What is the primary chemical name for 13-Hydroxyoctadecadienoic acid (13-HODE)?

The primary chemical name for 13-HODE is 13(S)-hydroxy-9Z,11E-octadecadienoic acid. This specific isomer is often the focus of studies due to its bioactivity.

What are the cis-trans isomers of 13-HODE that may also be produced?

Two other naturally occurring isomers that may accompany 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 differ from the primary form in the configuration of their double bonds.

Why is the general term "13-HODE" sometimes used in scientific literature even when specific isomers might be relevant?

The term "13-HODE" is sometimes used generically when studies have not distinguished between the different isomers, as many methods for identification and quantification may not differentiate between them. This reflects a common challenge in lipid mediator research where precise isomer identification can be difficult.

What are "OXLAMs" and what physiological role have they been proposed to play?

OXLAMs stand for oxidized linoleic acid metabolites, which include various HODEs and their ketone derivatives like 13-oxoODE. These compounds have been implicated in signaling pathways related to pain perception, suggesting they play a role in sensory processes.

What is the chemical formula and molar mass of 13-Hydroxyoctadecadienoic acid?

The chemical formula for 13-Hydroxyoctadecadienoic acid is C18H32O3, and its molar mass is approximately 296.451 g/mol. These are fundamental properties defining its molecular composition.

Which enzyme is primarily known for converting linoleic acid into 13-hydroperoxy-9Z,11E-octadecadienoic acid (13-HpODE)?

The enzyme 15-lipoxygenase 1 (ALOX15) is primarily known for converting linoleic acid into 13-hydroperoxy-9Z,11E-octadecadienoic acid (13-HpODE). This is a key step in the production pathway of 13-HODE.

How does 15-lipoxygenase 1 (ALOX15) act on linoleic acid in terms of stereochemistry?

ALOX15 acts in a highly stereospecific manner, predominantly forming the 13(S)-hydroperoxy-9Z,11E-octadecadienoic acid (13(S)-HpODE) isomer. This specificity is crucial for the biological activity of the resulting metabolites.

What happens to 13(S)-HpODE within cells to form 13(S)-HODE?

Within cells, 13(S)-HpODE is rapidly reduced by peroxidases to form 13(S)-HODE. This enzymatic reduction is a common step in the metabolic pathway of lipid hydroperoxides, converting them into more stable hydroxylated forms.

Can 15-lipoxygenase 1 metabolize linoleic acid when it's bound to other molecules like phospholipids or cholesterol?

Yes, ALOX15 is capable of metabolizing linoleic acid that is bound to phospholipids or cholesterol, forming the corresponding 13(S)-HpODE-bound molecules, which are then converted to their 13(S)-HODE-bound products. This indicates its action within cellular membrane structures.

How does 15-lipoxygenase 2 (ALOX15B) differ from 15-lipoxygenase 1 (ALOX15) in its metabolism of linoleic acid?

ALOX15B strongly prefers arachidonic acid over linoleic acid, making it relatively less efficient in metabolizing linoleic acid to 13(S)-HpODE compared to ALOX15. However, it can still contribute to the production of these metabolites.

Which cyclooxygenase enzyme (COX-1 or COX-2) shows a higher preference for linoleic acid and produces more 13(S)-HODE?

Cyclooxygenase 2 (COX-2) exhibits a higher preference for linoleic acid and consequently produces significantly more 13(S)-HODE than COX-1. COX-2 is therefore considered the principal COX enzyme responsible for making 13(S)-HODE in cells expressing both.

What other HODE isomer is produced concurrently by cyclooxygenases 1 and 2 when metabolizing linoleic acid?

Along with 13(S)-HODE, cyclooxygenases 1 and 2 also produce smaller amounts of 9(R)-HODE. This indicates that these enzymes can generate multiple hydroxylated fatty acid products from the same substrate.

How do Cytochrome P450 enzymes metabolize linoleic acid, and what is the typical stereoisomer outcome?

Cytochrome P450 microsomal enzymes metabolize linoleic acid into a mixture of 13-HODEs and 9-HODEs. These reactions typically produce racemic mixtures, meaning both R and S stereoisomers are formed, with the R isomer often predominating (e.g., an 80%/20% R/S ratio in human liver microsomes).

