What is uric acid and what is its chemical formula?

Uric acid is a heterocyclic compound composed of carbon, nitrogen, oxygen, and hydrogen. Its chemical formula is C5H4N4O3. It is a product of the metabolic breakdown of purine nucleotides and is a normal component found in urine.

What are urates and acid urates?

Urates and acid urates are ions and salts formed by uric acid. Examples include ammonium acid urate. These are derived from uric acid, which is the final product of purine metabolism in humans.

What health conditions are associated with high blood concentrations of uric acid?

High blood concentrations of uric acid, a condition known as hyperuricemia, can lead to gout. It is also associated with other medical conditions such as diabetes and the formation of ammonium acid urate kidney stones.

Who first isolated uric acid and from where?

Carl Wilhelm Scheele, a Swedish chemist, first isolated uric acid from kidney stones in 1776.

How was uric acid first synthesized, and by whom?

The Ukrainian chemist Ivan Horbaczewski first synthesized uric acid in 1882 by melting urea with glycine.

What type of chemical phenomenon does uric acid exhibit regarding its structure?

Uric acid exhibits lactam-lactim tautomerism, a form of isomerism where a molecule can exist in two forms that differ by the position of a proton and a double bond. It crystallizes in the lactam form, which computational chemistry indicates is the most stable tautomer.

What are the pKa values for uric acid, and what form predominates at physiological pH?

Uric acid is a diprotic acid with pKa values of 5.4 and 10.3. At physiological pH, the hydrogen urate ion predominates in solution.

What enzyme catalyzes the formation of uric acid from xanthine and hypoxanthine?

The enzyme xanthine oxidase (XO) catalyzes the formation of uric acid from xanthine and hypoxanthine. Xanthine is itself produced from other purines.

What is the role of molybdenum in xanthine oxidase?

Xanthine oxidase, despite its name, primarily functions as a dehydrogenase. Its active site contains molybdenum, which is bound to sulfur and oxygen, playing a crucial role in its catalytic activity.

Under what physiological conditions is uric acid released?

Uric acid is released under hypoxic conditions, which are characterized by low oxygen saturation.

How does the water solubility of uric acid and its salts generally behave?

The water solubility of uric acid and its alkali metal and alkaline earth salts is generally low. However, these salts are more soluble in hot water than in cold water, which facilitates their recrystallization.

What is the significance of uric acid's low water solubility in relation to health?

The low water solubility of uric acid is significant in the etiology of gout, a condition where uric acid crystals precipitate in joints and tissues.

How does the solubility of urate salts in ethanol compare to their solubility in water?

The solubility of urate salts in ethanol is very low or negligible. In mixtures of ethanol and water, their solubilities fall between the values for pure ethanol and pure water.

In most mammals, what is the further metabolic breakdown product of uric acid?

In most mammals, the enzyme uricase further oxidizes uric acid into allantoin. Humans, however, lack this enzyme and excrete uric acid directly.

What is the suggested functional similarity between uric acid and ascorbic acid in higher primates?

The loss of uricase in higher primates, similar to the loss of the ability to synthesize ascorbic acid (Vitamin C), has led to the suggestion that urate may partially substitute for ascorbate. Both compounds are strong reducing agents and potent antioxidants.

What proportion of the antioxidant capacity of human blood plasma is attributed to hydrogen urate ion?

In humans, the hydrogen urate ion contributes over half of the antioxidant capacity found in blood plasma. This highlights its role as a significant endogenous antioxidant.

What are the typical reference ranges for uric acid in human blood for men and women?

The normal concentration range for uric acid in human blood is generally cited as 25 to 80 mg/L for men and 15 to 60 mg/L for women. However, some sources indicate slightly different values, and individuals can have higher levels without symptoms of gout.

How is uric acid primarily eliminated from the body in humans?

In humans, approximately 70% of daily uric acid is disposed of through the kidneys. Impaired kidney excretion is a common cause of hyperuricemia in about 5-25% of the population.

What is the normal daily excretion of uric acid in human urine compared to urea?

Normal daily excretion of uric acid in urine is about 270 to 360 mg. This is roughly 1% of the daily excretion of urea. The concentration in urine is higher than uric acid's solubility limit because it is excreted as dissolved acid urates.

