Related Concepts:

• Identify the primary chemical name for 13-Hydroxyoctadecadienoic acid (13-HODE).: The primary chemical designation for 13-HODE is 13(S)-hydroxy-9Z,11E-octadecadienoic acid. This particular isomer is frequently the subject of investigation owing to its significant bioactivity.
• In addition to 13(S)-HODE, what other stereoisomer is frequently produced concurrently?: The synthesis of 13(S)-HODE is frequently accompanied by its stereoisomer, 13(R)-hydroxy-9Z,11E-octadecadienoic acid (13(R)-HODE). These isomers are distinguished by the spatial configuration of the hydroxyl group.

Related Concepts:

• State the chemical formula and approximate molar mass of 13-Hydroxyoctadecadienoic acid.: The molecular formula for 13-Hydroxyoctadecadienoic acid is C18H32O3, and its molar mass is approximately 296.451 g/mol. These fundamental properties define its molecular composition.
• Identify the primary chemical name for 13-Hydroxyoctadecadienoic acid (13-HODE).: The primary chemical designation for 13-HODE is 13(S)-hydroxy-9Z,11E-octadecadienoic acid. This particular isomer is frequently the subject of investigation owing to its significant bioactivity.

Related Concepts:

• Identify the primary chemical name for 13-Hydroxyoctadecadienoic acid (13-HODE).: The primary chemical designation for 13-HODE is 13(S)-hydroxy-9Z,11E-octadecadienoic acid. This particular isomer is frequently the subject of investigation owing to its significant bioactivity.
• State the chemical formula and approximate molar mass of 13-Hydroxyoctadecadienoic acid.: The molecular formula for 13-Hydroxyoctadecadienoic acid is C18H32O3, and its molar mass is approximately 296.451 g/mol. These fundamental properties define its molecular composition.

Related Concepts:

• Identify the primary chemical name for 13-Hydroxyoctadecadienoic acid (13-HODE).: The primary chemical designation for 13-HODE is 13(S)-hydroxy-9Z,11E-octadecadienoic acid. This particular isomer is frequently the subject of investigation owing to its significant bioactivity.
• In addition to 13(S)-HODE, what other stereoisomer is frequently produced concurrently?: The synthesis of 13(S)-HODE is frequently accompanied by its stereoisomer, 13(R)-hydroxy-9Z,11E-octadecadienoic acid (13(R)-HODE). These isomers are distinguished by the spatial configuration of the hydroxyl group.

Related Concepts:

• Identify the primary chemical name for 13-Hydroxyoctadecadienoic acid (13-HODE).: The primary chemical designation for 13-HODE is 13(S)-hydroxy-9Z,11E-octadecadienoic acid. This particular isomer is frequently the subject of investigation owing to its significant bioactivity.
• Under what circumstances is the generalized term '13-HODE' sometimes employed in scientific literature, even when specific isomers are potentially relevant?: The designation '13-HODE' is occasionally utilized generically when research studies have not differentiated between the specific isomers. This often occurs because many analytical methods employed for identification and quantification may lack the precision to distinguish between them, reflecting a common challenge in lipid mediator research.

Related Concepts:

• State the chemical formula and approximate molar mass of 13-Hydroxyoctadecadienoic acid.: The molecular formula for 13-Hydroxyoctadecadienoic acid is C18H32O3, and its molar mass is approximately 296.451 g/mol. These fundamental properties define its molecular composition.

Related Concepts:

• Describe the effects of 13-HODE and 9-HODE on neutrophils and natural killer cells.: 13-HODE and 9-HODE function as moderate stimulators of neutrophil chemotaxis (directed migration) in vitro. In contrast, their R-stereoisomers and 9(S)-HODE exhibit weak stimulatory effects on natural killer cell migration, potentially contributing to inflammatory responses.

Related Concepts:

• What cis-trans isomers of 13-HODE may also be generated during its synthesis?: Two additional naturally occurring isomers that may be found alongside 13(S)-HODE are 13(S)-hydroxy-9E,11E-octadecadienoic acid (13(S)-EE-HODE) and 13(R)-hydroxy-9E,11E-octadecadienoic acid (13(R)-EE-HODE). These isomers differ from the primary form in the configuration of their conjugated double bonds.
• Under what circumstances is the generalized term '13-HODE' sometimes employed in scientific literature, even when specific isomers are potentially relevant?: The designation '13-HODE' is occasionally utilized generically when research studies have not differentiated between the specific isomers. This often occurs because many analytical methods employed for identification and quantification may lack the precision to distinguish between them, reflecting a common challenge in lipid mediator research.
• Identify the primary chemical name for 13-Hydroxyoctadecadienoic acid (13-HODE).: The primary chemical designation for 13-HODE is 13(S)-hydroxy-9Z,11E-octadecadienoic acid. This particular isomer is frequently the subject of investigation owing to its significant bioactivity.

Related Concepts:

• Under what circumstances is the generalized term '13-HODE' sometimes employed in scientific literature, even when specific isomers are potentially relevant?: The designation '13-HODE' is occasionally utilized generically when research studies have not differentiated between the specific isomers. This often occurs because many analytical methods employed for identification and quantification may lack the precision to distinguish between them, reflecting a common challenge in lipid mediator research.
• Identify the primary chemical name for 13-Hydroxyoctadecadienoic acid (13-HODE).: The primary chemical designation for 13-HODE is 13(S)-hydroxy-9Z,11E-octadecadienoic acid. This particular isomer is frequently the subject of investigation owing to its significant bioactivity.

Related Concepts:

• Describe the stereochemical action of 15-lipoxygenase 1 (ALOX15) on linoleic acid.: ALOX15 operates with high stereospecificity, predominantly forming the 13(S)-hydroperoxy-9Z,11E-octadecadienoic acid (13(S)-HpODE) isomer. This stereochemical precision is crucial for the subsequent biological activities of the derived metabolites.
• Describe the difference in linoleic acid metabolism between 15-lipoxygenase 2 (ALOX15B) and 15-lipoxygenase 1 (ALOX15).: ALOX15B exhibits a pronounced preference for arachidonic acid over linoleic acid, rendering it comparatively less efficient in metabolizing linoleic acid to 13(S)-HpODE relative to ALOX15. Nevertheless, it can still contribute to the overall production of these metabolites.
• Identify the enzyme primarily recognized for catalyzing the conversion of linoleic acid into 13-hydroperoxy-9Z,11E-octadecadienoic acid (13-HpODE).: The enzyme 15-lipoxygenase 1 (ALOX15) is primarily recognized for catalyzing the conversion of linoleic acid into 13-hydroperoxy-9Z,11E-octadecadienoic acid (13(S)-HpODE). This represents a critical initial step in the biosynthetic pathway leading to 13-HODE.