What are the main non-enzymatic pathways that produce HODEs from linoleic acid, and what is their typical stereoisomer outcome?

Free radical and singlet oxygen oxidations are the main non-enzymatic pathways that produce HODEs from linoleic acid. These reactions are generally not stereospecific, producing approximately equal amounts of the S and R stereoisomers.

What is 4-Hydroxynonenal (HNE) and how is it related to 13-HpODE?

4-Hydroxynonenal (HNE) is a lipid peroxidation product that is formed from 13-HpODE. HNE is a reactive aldehyde implicated in cellular damage and is often studied in the context of oxidative stress.

What roles are suggested for 13-HODE and its related metabolites in stimulating peroxisome proliferator-activated receptors (PPARs)?

13-HODE, along with 13-oxoODE and 13-EE-HODE, can directly activate the peroxisome proliferator-activated receptor gamma (PPARγ). This activation is thought to be responsible for inducing gene transcription and promoting the maturation of monocytes into macrophages. They can also activate PPARβ.

Which receptor, besides PPARs, is stimulated by 13-HODE and related oxidized linoleic acid metabolites (OXLAMs)?

13-HODE and related OXLAMs also stimulate the TRPV1 receptor, which is known as the capsaicin receptor or vanilloid receptor 1. This interaction is believed to be involved in mediating pain sensation.

What is the significance of 13(S)-HODE's interaction with the TRPV1 receptor in the context of asthma?

The interaction of 13(S)-HODE with TRPV1 is significant because TRPV1 is highly expressed in airway epithelial cells, and blocking this receptor can inhibit airway responses to 13(S)-HODE. This suggests a potential mechanism by which 13-HODE contributes to airway damage in severe asthma.

How is 13(S)-HODE typically metabolized or incorporated into cellular structures?

13(S)-HODE is rapidly and quantitatively incorporated into cellular phospholipids, becoming esterified within cell membranes. This incorporation is a key aspect of its cellular fate and potential signaling functions.

What is 13-oxoODE, and how is it formed from 13(S)-HODE?

13-oxoODE is formed when 13(S)-HODE is oxidized by an NAD+-dependent 13-HODE dehydrogenase enzyme. This oxidation converts the hydroxyl group to a ketone group, creating a different metabolite.

What is the biological significance of 13-oxoODE, and why is it studied?

13-oxoODE accumulates in tissues, is bioactive, and is considered a potential marker for certain diseases. Its biological activities and role as a marker make it an important subject of study in lipid metabolism research.

How can 13-oxoODE be conjugated with glutathione, and what is the significance of this reaction?

13-oxoODE can react with glutathione, either non-enzymatically via a Michael reaction or enzymatically via a glutathione transferase. This conjugation forms products that are then often exported from the cell, potentially serving to limit 13-oxoODE's activity.

What role is suggested for phospholipid-bound 13(S)-HODE in the maturation of red blood cells?

Phospholipid-bound 13(S)-HODE accumulation in mitochondrial membranes is suggested to be a critical step in triggering mitochondrial degradation, thereby facilitating the maturation of reticulocytes into mature erythrocytes. This highlights a role in cellular differentiation processes.

How do 13-HODE and 9-HODE affect neutrophils and natural killer cells?

13-HODE and 9-HODE act as moderate stimulators of neutrophil chemotaxis (directed migration) in vitro. Conversely, their R-stereoisomers and 9(S)-HODE are weak stimulators of natural killer cell migration, potentially contributing to inflammatory responses.

What is the observed presence of 13-HODE in atheromatous plaques, and what does this suggest about its role in atherosclerosis?

13-HODE is a dominant component of atheromatous plaques in atherosclerosis, often esterified to cholesterol and phospholipids. Its presence suggests a significant role in the development and progression of this cardiovascular disease.

How does 13(S)-HODE contribute to the progression of atherosclerosis through the PPARγ pathway?

13(S)-HODE activates the transcription factor PPARγ, which in turn increases the production of CD36 and aP2 receptors on macrophages. This leads to increased uptake of lipids, formation of foam cells, and potentially apoptosis of macrophages, all contributing to plaque growth.

What is the observed effect of 13(S)-HODE on airway hyperresponsiveness in animal models, and how might this relate to asthma?