What is unique about uric acid metabolism in Dalmatian dogs?

Dalmatian dogs have a genetic defect affecting their liver and kidney uptake of uric acid. This results in them excreting uric acid in their urine, rather than converting it to allantoin like most other mammals.

In which animal groups is uric acid the final product of purine metabolism and excreted in feces?

In birds, reptiles, and certain desert-dwelling mammals like the kangaroo rat, uric acid is the end product of purine metabolism. It is excreted as a dry mass in feces, which helps conserve water and prevent dehydration.

What role does uric acid play in the marine polychaete worm *Platynereis dumerilii*?

In *Platynereis dumerilii*, uric acid functions as a sexual pheromone. The female releases it during mating to induce males to release sperm.

How do gut bacteria metabolize uric acid in humans?

Approximately one-fifth of human gut bacteria species metabolize uric acid anaerobically. This process involves enzymes like ammonia lyase, peptidase, carbamoyl transferase, and oxidoreductase, converting uric acid into substances like xanthine, lactate, acetate, and butyrate.

What is the genetic contribution to high serum urate levels compared to diet?

While dietary factors like meat and seafood can elevate serum urate levels, genetic variation is considered a much greater contributor to high serum urate concentrations.

Which gene is known to encode GLUT9, a transporter for both uric acid and fructose?

The SLC2A9 gene encodes GLUT9, a transporter protein that is known to transport both uric acid and fructose. Variants in this gene have been linked to serum urate levels.

What is myogenic hyperuricemia and in which conditions is it observed?

Myogenic hyperuricemia occurs when the purine nucleotide cycle is active due to low ATP reserves in muscle cells. This is a common feature in metabolic myopathies, such as Glycogen Storage Disease type III, where it is exercise-induced, leading to increased plasma levels of inosine, hypoxanthine, and uric acid.

What are the typical reference ranges for uric acid in human blood plasma in mg per 100 mL?

The typical reference range for uric acid in human blood plasma is 3.4 to 7.2 mg per 100 mL for men and 2.4 to 6.1 mg per 100 mL for women. Levels outside these ranges are termed hyperuricemia (high) or hypouricemia (low).

What dietary factors can increase uric acid levels?

High intake of dietary purines, high-fructose corn syrup, and sucrose can increase uric acid levels in the blood, potentially contributing to hyperuricemia.

How can certain medications affect uric acid levels?

Some medications, such as thiazide diuretics, can increase blood uric acid levels by interfering with the kidneys' ability to clear uric acid.

What is tumor lysis syndrome and how does it relate to uric acid?

Tumor lysis syndrome is a metabolic complication of certain cancers or chemotherapy. It leads to high uric acid levels in the blood when tumor cells release their contents, including nucleobases, into the plasma. This can cause uric acid crystals to deposit in the kidneys, potentially leading to acute kidney injury.

What is gout and how does it manifest?

Gout is a painful condition caused by excess uric acid in the blood (hyperuricemia). It manifests when needle-like crystals of monosodium urate precipitate in joints, capillaries, skin, and other tissues.

What is the prevalence of gout and hyperuricemia in the United States according to a 2011 survey?

A 2011 survey in the United States indicated that approximately 3.9% of the population had gout, while 21.4% had hyperuricemia without experiencing symptoms.

What types of foods are particularly rich in purines and can increase gout risk?

Purine-rich foods that can increase gout risk include organ meats like liver and kidney, and certain seafood such as anchovies, herring, sardines, mussels, scallops, trout, haddock, mackerel, and tuna.

Is there an association between moderate intake of purine-rich vegetables and gout risk?

No, moderate consumption of purine-rich vegetables is not associated with an increased risk of gout, unlike the consumption of purine-rich meats and seafood.

What were historical and current treatments for gout?

In the 19th century, lithium salts were used to treat gout because lithium urate is more soluble. Current treatments include NSAIDs, colchicine, or corticosteroids for inflammation during attacks, and allopurinol to manage urate levels by inhibiting xanthine oxidase.

How is tumor lysis syndrome treated in relation to uric acid levels?