Related Concepts:

• Which cyclooxygenase enzyme, COX-1 or COX-2, demonstrates a higher affinity for linoleic acid and consequently produces a greater quantity of 13(S)-HODE?: Cyclooxygenase 2 (COX-2) displays a superior preference for linoleic acid, leading to the production of substantially greater amounts of 13(S)-HODE compared to COX-1. Consequently, COX-2 is regarded as the principal COX enzyme responsible for 13(S)-HODE synthesis in cells co-expressing both enzymes.
• Identify the enzyme primarily recognized for catalyzing the conversion of linoleic acid into 13-hydroperoxy-9Z,11E-octadecadienoic acid (13-HpODE).: The enzyme 15-lipoxygenase 1 (ALOX15) is primarily recognized for catalyzing the conversion of linoleic acid into 13-hydroperoxy-9Z,11E-octadecadienoic acid (13(S)-HpODE). This represents a critical initial step in the biosynthetic pathway leading to 13-HODE.
• When cyclooxygenases 1 and 2 metabolize linoleic acid, what other HODE isomer is produced concurrently?: In addition to 13(S)-HODE, cyclooxygenases 1 and 2 also generate minor quantities of 9(R)-HODE during the metabolism of linoleic acid. This observation underscores the capacity of these enzymes to yield multiple hydroxylated fatty acid products from a single substrate.

Related Concepts:

• Is 15-lipoxygenase 1 capable of metabolizing linoleic acid when it is covalently bound to other molecules, such as phospholipids or cholesterol?: Affirmatively, ALOX15 demonstrates the capacity to metabolize linoleic acid even when it is esterified within phospholipid or cholesterol molecules, thereby generating the corresponding bound hydroperoxy and hydroxy products. This capability highlights its functional relevance within cellular membrane structures.
• Describe the difference in linoleic acid metabolism between 15-lipoxygenase 2 (ALOX15B) and 15-lipoxygenase 1 (ALOX15).: ALOX15B exhibits a pronounced preference for arachidonic acid over linoleic acid, rendering it comparatively less efficient in metabolizing linoleic acid to 13(S)-HpODE relative to ALOX15. Nevertheless, it can still contribute to the overall production of these metabolites.
• Identify the enzyme primarily recognized for catalyzing the conversion of linoleic acid into 13-hydroperoxy-9Z,11E-octadecadienoic acid (13-HpODE).: The enzyme 15-lipoxygenase 1 (ALOX15) is primarily recognized for catalyzing the conversion of linoleic acid into 13-hydroperoxy-9Z,11E-octadecadienoic acid (13(S)-HpODE). This represents a critical initial step in the biosynthetic pathway leading to 13-HODE.

Related Concepts:

• Describe the difference in linoleic acid metabolism between 15-lipoxygenase 2 (ALOX15B) and 15-lipoxygenase 1 (ALOX15).: ALOX15B exhibits a pronounced preference for arachidonic acid over linoleic acid, rendering it comparatively less efficient in metabolizing linoleic acid to 13(S)-HpODE relative to ALOX15. Nevertheless, it can still contribute to the overall production of these metabolites.
• Is 15-lipoxygenase 1 capable of metabolizing linoleic acid when it is covalently bound to other molecules, such as phospholipids or cholesterol?: Affirmatively, ALOX15 demonstrates the capacity to metabolize linoleic acid even when it is esterified within phospholipid or cholesterol molecules, thereby generating the corresponding bound hydroperoxy and hydroxy products. This capability highlights its functional relevance within cellular membrane structures.
• Describe the stereochemical action of 15-lipoxygenase 1 (ALOX15) on linoleic acid.: ALOX15 operates with high stereospecificity, predominantly forming the 13(S)-hydroperoxy-9Z,11E-octadecadienoic acid (13(S)-HpODE) isomer. This stereochemical precision is crucial for the subsequent biological activities of the derived metabolites.

Related Concepts:

• Which cyclooxygenase enzyme, COX-1 or COX-2, demonstrates a higher affinity for linoleic acid and consequently produces a greater quantity of 13(S)-HODE?: Cyclooxygenase 2 (COX-2) displays a superior preference for linoleic acid, leading to the production of substantially greater amounts of 13(S)-HODE compared to COX-1. Consequently, COX-2 is regarded as the principal COX enzyme responsible for 13(S)-HODE synthesis in cells co-expressing both enzymes.
• Identify the enzyme primarily recognized for catalyzing the conversion of linoleic acid into 13-hydroperoxy-9Z,11E-octadecadienoic acid (13-HpODE).: The enzyme 15-lipoxygenase 1 (ALOX15) is primarily recognized for catalyzing the conversion of linoleic acid into 13-hydroperoxy-9Z,11E-octadecadienoic acid (13(S)-HpODE). This represents a critical initial step in the biosynthetic pathway leading to 13-HODE.
• When cyclooxygenases 1 and 2 metabolize linoleic acid, what other HODE isomer is produced concurrently?: In addition to 13(S)-HODE, cyclooxygenases 1 and 2 also generate minor quantities of 9(R)-HODE during the metabolism of linoleic acid. This observation underscores the capacity of these enzymes to yield multiple hydroxylated fatty acid products from a single substrate.

Related Concepts:

• When cyclooxygenases 1 and 2 metabolize linoleic acid, what other HODE isomer is produced concurrently?: In addition to 13(S)-HODE, cyclooxygenases 1 and 2 also generate minor quantities of 9(R)-HODE during the metabolism of linoleic acid. This observation underscores the capacity of these enzymes to yield multiple hydroxylated fatty acid products from a single substrate.
• Which cyclooxygenase enzyme, COX-1 or COX-2, demonstrates a higher affinity for linoleic acid and consequently produces a greater quantity of 13(S)-HODE?: Cyclooxygenase 2 (COX-2) displays a superior preference for linoleic acid, leading to the production of substantially greater amounts of 13(S)-HODE compared to COX-1. Consequently, COX-2 is regarded as the principal COX enzyme responsible for 13(S)-HODE synthesis in cells co-expressing both enzymes.
• Describe the metabolic process of linoleic acid by Cytochrome P450 enzymes and the typical stereoisomeric outcome.: Microsomal Cytochrome P450 enzymes metabolize linoleic acid into a mixture comprising both 13-HODEs and 9-HODEs. These enzymatic reactions characteristically yield racemic mixtures, wherein both R and S stereoisomers are generated, with the R isomer frequently predominating (e.g., an approximate 80%/20% R/S ratio observed in human liver microsomes).