In guinea pigs, 13(S)-HODE causes airway narrowing and mimics asthmatic hypersensitivity by increasing responses to bronchoconstrictors. This suggests a direct role for 13-HODE in the pathophysiology of asthma.

What is the relationship between 15-lipoxygenase 1, 13-HODE, and the progression of colon cancer?

Studies show progressive reductions in both 15-lipoxygenase 1 and its product, 13-HODE, as colon cancer advances from polyp to malignant stages. Conversely, higher levels of 15-LOX 1 and 13-HODE appear to inhibit cancer development, suggesting they act as tumor suppressors in this context.

What effect does 13(S)-HODE have on human breast cancer cells, and what does this suggest about its role?

13(S)-HODE stimulates the proliferation of various human breast cancer cell lines in culture and appears necessary for growth factors to promote proliferation. This suggests that 13(S)-HODE may play a role in promoting breast cancer growth in humans.

How is 15-lipoxygenase 1 (15-LOX 1) expression related to prostate cancer progression and severity?

15-LOX 1 is overexpressed in prostate cancerous tissue compared to normal tissue, and its expression levels correlate positively with cancer proliferation rates and severity (Gleason score). This enzyme's activity, primarily through 13(S)-HODE production, appears to promote prostate cancer growth and survival.

In what specific diseases have elevated levels of 13-HODE been observed?

Elevated 13-HODE levels have been observed in conditions such as rheumatoid arthritis, diabetes, polycystic kidney disease, chronic pancreatitis, steatohepatitis (both alcoholic and non-alcoholic), Alzheimer's disease, and vascular dementia. These findings suggest a link between 13-HODE and diseases involving oxidative stress or inflammation.

What are the limitations regarding the clinical usefulness of HODEs as disease markers?

Despite elevated levels in various diseases, HODEs are not yet clinically useful markers due to significant variations in reported values, influence from dietary linoleic acid intake, potential formation during tissue processing, and a lack of specific linkage to a single disease. More research is needed to establish their diagnostic value.

What is the preferred IUPAC name for 13-Hydroxyoctadecadienoic acid?

The preferred IUPAC name for 13-Hydroxyoctadecadienoic acid is (9Z,11E,13S)-13-Hydroxyoctadeca-9,11-dienoic acid. This systematic name precisely describes the molecule's structure and stereochemistry.

What are the different identifiers provided for 13-HODE in the source text?

The source text provides several identifiers, including CAS Registry Numbers (e.g., 29623-28-7, 5204-88-6, 10219-69-9), ChEBI IDs (CHEBI:137495, CHEBI:34154), ChEMBL IDs (ChEMBL451721), ChemSpider IDs (4947055), KEGG IDs (C14762), PubChem Compound IDs (5282948, 6443013, 13723970), UNII (53CYY2A5PM), CompTox Dashboard ID (DTXSID201017286), InChI strings, and SMILES notations. These are standard ways to uniquely identify chemical compounds.

What is the significance of the stereochemistry (S vs. R) of 13-HODE in its biological activities?

The stereochemistry of 13-HODE is significant, as studies indicate that different isomers can have distinct biological activities. For example, 13(S)-HODE activates PPARγ, while 13(R)-HODE lacks this ability, and their potencies in activating receptors like TRPV1 can also differ.

What is the proposed mechanism for mitochondrial degradation during red blood cell maturation involving 13(S)-HODE?

It is suggested that the accumulation of 13(S)-HODE bound to mitochondrial membranes increases their permeability. This increased permeability is thought to trigger the degradation of mitochondria, a necessary step for red blood cells to mature and lose their organelles.

How do 13-HODE and its counterparts activate PPARγ, and what are the downstream effects?

13-HODE, 13-oxoODE, and 13-EE-HODE activate PPARγ, which then induces the transcription of genes in monocytes, promoting their differentiation into macrophages. This pathway is involved in inflammatory and immune responses.

What is the relationship between 13-HODE and the development of foam cells in atherosclerosis?

13(S)-HODE, via PPARγ activation, increases the expression of CD36 and aP2 on macrophages. These receptors enhance the uptake of lipids, leading to the transformation of macrophages into lipid-laden foam cells, a hallmark of atherosclerotic plaques.