Treatment for tumor lysis syndrome involves measures to reduce uric acid levels, such as hyperhydration to dilute and excrete uric acid, rasburicase to break down poorly soluble uric acid, or allopurinol to inhibit purine catabolism.

What are the neurological and physical manifestations of Lesch-Nyhan syndrome?

Lesch-Nyhan syndrome, a rare inherited disorder associated with high serum uric acid, can cause spasticity, involuntary movements, cognitive retardation, and symptoms similar to gout.

What is the relationship between hyperuricemia and cardiovascular disease?

Hyperuricemia is associated with increased risk factors for cardiovascular disease. However, whether high uric acid levels causally contribute to atherosclerotic cardiovascular disease is still a subject of debate and conflicting data.

How do uric acid stones form in the kidneys, and are they visible on X-ray?

Kidney stones can form from deposits of sodium urate microcrystals. Uric acid stones are radiolucent, meaning they do not appear on standard abdominal X-rays. Uric acid crystals can also act as 'seed crystals' promoting the formation of calcium oxalate stones.

What is the association between hyperuricemia and metabolic syndrome?

Hyperuricemia is associated with components of metabolic syndrome, and this association has been observed in both adults and children.

What are potential causes for low uric acid levels (hypouricemia)?

Low uric acid levels can be caused by factors such as low dietary zinc intake, which can be exacerbated by oral contraceptive use in women. The medication sevelamer, used for chronic kidney failure, can also significantly reduce serum uric acid.

What has been observed regarding serum uric acid levels in patients with multiple sclerosis?

A meta-analysis of studies suggests that patients with multiple sclerosis have significantly lower serum uric acid levels compared to healthy individuals, potentially indicating a diagnostic biomarker for the condition.

How can low or deficient zinc levels be addressed in relation to uric acid?

Correcting low zinc levels through supplementation can help elevate serum uric acid levels in individuals experiencing hypouricemia.

What is the role of hypoxanthine and xanthine in the metabolic pathway leading to uric acid?

Hypoxanthine and xanthine are intermediate products in the catabolism of purines. Xanthine oxidase converts both hypoxanthine and xanthine into uric acid, which is the final product of purine metabolism in humans.

What is the significance of the 'lactam' and 'lactim' forms of uric acid?

Uric acid exhibits lactam-lactim tautomerism, meaning it can exist in two structural forms. It crystallizes in the lactam form, which is considered the most stable tautomer based on computational chemistry studies.

What is the relationship between fasting or rapid weight loss and uric acid levels?

Fasting or rapid weight loss can temporarily elevate uric acid levels in the blood. This is a known factor that can influence serum urate concentrations.

What is pseudohypoxia in the context of uric acid metabolism?

Pseudohypoxia, characterized by a disrupted NADH/NAD+ ratio, can lead to elevated uric acid levels. This condition is associated with factors like diabetic hyperglycemia and excessive alcohol consumption.

What is the function of allopurinol in managing uric acid levels?

Allopurinol is a medication used to manage uric acid levels, particularly in conditions like gout. It functions as a weak inhibitor of xanthine oxidase, an enzyme involved in purine breakdown, thereby reducing uric acid production. It is structurally similar to hypoxanthine.

What is the difference between hyperuricosuria and hypouricosuria?

Hyperuricosuria refers to abnormally high concentrations of uric acid in the urine, while hypouricosuria refers to abnormally low concentrations of uric acid in the urine.

Can uric acid levels in saliva be indicative of blood uric acid levels?

Yes, uric acid concentrations found in saliva may be associated with the levels of uric acid present in the blood.

What is the role of uric acid in the purine nucleotide cycle?

In the purine nucleotide cycle, excess adenosine monophosphate (AMP) can be converted into uric acid through a series of intermediate steps: IMP -> Inosine -> Hypoxanthine -> Xanthine -> Uric Acid. This process can contribute to hyperuricemia, particularly in conditions like metabolic myopathies.

Uric Acid Wiki: Uric Acid Unveiled: A Biochemical Perspective

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Introduction

Molecular Identity

Uric acid is a heterocyclic compound composed of carbon, nitrogen, oxygen, and hydrogen, with the chemical formula C₅H₄N₄O₃. It exists as ions and salts known as urates and acid urates. Physiologically, it represents the terminal product of purine nucleotide catabolism and is a natural constituent of urine.