Related Concepts:

• Describe the metabolic process of linoleic acid by Cytochrome P450 enzymes and the typical stereoisomeric outcome.: Microsomal Cytochrome P450 enzymes metabolize linoleic acid into a mixture comprising both 13-HODEs and 9-HODEs. These enzymatic reactions characteristically yield racemic mixtures, wherein both R and S stereoisomers are generated, with the R isomer frequently predominating (e.g., an approximate 80%/20% R/S ratio observed in human liver microsomes).
• Which cyclooxygenase enzyme, COX-1 or COX-2, demonstrates a higher affinity for linoleic acid and consequently produces a greater quantity of 13(S)-HODE?: Cyclooxygenase 2 (COX-2) displays a superior preference for linoleic acid, leading to the production of substantially greater amounts of 13(S)-HODE compared to COX-1. Consequently, COX-2 is regarded as the principal COX enzyme responsible for 13(S)-HODE synthesis in cells co-expressing both enzymes.
• Identify the principal non-enzymatic pathways responsible for HODE production from linoleic acid and describe their typical stereoisomeric outcome.: Free radical and singlet oxygen oxidations constitute the primary non-enzymatic pathways for HODE generation from linoleic acid. These reactions are generally characterized by a lack of stereospecificity, resulting in the production of roughly equivalent quantities of the S and R stereoisomers.

Related Concepts:

• Identify the enzyme primarily recognized for catalyzing the conversion of linoleic acid into 13-hydroperoxy-9Z,11E-octadecadienoic acid (13-HpODE).: The enzyme 15-lipoxygenase 1 (ALOX15) is primarily recognized for catalyzing the conversion of linoleic acid into 13-hydroperoxy-9Z,11E-octadecadienoic acid (13(S)-HpODE). This represents a critical initial step in the biosynthetic pathway leading to 13-HODE.
• Describe the metabolic process of linoleic acid by Cytochrome P450 enzymes and the typical stereoisomeric outcome.: Microsomal Cytochrome P450 enzymes metabolize linoleic acid into a mixture comprising both 13-HODEs and 9-HODEs. These enzymatic reactions characteristically yield racemic mixtures, wherein both R and S stereoisomers are generated, with the R isomer frequently predominating (e.g., an approximate 80%/20% R/S ratio observed in human liver microsomes).
• Describe the difference in linoleic acid metabolism between 15-lipoxygenase 2 (ALOX15B) and 15-lipoxygenase 1 (ALOX15).: ALOX15B exhibits a pronounced preference for arachidonic acid over linoleic acid, rendering it comparatively less efficient in metabolizing linoleic acid to 13(S)-HpODE relative to ALOX15. Nevertheless, it can still contribute to the overall production of these metabolites.

Related Concepts:

• Which cyclooxygenase enzyme, COX-1 or COX-2, demonstrates a higher affinity for linoleic acid and consequently produces a greater quantity of 13(S)-HODE?: Cyclooxygenase 2 (COX-2) displays a superior preference for linoleic acid, leading to the production of substantially greater amounts of 13(S)-HODE compared to COX-1. Consequently, COX-2 is regarded as the principal COX enzyme responsible for 13(S)-HODE synthesis in cells co-expressing both enzymes.
• When cyclooxygenases 1 and 2 metabolize linoleic acid, what other HODE isomer is produced concurrently?: In addition to 13(S)-HODE, cyclooxygenases 1 and 2 also generate minor quantities of 9(R)-HODE during the metabolism of linoleic acid. This observation underscores the capacity of these enzymes to yield multiple hydroxylated fatty acid products from a single substrate.
• Describe the difference in linoleic acid metabolism between 15-lipoxygenase 2 (ALOX15B) and 15-lipoxygenase 1 (ALOX15).: ALOX15B exhibits a pronounced preference for arachidonic acid over linoleic acid, rendering it comparatively less efficient in metabolizing linoleic acid to 13(S)-HpODE relative to ALOX15. Nevertheless, it can still contribute to the overall production of these metabolites.

Related Concepts:

• Describe the metabolic process of linoleic acid by Cytochrome P450 enzymes and the typical stereoisomeric outcome.: Microsomal Cytochrome P450 enzymes metabolize linoleic acid into a mixture comprising both 13-HODEs and 9-HODEs. These enzymatic reactions characteristically yield racemic mixtures, wherein both R and S stereoisomers are generated, with the R isomer frequently predominating (e.g., an approximate 80%/20% R/S ratio observed in human liver microsomes).
• Identify the principal non-enzymatic pathways responsible for HODE production from linoleic acid and describe their typical stereoisomeric outcome.: Free radical and singlet oxygen oxidations constitute the primary non-enzymatic pathways for HODE generation from linoleic acid. These reactions are generally characterized by a lack of stereospecificity, resulting in the production of roughly equivalent quantities of the S and R stereoisomers.

Related Concepts:

• Describe the difference in linoleic acid metabolism between 15-lipoxygenase 2 (ALOX15B) and 15-lipoxygenase 1 (ALOX15).: ALOX15B exhibits a pronounced preference for arachidonic acid over linoleic acid, rendering it comparatively less efficient in metabolizing linoleic acid to 13(S)-HpODE relative to ALOX15. Nevertheless, it can still contribute to the overall production of these metabolites.
• Is 15-lipoxygenase 1 capable of metabolizing linoleic acid when it is covalently bound to other molecules, such as phospholipids or cholesterol?: Affirmatively, ALOX15 demonstrates the capacity to metabolize linoleic acid even when it is esterified within phospholipid or cholesterol molecules, thereby generating the corresponding bound hydroperoxy and hydroxy products. This capability highlights its functional relevance within cellular membrane structures.
• Identify the enzyme primarily recognized for catalyzing the conversion of linoleic acid into 13-hydroperoxy-9Z,11E-octadecadienoic acid (13-HpODE).: The enzyme 15-lipoxygenase 1 (ALOX15) is primarily recognized for catalyzing the conversion of linoleic acid into 13-hydroperoxy-9Z,11E-octadecadienoic acid (13(S)-HpODE). This represents a critical initial step in the biosynthetic pathway leading to 13-HODE.

Related Concepts:

• Identify the principal non-enzymatic pathways responsible for HODE production from linoleic acid and describe their typical stereoisomeric outcome.: Free radical and singlet oxygen oxidations constitute the primary non-enzymatic pathways for HODE generation from linoleic acid. These reactions are generally characterized by a lack of stereospecificity, resulting in the production of roughly equivalent quantities of the S and R stereoisomers.
• What is the significance of the stereochemistry (S versus R configuration) of 13-HODE in the context of atherosclerotic plaque progression?: The observation that early atherosclerotic plaques predominantly contain the S-isomer of 13-HODE, whereas mature plaques exhibit comparable amounts of both S and R isomers, suggests that distinct metabolic pathways (e.g., 15-LOX-1 contributing the S-isomer, and cytochrome/free radical pathways contributing the R-isomer) play differential roles in plaque development over time.
• Define 13-oxoODE and explain its formation from 13(S)-HODE.: 13-oxoODE is a metabolite formed when 13(S)-HODE undergoes oxidation, catalyzed by an NAD+-dependent 13-HODE dehydrogenase enzyme. This process converts the hydroxyl group into a ketone functional group, yielding a distinct metabolite.