What evidence links 13-HODE to asthma pathology?

Evidence includes 13(S)-HODE causing airway hyperresponsiveness in guinea pigs, elevated levels in human asthma patients' samples, significant production by eosinophils (key asthma cells), and the molecule causing mitochondrial damage in airway epithelial cells, potentially via TRPV1 activation.

How might dietary interventions influence 13-HODE levels and prostate cancer growth?

Increasing dietary linoleic acid (an omega-6 fatty acid) may promote prostate cancer growth by increasing 13-HODE production, while increasing dietary stearidonic acid (an omega-3 fatty acid) may inhibit growth by promoting the production of inhibitory docosahexaenoic acid metabolites. This suggests a link between diet, lipid metabolism, and cancer progression.

What is the significance of the stereochemistry (S vs. R) of 13-HODE in the context of atherosclerosis plaque progression?

The observation that early atherosclerotic plaques contain primarily the S-isomer of 13-HODE, while mature plaques have equal amounts of S and R isomers, suggests that different metabolic pathways (e.g., 15-LOX-1 for S-isomer, cytochrome/free radical for R-isomer) contribute to plaque development over time.

What is the role of 13-HODE in the context of colon cancer cell proliferation and apoptosis?

13(S)-HODE has been shown to inhibit the proliferation and induce apoptosis (programmed cell death) in cultured human colon cancer cells. This suggests a potential anti-cancer effect of this metabolite.

What are the potential therapeutic implications of targeting 13-HODE pathways in diseases like atherosclerosis or asthma?

Targeting pathways that produce or utilize 13-HODE, such as inhibiting 15-LOX-1 or blocking TRPV1 activation, are being explored as potential therapeutic strategies for conditions like atherosclerosis and severe asthma. This highlights the molecule's relevance in drug development.

What is the relationship between 13-HODE and the activation of GPR132?

13(S)-HpODE and 13(S)-HODE can activate human GPR132, although they are weaker activators compared to their 9-HODE counterparts. The precise physiological role of this activation is still under investigation.

What is 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 levels in tumor tissue further support its role in cancer progression.

What is the proposed mechanism by which 13(S)-HODE might contribute to cell injury?

The accumulation of 13(S)-HODE bound to phospholipids in mitochondrial membranes may increase their permeability. This increased permeability is thought to trigger the degradation of mitochondria, leading to the release of damaging substances and subsequent cell injury.

13-hydroxyoctadecadienoic Acid Wiki: 13-HODE Unveiled: The Molecular Messenger of Cellular Processes

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Overview

Chemical Identity

13-Hydroxyoctadecadienoic acid, commonly abbreviated as 13-HODE, specifically refers to 13(S)-hydroxy-9Z,11E-octadecadienoic acid. Its production is often accompanied by its stereoisomer, 13(R)-hydroxy-9Z,11E-octadecadienoic acid (13(R)-HODE). The molecule is an 18-carbon polyunsaturated fatty acid derivative with hydroxyl and conjugated double bonds.

Isomeric Forms and Nomenclature

Beyond the primary (S) and (R) forms at the C13 position, other naturally occurring isomers exist, such as the (9E,11E) isomers (13(S)-EE-HODE and 13(R)-EE-HODE). Studies often use the general term "13-HODE" when isomer distinction was not performed. Similar sets of 9-hydroxyoctadecadienoic acid (9-HODE) metabolites also occur, particularly under oxidative stress, with overlapping but distinct activities.

Biological Significance

Both 13(S)-HODE and 13(R)-HODE have been associated with various clinically relevant bioactivities. Research suggests these metabolites can mediate physiological and pathological responses, serve as markers for certain human diseases, and potentially contribute to disease progression. Their precise roles are areas of ongoing investigation.