Physiological Balance

Maintaining appropriate blood concentrations of uric acid is crucial. Elevated levels, termed hyperuricemia, are strongly associated with conditions such as gout and can also be linked to diabetes and the formation of ammonium acid urate kidney stones.

Historical Context

First isolated from kidney stones in 1776 by Carl Wilhelm Scheele, uric acid's synthesis was later achieved by Ivan Horbaczewski in 1882 through the thermal decomposition of urea and glycine. Its chemical properties and biological roles have been subjects of extensive study since.

Chemical Properties

Nomenclature and Identifiers

The preferred IUPAC name for uric acid is 7,9-Dihydro-1H-purine-2,6,8(3H)-trione. It is also known by various other names, including 2,6,8-Trioxypurine. Key identifiers include its CAS Registry Number (69-93-2) and numerous database entries like PubChem CID 1175.

Structure and Tautomerism

Uric acid exhibits lactam–lactim tautomerism, with the lactam form being the most stable and prevalent crystalline structure. Computational studies further support this stability. It functions as a diprotic acid with pK_a1 = 5.4 and pK_a2 = 10.3, meaning it predominantly exists as the hydrogen urate ion at physiological pH.

Solubility Characteristics

Uric acid and its alkali and alkaline earth salts generally exhibit low water solubility. Solubility increases with temperature, facilitating recrystallization. This property is critically relevant to the etiology of gout, where urate crystals precipitate in joints. The table below details the solubility of various urate salts.

Solubility of Urate Salts (grams of water per gram of compound)
Compound	Cold water	Boiling water
Uric acid	15,000	2,000
Ammonium hydrogen urate	—	1,600
Lithium hydrogen urate	370	39
Sodium hydrogen urate	1,175	124
Potassium hydrogen urate	790	75
Magnesium dihydrogen diurate	3,750	160
Calcium dihydrogen diurate	603	276
Disodium urate	77	—
Dipotassium urate	44	35
Calcium urate	1,500	1,440
Strontium urate	4,300	1,790
Barium urate	7,900	2,700

Note: Lower numbers indicate greater solubility.

Biochemical Pathways

Purine Catabolism

Uric acid is the final product of purine metabolism in humans. The enzyme xanthine oxidase (XO) catalyzes the conversion of xanthine and hypoxanthine into uric acid. This process is crucial for nitrogenous waste excretion, particularly in species lacking the uricase enzyme, which further metabolizes uric acid into allantoin.

Antioxidant Properties

In humans, the hydrogen urate ion, present at physiological pH, contributes significantly to the antioxidant capacity of blood plasma. This role has led to speculation that uric acid may partially substitute for ascorbic acid (Vitamin C) in species that have lost the ability to synthesize it, given that both are potent reducing agents and electron donors.

Metabolic Regulation

The body's handling of uric acid involves complex regulation of both production and excretion. Factors influencing these processes include genetic predispositions, dietary intake of purines and fructose, and the efficiency of renal and intestinal clearance mechanisms. Disruptions in this balance can lead to significant health issues.

Genetic and Species Diversity

Primate vs. Mammalian Differences

Unlike most mammals, higher primates, including humans, lack the functional uricase enzyme. This evolutionary divergence means uric acid is the terminal purine metabolite, excreted in urine, whereas in many other mammals, it is further broken down. This loss is paralleled by the loss of ascorbic acid synthesis, suggesting a potential compensatory antioxidant role for urate.

Canine Excretion Anomaly

The Dalmatian breed of dog exhibits a unique genetic defect affecting uric acid transport in the liver and kidneys. This results in a significantly reduced conversion of uric acid to allantoin, leading to its excretion in urine, a trait uncommon in other canine breeds.

Avian and Reptilian Excretion

Birds, reptiles, and certain desert-dwelling mammals excrete uric acid as their primary nitrogenous waste product. This process occurs in the feces as a dry mass, a mechanism that conserves water effectively, albeit at a higher metabolic cost compared to urea or ammonia excretion.