Related Concepts:

• Describe the intracellular transformation of 13(S)-HpODE into 13(S)-HODE.: Intracellularly, 13(S)-HpODE undergoes rapid reduction, catalyzed by peroxidases, to yield 13(S)-HODE. This enzymatic reduction is a characteristic step in the metabolic processing of lipid hydroperoxides, converting them into more stable hydroxylated derivatives.
• Define 13-oxoODE and explain its formation from 13(S)-HODE.: 13-oxoODE is a metabolite formed when 13(S)-HODE undergoes oxidation, catalyzed by an NAD+-dependent 13-HODE dehydrogenase enzyme. This process converts the hydroxyl group into a ketone functional group, yielding a distinct metabolite.
• Describe the typical metabolic fate or incorporation of 13(S)-HODE into cellular structures.: 13(S)-HODE undergoes rapid and quantitative incorporation into cellular phospholipids, becoming esterified within cell membranes. This incorporation is a fundamental aspect of its cellular fate and its potential roles in signaling processes.

Related Concepts:

• Define 4-Hydroxynonenal (HNE) and elucidate its relationship to 13-HpODE.: 4-Hydroxynonenal (HNE) is recognized as a product of lipid peroxidation that is generated from 13-HpODE. HNE is a reactive aldehyde implicated in cellular damage and is frequently investigated within the context of oxidative stress.
• Describe the intracellular transformation of 13(S)-HpODE into 13(S)-HODE.: Intracellularly, 13(S)-HpODE undergoes rapid reduction, catalyzed by peroxidases, to yield 13(S)-HODE. This enzymatic reduction is a characteristic step in the metabolic processing of lipid hydroperoxides, converting them into more stable hydroxylated derivatives.
• Define 13-oxoODE and explain its formation from 13(S)-HODE.: 13-oxoODE is a metabolite formed when 13(S)-HODE undergoes oxidation, catalyzed by an NAD+-dependent 13-HODE dehydrogenase enzyme. This process converts the hydroxyl group into a ketone functional group, yielding a distinct metabolite.

Related Concepts:

• Describe the typical metabolic fate or incorporation of 13(S)-HODE into cellular structures.: 13(S)-HODE undergoes rapid and quantitative incorporation into cellular phospholipids, becoming esterified within cell membranes. This incorporation is a fundamental aspect of its cellular fate and its potential roles in signaling processes.
• Describe the intracellular transformation of 13(S)-HpODE into 13(S)-HODE.: Intracellularly, 13(S)-HpODE undergoes rapid reduction, catalyzed by peroxidases, to yield 13(S)-HODE. This enzymatic reduction is a characteristic step in the metabolic processing of lipid hydroperoxides, converting them into more stable hydroxylated derivatives.
• What role is suggested for phospholipid-bound 13(S)-HODE in the process of red blood cell maturation?: The accumulation of phospholipid-bound 13(S)-HODE within mitochondrial membranes is proposed as a critical event that initiates mitochondrial degradation. This process is essential for facilitating the maturation of reticulocytes into erythrocytes, underscoring its role in cellular differentiation.

Related Concepts:

• Define 13-oxoODE and explain its formation from 13(S)-HODE.: 13-oxoODE is a metabolite formed when 13(S)-HODE undergoes oxidation, catalyzed by an NAD+-dependent 13-HODE dehydrogenase enzyme. This process converts the hydroxyl group into a ketone functional group, yielding a distinct metabolite.
• Describe the intracellular transformation of 13(S)-HpODE into 13(S)-HODE.: Intracellularly, 13(S)-HpODE undergoes rapid reduction, catalyzed by peroxidases, to yield 13(S)-HODE. This enzymatic reduction is a characteristic step in the metabolic processing of lipid hydroperoxides, converting them into more stable hydroxylated derivatives.

Related Concepts:

• Describe the process by which 13-oxoODE can be conjugated with glutathione and elucidate the significance of this reaction.: 13-oxoODE can react with glutathione through either non-enzymatic Michael addition or enzymatic conjugation mediated by glutathione transferases. This conjugation generates products that are frequently exported from the cell, potentially serving to mitigate the intracellular activity of 13-oxoODE.
• Describe the intracellular transformation of 13(S)-HpODE into 13(S)-HODE.: Intracellularly, 13(S)-HpODE undergoes rapid reduction, catalyzed by peroxidases, to yield 13(S)-HODE. This enzymatic reduction is a characteristic step in the metabolic processing of lipid hydroperoxides, converting them into more stable hydroxylated derivatives.

Related Concepts:

• What role is suggested for phospholipid-bound 13(S)-HODE in the process of red blood cell maturation?: The accumulation of phospholipid-bound 13(S)-HODE within mitochondrial membranes is proposed as a critical event that initiates mitochondrial degradation. This process is essential for facilitating the maturation of reticulocytes into erythrocytes, underscoring its role in cellular differentiation.
• Describe the typical metabolic fate or incorporation of 13(S)-HODE into cellular structures.: 13(S)-HODE undergoes rapid and quantitative incorporation into cellular phospholipids, becoming esterified within cell membranes. This incorporation is a fundamental aspect of its cellular fate and its potential roles in signaling processes.

Related Concepts:

• Describe the intracellular transformation of 13(S)-HpODE into 13(S)-HODE.: Intracellularly, 13(S)-HpODE undergoes rapid reduction, catalyzed by peroxidases, to yield 13(S)-HODE. This enzymatic reduction is a characteristic step in the metabolic processing of lipid hydroperoxides, converting them into more stable hydroxylated derivatives.
• Define 13-oxoODE and explain its formation from 13(S)-HODE.: 13-oxoODE is a metabolite formed when 13(S)-HODE undergoes oxidation, catalyzed by an NAD+-dependent 13-HODE dehydrogenase enzyme. This process converts the hydroxyl group into a ketone functional group, yielding a distinct metabolite.
• Describe the typical metabolic fate or incorporation of 13(S)-HODE into cellular structures.: 13(S)-HODE undergoes rapid and quantitative incorporation into cellular phospholipids, becoming esterified within cell membranes. This incorporation is a fundamental aspect of its cellular fate and its potential roles in signaling processes.