Metabolic Pathways

Enzymatic Synthesis

13-HODEs are primarily synthesized through the action of specific enzymes on linoleic acid:

15-Lipoxygenase 1 (15-LOX-1): This enzyme preferentially converts linoleic acid to 13(S)-hydroperoxy-octadecadienoic acid (13(S)-HpODE), which is then reduced to 13(S)-HODE. It can metabolize linoleic acid bound to phospholipids and cholesterol.
Cyclooxygenases (COX-1 and COX-2): COX-2, in particular, metabolizes linoleic acid to 13(S)-HODE, often producing smaller amounts of 9(R)-HODE concurrently.
Cytochrome P450 Enzymes: These microsomal enzymes convert linoleic acid into a mixture of 13-HODEs and 9-HODEs, typically yielding a predominance of the R-stereoisomer.
15-Lipoxygenase 2 (15-LOX-2): While preferring arachidonic acid, this enzyme can also contribute to 13-HODE production from linoleic acid, though less efficiently than 15-LOX-1.

Non-Enzymatic Oxidation

Under conditions of oxidative stress, free radicals and singlet oxygen can non-enzymatically oxidize linoleic acid. These processes generate various hydroperoxides and hydroxy acids, including 13-HpODEs and 13-HODEs. These reactions are thought to produce approximately equal amounts of S and R stereoisomers. Products like 4-hydroxynonenal (HNE) can also form from 13-HpODE peroxidation.

Non-enzymatic oxidations can yield a complex mixture of products:

Free radical oxidation produces 13-HpODEs, 9-HpODEs, 13-HODEs, 9-HODEs, and isomers like 13-EE-HODE.
Singlet oxygen oxidation generates presumed racemic mixtures of 9-hydroxy-10E,12-Z-octadecadienoic acid, 10-hydroxy-8E,12Z-octadecadienoic acid, and 12-hydroxy-9Z-13-E-octadecadienoic acid.
These pathways are considered major contributors to 13-HODE formation in tissues experiencing oxidative stress, such as sites of inflammation, cardiovascular disease, and neurodegenerative disease.

Metabolism & Fate

Cellular Incorporation

Following its formation, 13(S)-HODE is rapidly and quantitatively incorporated into cellular phospholipids. It is often esterified at the sn-2 position of phosphatidylcholine, phosphatidylinositol, and phosphatidylethanolamine. Lower levels of 13(S)-HODE esterified to phospholipids have been observed in psoriatic skin lesions compared to normal skin, suggesting a potential inactivation pathway.

Chain Shortening

13(S)-HODE can undergo metabolism via peroxisome-dependent β-oxidation. This process breaks down the fatty acid chain, producing shorter metabolites (16-, 14-, and 12-carbon products) that are subsequently released from the cell. This pathway may serve to inactivate and eliminate 13(S)-HODE.

Oxidation and Conjugation

13(S)-HODE can be oxidized to 13-oxo-octadecadienoic acid (13-oxoODE) by a specific dehydrogenase enzyme. 13-oxoODE itself has biological activity and may accumulate in tissues. It can also react with glutathione, either non-enzymatically or via glutathione transferase, forming conjugates. These conjugates may be exported from the cell, potentially serving as a mechanism to limit 13-oxoODE activity.

Biological Activities

Receptor Activation

13-HODEs (including 13(S)-HODE, 13(R)-HODE, and 13-oxoODE) interact with key cellular receptors:

Peroxisome Proliferator-Activated Receptor gamma (PPARγ): 13-HODE and related metabolites directly activate PPARγ. This activation is linked to the induction of PPARγ-target genes in monocytes, promoting their differentiation into macrophages.
Transient Receptor Potential Vanilloid 1 (TRPV1): These HODEs stimulate TRPV1, a receptor involved in pain and inflammation signaling. This interaction occurs in neurons and airway epithelial cells and is implicated in pain sensation and airway hyperresponsiveness.
G Protein-Coupled Receptor 132 (GPR132): 13(S)-HpODE and 13(S)-HODE activate human GPR132, although they are weaker activators compared to their 9-HODE counterparts. The physiological relevance in humans is still under investigation due to species-specific differences in receptor activation.

Cellular Effects

The activities of 13-HODEs translate to significant cellular effects:

Mitochondrial Degradation: In erythropoiesis (red blood cell development), phospholipid-bound 13(S)-HODE accumulation in mitochondria may increase membrane permeability, triggering degradation and facilitating cell maturation.
Leukocyte Stimulation: 13-HODEs act as chemoattractants for neutrophils in vitro. They also weakly stimulate natural killer cells, potentially contributing to pro-inflammatory and tissue-injuring actions.
Apoptosis Regulation: In certain contexts, like macrophages within atherosclerotic plaques, the 13(S)-HODE/PPARγ pathway can induce apoptosis, potentially influencing plaque progression.