Microbial Metabolism

Gut bacteria play a role in uric acid metabolism. Certain anaerobic bacteria can convert uric acid into xanthine, lactate, and short-chain fatty acids. Studies suggest that disruptions to this gut microbiome, such as through antibiotic use, might influence uric acid levels and potentially increase gout risk.

Human Genetic Factors

While diet influences serum urate levels, genetic variations are major contributors. Mutations in genes encoding urate transporters, such as SLC2A9 (encoding GLUT9), ABCG2, and others, significantly impact renal excretion and serum concentrations, predisposing individuals to hyperuricemia and gout.

Clinical Significance

Hyperuricemia and Gout

Elevated serum uric acid levels (hyperuricemia) can lead to the deposition of monosodium urate crystals in joints and tissues, causing the inflammatory condition known as gout. While dietary factors contribute, genetic predisposition plays a larger role. Treatment involves managing inflammation and reducing urate levels with medications like allopurinol.

Cardiovascular and Metabolic Links

Hyperuricemia is associated with increased risk factors for cardiovascular disease and metabolic syndrome. Emerging research suggests a potential causal role for high uric acid levels in the pathogenesis of atherosclerosis, although this remains a subject of ongoing investigation and debate.

Renal Stone Formation

Supersaturation of uric acid in the kidneys can lead to the formation of uric acid kidney stones. These stones are radiolucent and may also act as nucleation sites for calcium oxalate stones. Maintaining adequate hydration and managing urinary pH are key preventive strategies.

Tumor Lysis Syndrome

In conditions like tumor lysis syndrome, rapid cell breakdown releases large amounts of purines, leading to a surge in uric acid production. This can cause acute kidney injury if uric acid crystals precipitate within the renal tubules. Management includes hydration and agents that reduce uric acid levels.

Hypouricemia and Neurological Conditions

Conversely, low serum uric acid levels (hypouricemia) can result from factors like zinc deficiency or certain medications. Intriguingly, meta-analyses suggest lower uric acid levels may be associated with multiple sclerosis, potentially serving as a diagnostic biomarker, though the exact relationship requires further elucidation.

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References

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This content has been generated by an Artificial Intelligence model and is intended for educational and informational purposes only. It is based on data available from public sources, which may not be exhaustive or entirely up-to-date.

This is not medical advice. The information provided herein should not be considered a substitute for professional medical consultation, diagnosis, or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it due to information obtained from this resource.

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Uric Acid Unveiled

💡 Dive in with Flashcard Learning! 💡

Introduction ℹ️

🧪 Molecular Identity

⚖️ Physiological Balance

🔬 Historical Context

Chemical Properties ⚗️

🏷️ Nomenclature and Identifiers

⚛️ Structure and Tautomerism

💧 Solubility Characteristics

Biochemical Pathways 🧬

🔄 Purine Catabolism

🛡️ Antioxidant Properties

📉 Metabolic Regulation

Genetic and Species Diversity 🌐

🐒 Primate vs. Mammalian Differences

🐕 Canine Excretion Anomaly

🐦 Avian and Reptilian Excretion

🦠 Microbial Metabolism

🧬 Human Genetic Factors

Clinical Significance 🩺

📈 Hyperuricemia and Gout

❤️ Cardiovascular and Metabolic Links

💎 Renal Stone Formation

⚡ Tumor Lysis Syndrome

🧠 Hypouricemia and Neurological Conditions

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📜 Important Notice

Dive in with Flashcard Learning!

Introduction

Molecular Identity

Physiological Balance

Historical Context

Chemical Properties

Nomenclature and Identifiers

Structure and Tautomerism

Solubility Characteristics

Biochemical Pathways

Purine Catabolism

Antioxidant Properties

Metabolic Regulation

Genetic and Species Diversity

Primate vs. Mammalian Differences

Canine Excretion Anomaly

Avian and Reptilian Excretion

Microbial Metabolism

Human Genetic Factors

Clinical Significance

Hyperuricemia and Gout

Cardiovascular and Metabolic Links

Renal Stone Formation

Tumor Lysis Syndrome

Hypouricemia and Neurological Conditions

Teacher's Corner

True or False?

Test Your Knowledge!

Gamer's Corner

Discover other topics to study!

References

Feedback & Support

Disclaimer

Important Notice