Related Concepts:

• Describe the typical metabolic fate or incorporation of 13(S)-HODE into cellular structures.: 13(S)-HODE undergoes rapid and quantitative incorporation into cellular phospholipids, becoming esterified within cell membranes. This incorporation is a fundamental aspect of its cellular fate and its potential roles in signaling processes.
• Describe the intracellular transformation of 13(S)-HpODE into 13(S)-HODE.: Intracellularly, 13(S)-HpODE undergoes rapid reduction, catalyzed by peroxidases, to yield 13(S)-HODE. This enzymatic reduction is a characteristic step in the metabolic processing of lipid hydroperoxides, converting them into more stable hydroxylated derivatives.
• What role is suggested for phospholipid-bound 13(S)-HODE in the process of red blood cell maturation?: The accumulation of phospholipid-bound 13(S)-HODE within mitochondrial membranes is proposed as a critical event that initiates mitochondrial degradation. This process is essential for facilitating the maturation of reticulocytes into erythrocytes, underscoring its role in cellular differentiation.

Related Concepts:

• Describe the process by which 13-oxoODE can be conjugated with glutathione and elucidate the significance of this reaction.: 13-oxoODE can react with glutathione through either non-enzymatic Michael addition or enzymatic conjugation mediated by glutathione transferases. This conjugation generates products that are frequently exported from the cell, potentially serving to mitigate the intracellular activity of 13-oxoODE.
• Define 13-oxoODE and explain its formation from 13(S)-HODE.: 13-oxoODE is a metabolite formed when 13(S)-HODE undergoes oxidation, catalyzed by an NAD+-dependent 13-HODE dehydrogenase enzyme. This process converts the hydroxyl group into a ketone functional group, yielding a distinct metabolite.
• Describe the intracellular transformation of 13(S)-HpODE into 13(S)-HODE.: Intracellularly, 13(S)-HpODE undergoes rapid reduction, catalyzed by peroxidases, to yield 13(S)-HODE. This enzymatic reduction is a characteristic step in the metabolic processing of lipid hydroperoxides, converting them into more stable hydroxylated derivatives.

Related Concepts:

• What role is suggested for phospholipid-bound 13(S)-HODE in the process of red blood cell maturation?: The accumulation of phospholipid-bound 13(S)-HODE within mitochondrial membranes is proposed as a critical event that initiates mitochondrial degradation. This process is essential for facilitating the maturation of reticulocytes into erythrocytes, underscoring its role in cellular differentiation.
• Describe the typical metabolic fate or incorporation of 13(S)-HODE into cellular structures.: 13(S)-HODE undergoes rapid and quantitative incorporation into cellular phospholipids, becoming esterified within cell membranes. This incorporation is a fundamental aspect of its cellular fate and its potential roles in signaling processes.

Related Concepts:

• What role is suggested for phospholipid-bound 13(S)-HODE in the process of red blood cell maturation?: The accumulation of phospholipid-bound 13(S)-HODE within mitochondrial membranes is proposed as a critical event that initiates mitochondrial degradation. This process is essential for facilitating the maturation of reticulocytes into erythrocytes, underscoring its role in cellular differentiation.
• Describe the typical metabolic fate or incorporation of 13(S)-HODE into cellular structures.: 13(S)-HODE undergoes rapid and quantitative incorporation into cellular phospholipids, becoming esterified within cell membranes. This incorporation is a fundamental aspect of its cellular fate and its potential roles in signaling processes.

Related Concepts:

• Define 'OXLAMs' and describe the physiological role that has been proposed for them.: OXLAMs is an acronym for oxidized linoleic acid metabolites, encompassing various HODEs and their ketone derivatives, such as 13-oxoODE. These compounds have been implicated in signaling pathways associated with pain perception, suggesting a role in sensory transduction processes.

Related Concepts:

• What roles have been proposed for 13-HODE and its related metabolites concerning the stimulation of peroxisome proliferator-activated receptors (PPARs)?: 13-HODE, in conjunction with 13-oxoODE and 13-EE-HODE, possesses the capacity to directly activate the peroxisome proliferator-activated receptor gamma (PPARγ). This activation is hypothesized to be responsible for inducing specific gene transcription and fostering the maturation of monocytes into macrophages. Activation of PPARβ has also been noted.

Related Concepts:

• Beyond PPARs, which receptor is stimulated by 13-HODE and related oxidized linoleic acid metabolites (OXLAMs)?: 13-HODE and related OXLAMs also stimulate the transient receptor potential vanilloid 1 (TRPV1) receptor, also identified as the capsaicin receptor or vanilloid receptor 1. This interaction is posited to be involved in the mediation of pain sensation.
• In the context of asthma, what is the significance of the interaction between 13(S)-HODE and the TRPV1 receptor?: The interaction of 13(S)-HODE with TRPV1 is significant due to the high expression of TRPV1 in airway epithelial cells. Furthermore, blockade of this receptor has been shown to inhibit airway responses elicited by 13(S)-HODE, suggesting a potential mechanistic link between 13-HODE and airway pathology in severe asthma.
• What are the potential therapeutic implications of targeting pathways involving 13-HODE in diseases such as atherosclerosis or asthma?: Strategies targeting the pathways responsible for the production or utilization of 13-HODE, such as the inhibition of 15-LOX-1 or the blockade of TRPV1 activation, are under investigation as potential therapeutic interventions for conditions including atherosclerosis and severe asthma. This underscores the molecule's significance in the realm of drug development.

Related Concepts:

• In the context of asthma, what is the significance of the interaction between 13(S)-HODE and the TRPV1 receptor?: The interaction of 13(S)-HODE with TRPV1 is significant due to the high expression of TRPV1 in airway epithelial cells. Furthermore, blockade of this receptor has been shown to inhibit airway responses elicited by 13(S)-HODE, suggesting a potential mechanistic link between 13-HODE and airway pathology in severe asthma.
• What are the potential therapeutic implications of targeting pathways involving 13-HODE in diseases such as atherosclerosis or asthma?: Strategies targeting the pathways responsible for the production or utilization of 13-HODE, such as the inhibition of 15-LOX-1 or the blockade of TRPV1 activation, are under investigation as potential therapeutic interventions for conditions including atherosclerosis and severe asthma. This underscores the molecule's significance in the realm of drug development.

Related Concepts:

• What roles have been proposed for 13-HODE and its related metabolites concerning the stimulation of peroxisome proliferator-activated receptors (PPARs)?: 13-HODE, in conjunction with 13-oxoODE and 13-EE-HODE, possesses the capacity to directly activate the peroxisome proliferator-activated receptor gamma (PPARγ). This activation is hypothesized to be responsible for inducing specific gene transcription and fostering the maturation of monocytes into macrophages. Activation of PPARβ has also been noted.

Related Concepts:

• Define 'OXLAMs' and describe the physiological role that has been proposed for them.: OXLAMs is an acronym for oxidized linoleic acid metabolites, encompassing various HODEs and their ketone derivatives, such as 13-oxoODE. These compounds have been implicated in signaling pathways associated with pain perception, suggesting a role in sensory transduction processes.