Role in Human Diseases

Atherosclerosis

13-HODE is a dominant component found esterified within lipids in atherosclerotic plaques. Its accumulation, particularly the S-isomer early in plaque development, is linked to disease progression. 13(S)-HODE activates PPARγ, leading to increased expression of scavenger receptors (CD36) and adipocyte protein 2 (aP2) on macrophages. This promotes the uptake of oxidized lipids, foam cell formation, and potentially macrophage apoptosis, all contributing to plaque growth. Statins, used to treat atherosclerosis, may exert some effects by inhibiting PPARγ.

Asthma

Elevated 13-HODE levels are found in individuals with asthma. In preclinical models, 13(S)-HODE induces airway hyperresponsiveness and epithelial injury, partly via TRPV1 activation. Eosinophils, key inflammatory cells in asthma, are significant producers of 13-HODE. These findings suggest 13-HODE may play a role in asthma pathogenesis, and TRPV1 inhibitors could be potential therapeutic agents.

Cancer

The role of 13-HODE in cancer is complex and context-dependent:

Colon Cancer: Reduced levels of 15-LOX-1 and its product, 13-HODE, are associated with the progression of both hereditary (APC/MUTYH) and non-hereditary colon cancers. Conversely, 13(S)-HODE has shown inhibitory effects on colon cancer cell proliferation and survival in vitro and in animal models.
Breast Cancer: 13(S)-HODE appears to stimulate the proliferation of human breast cancer cell lines in vitro and supports the growth of breast cancer xenografts in mice. Elevated levels correlate with faster-growing tumors.
Prostate Cancer: Overexpression of 15-LOX-1, leading to increased 13(S)-HODE production, is linked to increased proliferation, survival, vascularization, and metastasis of prostate cancer. Dietary fatty acids influence these processes.

Disease Markers

Potential Biomarkers

Elevated levels of 13-HODE (or total HODEs) have been reported in various conditions associated with oxidative stress, including:

Rheumatoid arthritis (in LDL fraction)
Diabetes (in HDL fraction)
Polycystic kidney disease and chronic pancreatitis (in serum)
Alcoholic and non-alcoholic steatohepatitis (in plasma)
Alzheimer's disease and vascular dementia (in plasma/erythrocytes)

Limitations and Future

Despite these associations, the clinical utility of HODEs as standalone biomarkers is limited. Factors such as variability in measurement methods, dietary influences (linoleic acid intake), potential formation during sample processing, and lack of absolute disease specificity hinder their widespread use. However, combined with other markers, HODEs might offer value in indicating disease presence, type, or progression in specific contexts.

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13-HODE Unveiled

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Overview ℹ️

🧬 Chemical Identity

⚖️ Isomeric Forms and Nomenclature

💡 Biological Significance

Metabolic Pathways ➡️

🌿 Enzymatic Synthesis

⚡ Non-Enzymatic Oxidation

Metabolism & Fate 🔄

🔗 Cellular Incorporation

📉 Chain Shortening

🧪 Oxidation and Conjugation

Biological Activities 🔬

🔑 Receptor Activation

💥 Cellular Effects

Role in Human Diseases 🏥

❤️ Atherosclerosis

🫁 Asthma

📈 Cancer

Disease Markers 📊

📍 Potential Biomarkers

⚠️ Limitations and Future

Teacher's Corner 🧑‍🏫

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📜 Important Notice

Dive in with Flashcard Learning!

Overview

Chemical Identity

Isomeric Forms and Nomenclature

Biological Significance

Metabolic Pathways

Enzymatic Synthesis

Non-Enzymatic Oxidation

Metabolism & Fate

Cellular Incorporation

Chain Shortening

Oxidation and Conjugation

Biological Activities

Receptor Activation

Cellular Effects

Role in Human Diseases

Atherosclerosis

Asthma

Cancer

Disease Markers

Potential Biomarkers

Limitations and Future

Teacher's Corner

True or False?

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Gamer's Corner

Discover other topics to study!

References

Feedback & Support

Disclaimer

Important Notice