Related Concepts:

• What roles have been proposed for 13-HODE and its related metabolites concerning the stimulation of peroxisome proliferator-activated receptors (PPARs)?: 13-HODE, in conjunction with 13-oxoODE and 13-EE-HODE, possesses the capacity to directly activate the peroxisome proliferator-activated receptor gamma (PPARγ). This activation is hypothesized to be responsible for inducing specific gene transcription and fostering the maturation of monocytes into macrophages. Activation of PPARβ has also been noted.

Related Concepts:

• In the context of asthma, what is the significance of the interaction between 13(S)-HODE and the TRPV1 receptor?: The interaction of 13(S)-HODE with TRPV1 is significant due to the high expression of TRPV1 in airway epithelial cells. Furthermore, blockade of this receptor has been shown to inhibit airway responses elicited by 13(S)-HODE, suggesting a potential mechanistic link between 13-HODE and airway pathology in severe asthma.
• Describe the observed effect of 13(S)-HODE on airway hyperresponsiveness in animal models and discuss its potential relationship to asthma.: In experimental models, specifically in guinea pigs, 13(S)-HODE induces airway narrowing and replicates asthmatic hypersensitivity by potentiating responses to bronchoconstrictors. This finding suggests a direct involvement of 13-HODE in the pathophysiology of asthma.

Related Concepts:

• Describe the effects of 13-HODE and 9-HODE on neutrophils and natural killer cells.: 13-HODE and 9-HODE function as moderate stimulators of neutrophil chemotaxis (directed migration) in vitro. In contrast, their R-stereoisomers and 9(S)-HODE exhibit weak stimulatory effects on natural killer cell migration, potentially contributing to inflammatory responses.
• Describe the role of 13-HODE in the context of breast cancer cell growth.: 13(S)-HODE appears to promote the growth of human breast cancer cells by stimulating their proliferation and potentially mediating the effects of growth factors. Elevated concentrations observed in tumor tissues further corroborate its role in cancer progression.
• What roles have been proposed for 13-HODE and its related metabolites concerning the stimulation of peroxisome proliferator-activated receptors (PPARs)?: 13-HODE, in conjunction with 13-oxoODE and 13-EE-HODE, possesses the capacity to directly activate the peroxisome proliferator-activated receptor gamma (PPARγ). This activation is hypothesized to be responsible for inducing specific gene transcription and fostering the maturation of monocytes into macrophages. Activation of PPARβ has also been noted.

Related Concepts:

• Describe the observed presence of 13-HODE in atheromatous plaques and infer its suggested role in atherosclerosis.: 13-HODE is identified as a dominant component within atheromatous plaques in the context of atherosclerosis, frequently found esterified to cholesterol and phospholipids. Its substantial presence strongly suggests a significant role in the pathogenesis and progression of this cardiovascular disease.
• What is the significance of the stereochemistry (S versus R configuration) of 13-HODE in the context of atherosclerotic plaque progression?: The observation that early atherosclerotic plaques predominantly contain the S-isomer of 13-HODE, whereas mature plaques exhibit comparable amounts of both S and R isomers, suggests that distinct metabolic pathways (e.g., 15-LOX-1 contributing the S-isomer, and cytochrome/free radical pathways contributing the R-isomer) play differential roles in plaque development over time.
• Elucidate the contribution of 13(S)-HODE to the progression of atherosclerosis via the PPARγ pathway.: 13(S)-HODE activates the transcription factor PPARγ, which subsequently upregulates the expression of CD36 and aP2 receptors on macrophages. This upregulation results in enhanced lipid uptake, leading to foam cell formation and potentially macrophage apoptosis, collectively contributing to atherosclerotic plaque expansion.

Related Concepts:

• Elucidate the contribution of 13(S)-HODE to the progression of atherosclerosis via the PPARγ pathway.: 13(S)-HODE activates the transcription factor PPARγ, which subsequently upregulates the expression of CD36 and aP2 receptors on macrophages. This upregulation results in enhanced lipid uptake, leading to foam cell formation and potentially macrophage apoptosis, collectively contributing to atherosclerotic plaque expansion.

Related Concepts:

• Describe the observed effect of 13(S)-HODE on airway hyperresponsiveness in animal models and discuss its potential relationship to asthma.: In experimental models, specifically in guinea pigs, 13(S)-HODE induces airway narrowing and replicates asthmatic hypersensitivity by potentiating responses to bronchoconstrictors. This finding suggests a direct involvement of 13-HODE in the pathophysiology of asthma.
• In the context of asthma, what is the significance of the interaction between 13(S)-HODE and the TRPV1 receptor?: The interaction of 13(S)-HODE with TRPV1 is significant due to the high expression of TRPV1 in airway epithelial cells. Furthermore, blockade of this receptor has been shown to inhibit airway responses elicited by 13(S)-HODE, suggesting a potential mechanistic link between 13-HODE and airway pathology in severe asthma.

Related Concepts:

• Describe the relationship observed between 15-lipoxygenase 1, 13-HODE, and the progression of colon cancer.: Research findings indicate progressive decreases in both 15-lipoxygenase 1 and its metabolite, 13-HODE, as colon cancer advances from polyp to malignant stages. Conversely, elevated levels of 15-LOX 1 and 13-HODE appear to exert an inhibitory effect on cancer development, suggesting a potential tumor-suppressive role in this context.

Related Concepts:

• Describe the role of 13-HODE in the context of breast cancer cell growth.: 13(S)-HODE appears to promote the growth of human breast cancer cells by stimulating their proliferation and potentially mediating the effects of growth factors. Elevated concentrations observed in tumor tissues further corroborate its role in cancer progression.
• What effect does 13-HODE exert on human breast cancer cells, and what implications does this have regarding its role in cancer progression?: 13(S)-HODE has been observed to stimulate the proliferation of diverse human breast cancer cell lines in vitro and appears requisite for growth factor-mediated proliferation. This observation suggests that 13(S)-HODE may contribute to the promotion of breast cancer growth in humans.
• Describe the role of 13-HODE in the context of colon cancer cell proliferation and apoptosis.: 13(S)-HODE has been demonstrated to inhibit the proliferation and induce apoptosis (programmed cell death) in human colon cancer cells cultured in vitro. This finding suggests a potential anti-cancer effect attributable to this metabolite.

Related Concepts:

• Describe the relationship between 15-lipoxygenase 1 (15-LOX 1) expression and the progression and severity of prostate cancer.: 15-LOX 1 exhibits overexpression in prostate cancerous tissue relative to normal tissue. Furthermore, its expression levels demonstrate a positive correlation with cancer proliferation rates and severity (as indicated by Gleason score). The activity of this enzyme, predominantly via 13(S)-HODE production, appears to foster prostate cancer growth and survival.

Related Concepts:

• In which specific diseases have elevated levels of 13-HODE been observed?: Elevated concentrations of 13-HODE have been documented in association with various pathological conditions, including rheumatoid arthritis, diabetes mellitus, polycystic kidney disease, chronic pancreatitis, steatohepatitis (both alcoholic and non-alcoholic), Alzheimer's disease, and vascular dementia. These observations suggest a correlation between 13-HODE and diseases characterized by oxidative stress or inflammatory processes.
• Describe the observed presence of 13-HODE in atheromatous plaques and infer its suggested role in atherosclerosis.: 13-HODE is identified as a dominant component within atheromatous plaques in the context of atherosclerosis, frequently found esterified to cholesterol and phospholipids. Its substantial presence strongly suggests a significant role in the pathogenesis and progression of this cardiovascular disease.
• What are the potential therapeutic implications of targeting pathways involving 13-HODE in diseases such as atherosclerosis or asthma?: Strategies targeting the pathways responsible for the production or utilization of 13-HODE, such as the inhibition of 15-LOX-1 or the blockade of TRPV1 activation, are under investigation as potential therapeutic interventions for conditions including atherosclerosis and severe asthma. This underscores the molecule's significance in the realm of drug development.

Related Concepts:

• Elucidate the contribution of 13(S)-HODE to the progression of atherosclerosis via the PPARγ pathway.: 13(S)-HODE activates the transcription factor PPARγ, which subsequently upregulates the expression of CD36 and aP2 receptors on macrophages. This upregulation results in enhanced lipid uptake, leading to foam cell formation and potentially macrophage apoptosis, collectively contributing to atherosclerotic plaque expansion.

Related Concepts:

• Describe the observed effect of 13(S)-HODE on airway hyperresponsiveness in animal models and discuss its potential relationship to asthma.: In experimental models, specifically in guinea pigs, 13(S)-HODE induces airway narrowing and replicates asthmatic hypersensitivity by potentiating responses to bronchoconstrictors. This finding suggests a direct involvement of 13-HODE in the pathophysiology of asthma.
• In the context of asthma, what is the significance of the interaction between 13(S)-HODE and the TRPV1 receptor?: The interaction of 13(S)-HODE with TRPV1 is significant due to the high expression of TRPV1 in airway epithelial cells. Furthermore, blockade of this receptor has been shown to inhibit airway responses elicited by 13(S)-HODE, suggesting a potential mechanistic link between 13-HODE and airway pathology in severe asthma.

Related Concepts:

• Describe the role of 13-HODE in the context of breast cancer cell growth.: 13(S)-HODE appears to promote the growth of human breast cancer cells by stimulating their proliferation and potentially mediating the effects of growth factors. Elevated concentrations observed in tumor tissues further corroborate its role in cancer progression.
• What effect does 13-HODE exert on human breast cancer cells, and what implications does this have regarding its role in cancer progression?: 13(S)-HODE has been observed to stimulate the proliferation of diverse human breast cancer cell lines in vitro and appears requisite for growth factor-mediated proliferation. This observation suggests that 13(S)-HODE may contribute to the promotion of breast cancer growth in humans.

Related Concepts:

• What is the significance of the stereochemistry (S versus R configuration) of 13-HODE in the context of atherosclerotic plaque progression?: The observation that early atherosclerotic plaques predominantly contain the S-isomer of 13-HODE, whereas mature plaques exhibit comparable amounts of both S and R isomers, suggests that distinct metabolic pathways (e.g., 15-LOX-1 contributing the S-isomer, and cytochrome/free radical pathways contributing the R-isomer) play differential roles in plaque development over time.
• Describe the observed presence of 13-HODE in atheromatous plaques and infer its suggested role in atherosclerosis.: 13-HODE is identified as a dominant component within atheromatous plaques in the context of atherosclerosis, frequently found esterified to cholesterol and phospholipids. Its substantial presence strongly suggests a significant role in the pathogenesis and progression of this cardiovascular disease.
• Elucidate the contribution of 13(S)-HODE to the progression of atherosclerosis via the PPARγ pathway.: 13(S)-HODE activates the transcription factor PPARγ, which subsequently upregulates the expression of CD36 and aP2 receptors on macrophages. This upregulation results in enhanced lipid uptake, leading to foam cell formation and potentially macrophage apoptosis, collectively contributing to atherosclerotic plaque expansion.

Related Concepts:

• Describe the role of 13-HODE in the context of breast cancer cell growth.: 13(S)-HODE appears to promote the growth of human breast cancer cells by stimulating their proliferation and potentially mediating the effects of growth factors. Elevated concentrations observed in tumor tissues further corroborate its role in cancer progression.
• Describe the role of 13-HODE in the context of colon cancer cell proliferation and apoptosis.: 13(S)-HODE has been demonstrated to inhibit the proliferation and induce apoptosis (programmed cell death) in human colon cancer cells cultured in vitro. This finding suggests a potential anti-cancer effect attributable to this metabolite.
• What effect does 13-HODE exert on human breast cancer cells, and what implications does this have regarding its role in cancer progression?: 13(S)-HODE has been observed to stimulate the proliferation of diverse human breast cancer cell lines in vitro and appears requisite for growth factor-mediated proliferation. This observation suggests that 13(S)-HODE may contribute to the promotion of breast cancer growth in humans.

Related Concepts:

• What are the potential therapeutic implications of targeting pathways involving 13-HODE in diseases such as atherosclerosis or asthma?: Strategies targeting the pathways responsible for the production or utilization of 13-HODE, such as the inhibition of 15-LOX-1 or the blockade of TRPV1 activation, are under investigation as potential therapeutic interventions for conditions including atherosclerosis and severe asthma. This underscores the molecule's significance in the realm of drug development.

Related Concepts:

• What role is suggested for phospholipid-bound 13(S)-HODE in the process of red blood cell maturation?: The accumulation of phospholipid-bound 13(S)-HODE within mitochondrial membranes is proposed as a critical event that initiates mitochondrial degradation. This process is essential for facilitating the maturation of reticulocytes into erythrocytes, underscoring its role in cellular differentiation.

Related Concepts:

• Elucidate the contribution of 13(S)-HODE to the progression of atherosclerosis via the PPARγ pathway.: 13(S)-HODE activates the transcription factor PPARγ, which subsequently upregulates the expression of CD36 and aP2 receptors on macrophages. This upregulation results in enhanced lipid uptake, leading to foam cell formation and potentially macrophage apoptosis, collectively contributing to atherosclerotic plaque expansion.
• Describe the observed presence of 13-HODE in atheromatous plaques and infer its suggested role in atherosclerosis.: 13-HODE is identified as a dominant component within atheromatous plaques in the context of atherosclerosis, frequently found esterified to cholesterol and phospholipids. Its substantial presence strongly suggests a significant role in the pathogenesis and progression of this cardiovascular disease.

Related Concepts:

• In which specific diseases have elevated levels of 13-HODE been observed?: Elevated concentrations of 13-HODE have been documented in association with various pathological conditions, including rheumatoid arthritis, diabetes mellitus, polycystic kidney disease, chronic pancreatitis, steatohepatitis (both alcoholic and non-alcoholic), Alzheimer's disease, and vascular dementia. These observations suggest a correlation between 13-HODE and diseases characterized by oxidative stress or inflammatory processes.
• Describe the observed presence of 13-HODE in atheromatous plaques and infer its suggested role in atherosclerosis.: 13-HODE is identified as a dominant component within atheromatous plaques in the context of atherosclerosis, frequently found esterified to cholesterol and phospholipids. Its substantial presence strongly suggests a significant role in the pathogenesis and progression of this cardiovascular disease.
• Describe the role of 13-HODE in the context of breast cancer cell growth.: 13(S)-HODE appears to promote the growth of human breast cancer cells by stimulating their proliferation and potentially mediating the effects of growth factors. Elevated concentrations observed in tumor tissues further corroborate its role in cancer progression.

Related Concepts:

• What effect does 13-HODE exert on human breast cancer cells, and what implications does this have regarding its role in cancer progression?: 13(S)-HODE has been observed to stimulate the proliferation of diverse human breast cancer cell lines in vitro and appears requisite for growth factor-mediated proliferation. This observation suggests that 13(S)-HODE may contribute to the promotion of breast cancer growth in humans.
• Describe the role of 13-HODE in the context of breast cancer cell growth.: 13(S)-HODE appears to promote the growth of human breast cancer cells by stimulating their proliferation and potentially mediating the effects of growth factors. Elevated concentrations observed in tumor tissues further corroborate its role in cancer progression.
• Describe the role of 13-HODE in the context of colon cancer cell proliferation and apoptosis.: 13(S)-HODE has been demonstrated to inhibit the proliferation and induce apoptosis (programmed cell death) in human colon cancer cells cultured in vitro. This finding suggests a potential anti-cancer effect attributable to this metabolite.

Related Concepts:

• Describe the relationship observed between 15-lipoxygenase 1, 13-HODE, and the progression of colon cancer.: Research findings indicate progressive decreases in both 15-lipoxygenase 1 and its metabolite, 13-HODE, as colon cancer advances from polyp to malignant stages. Conversely, elevated levels of 15-LOX 1 and 13-HODE appear to exert an inhibitory effect on cancer development, suggesting a potential tumor-suppressive role in this context.

Related Concepts:

• Describe the relationship between 15-lipoxygenase 1 (15-LOX 1) expression and the progression and severity of prostate cancer.: 15-LOX 1 exhibits overexpression in prostate cancerous tissue relative to normal tissue. Furthermore, its expression levels demonstrate a positive correlation with cancer proliferation rates and severity (as indicated by Gleason score). The activity of this enzyme, predominantly via 13(S)-HODE production, appears to foster prostate cancer growth and survival.

Related Concepts:

• Describe the typical metabolic fate or incorporation of 13(S)-HODE into cellular structures.: 13(S)-HODE undergoes rapid and quantitative incorporation into cellular phospholipids, becoming esterified within cell membranes. This incorporation is a fundamental aspect of its cellular fate and its potential roles in signaling processes.

Related Concepts:

• Describe the role of 13-HODE in the context of breast cancer cell growth.: 13(S)-HODE appears to promote the growth of human breast cancer cells by stimulating their proliferation and potentially mediating the effects of growth factors. Elevated concentrations observed in tumor tissues further corroborate its role in cancer progression.
• What effect does 13-HODE exert on human breast cancer cells, and what implications does this have regarding its role in cancer progression?: 13(S)-HODE has been observed to stimulate the proliferation of diverse human breast cancer cell lines in vitro and appears requisite for growth factor-mediated proliferation. This observation suggests that 13(S)-HODE may contribute to the promotion of breast cancer growth in humans.

Related Concepts:

• In which specific diseases have elevated levels of 13-HODE been observed?: Elevated concentrations of 13-HODE have been documented in association with various pathological conditions, including rheumatoid arthritis, diabetes mellitus, polycystic kidney disease, chronic pancreatitis, steatohepatitis (both alcoholic and non-alcoholic), Alzheimer's disease, and vascular dementia. These observations suggest a correlation between 13-HODE and diseases characterized by oxidative stress or inflammatory processes.
• Describe the role of 13-HODE in the context of breast cancer cell growth.: 13(S)-HODE appears to promote the growth of human breast cancer cells by stimulating their proliferation and potentially mediating the effects of growth factors. Elevated concentrations observed in tumor tissues further corroborate its role in cancer progression.
• What effect does 13-HODE exert on human breast cancer cells, and what implications does this have regarding its role in cancer progression?: 13(S)-HODE has been observed to stimulate the proliferation of diverse human breast cancer cell lines in vitro and appears requisite for growth factor-mediated proliferation. This observation suggests that 13(S)-HODE may contribute to the promotion of breast cancer growth in humans.

Related Concepts:

• Under what circumstances is the generalized term '13-HODE' sometimes employed in scientific literature, even when specific isomers are potentially relevant?: The designation '13-HODE' is occasionally utilized generically when research studies have not differentiated between the specific isomers. This often occurs because many analytical methods employed for identification and quantification may lack the precision to distinguish between them, reflecting a common challenge in lipid mediator research.
• Identify the primary chemical name for 13-Hydroxyoctadecadienoic acid (13-HODE).: The primary chemical designation for 13-HODE is 13(S)-hydroxy-9Z,11E-octadecadienoic acid. This particular isomer is frequently the subject of investigation owing to its significant bioactivity.
• In addition to 13(S)-HODE, what other stereoisomer is frequently produced concurrently?: The synthesis of 13(S)-HODE is frequently accompanied by its stereoisomer, 13(R)-hydroxy-9Z,11E-octadecadienoic acid (13(R)-HODE). These isomers are distinguished by the spatial configuration of the hydroxyl group.

Related Concepts:

Related Concepts:

Related Concepts:

• Under what circumstances is the generalized term '13-HODE' sometimes employed in scientific literature, even when specific isomers are potentially relevant?: The designation '13-HODE' is occasionally utilized generically when research studies have not differentiated between the specific isomers. This often occurs because many analytical methods employed for identification and quantification may lack the precision to distinguish between them, reflecting a common challenge in lipid mediator research.