Prabhakar singh iv sem-phenylketonuria, alkaptonuria, albinism, tyrosinosis
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This document discusses several inborn errors of metabolism including phenylketonuria (PKU), alkaptonuria, tyrosinosis, and albinism. PKU results from a defect in the enzyme phenylalanine hydroxylase, which converts the essential amino acid phenylalanine to tyrosine in the liver. This causes phenylalanine to accumulate and be excreted as the keto acid phenylpyruvate, giving PKU its name. Alkaptonuria is due to the inability to break down tyrosine and phenylalanine, causing homogentisic acid to accumulate and deposit in connective tissues, giving them a dark color. Tyrosinosis involves a
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Phenylalanine & tyrosine.pptx
This document summarizes the catabolism of phenylalanine and tyrosine. It discusses that phenylalanine is an essential amino acid that is converted to tyrosine. Tyrosine can then be incorporated into proteins or used to synthesize important compounds like catecholamines, thyroid hormones, and melanin. It also describes disorders that can occur if there are defects in the metabolic pathways of phenylalanine and tyrosine, including phenylketonuria (PKU), tyrosinemia types 1 and 2, and albinism. PKU is caused by a deficiency of phenylalanine hydroxylase and causes accumulation of phenylalanine that can lead to intellectual disability if left untreated.
Catabolism of phenylalanine and tyrosine and their metabolic disorders by BNP...
Catabolism of phenylalanine and tyrosine and their metabolic disorders by BNP...College of pharmaceutical sciences
Decarboxylation is the reaction by which CO2 is removed from the COOH group of an amino acid as a result an amine is formed. The reaction is catalyzed by the enzyme decarboxylase, which requires pyridoxal-P (B6-PO4) as coenzyme. Tissues like liver, kidney, brain possess the enzyme decarboxylase and also by microorganisms of intestinal tract. The enzyme removes CO2 from COOH and converts the amino acid to corresponding amine.
Phenylalanine is an essential, aromatic amino acid. The need for phenylalanine becomes minimal, if adequate tyrosine is supplied in the food. This is called the sparing action of tyrosine on phenylalanine.
Tyrosine is an aromatic amino acid. It is synthesized from phenylalanine, and so is a non-essential amino acid. The need for phenylalanine becomes minimal, if adequate tyrosine is supplied in the food. This is called the sparing action of tyrosine on the phenylalanine.
Seven amino acids produce acetyl CoA or acetoacetate and therefore are categorized as ketogenic. Of these, isoleucine, threonine, and the aromatic amino acids (phenylalanine, tyrosine, and tryptophan) are converted to compounds that produce both glucose and acetyl CoA or acetoacetate. Leucine and lysine do not produce glucose; they produce acetyl CoA and acetoacetate.
The name phenylketonuria is coined due to the fact that the metabolite phenylpyruvate is a keto acid (C6H5CH2−CO−COO−) excreted in urine in high amounts.
Phenylalanine cannot be converted to tyrosine. So, phenylalanine accumulates. Phenylalanine level in blood is elevated.Metabolism part i
The document discusses drug biotransformation and metabolism. It notes that biotransformation typically makes drugs more polar to enhance excretion, and may decrease or increase drug effects or toxicity. Drug metabolism mainly occurs in the liver, and can result in pharmacological inactivation, equal activity, or toxicological activation of metabolites. Phase I reactions include oxidation, reduction, and hydrolysis. Phase II involves conjugating metabolites to make them inactive and excretable, such as glucuronidation, acetylation, glycine addition, or sulfation.
keto.pptx
Phenylketonuria (PKU) is an inherited disorder that causes the body to be unable to break down an amino acid called phenylalanine. If left untreated, it can cause intellectual disabilities and other neurological problems. There are different types of PKU depending on severity. It is caused by mutations that impact the phenylalanine hydroxylase enzyme needed to metabolize phenylalanine. Symptoms usually appear between 3-6 months of age if untreated. Diagnosis involves newborn blood tests and managing PKU involves a lifelong low-phenylalanine diet to control symptoms and prevent complications.
Phenylketonuria Ppt
Phenylketonuria (PKU) is a genetic disorder caused by a mutation that prevents the breakdown of phenylalanine. This allows phenylalanine levels to accumulate in the blood and brain, which can cause intellectual disabilities if left untreated. The condition is usually diagnosed via newborn screening, which tests for high phenylalanine levels. Treatment requires a lifelong low-phenylalanine diet to prevent cognitive issues and other health problems associated with elevated phenylalanine. Strict dietary control is necessary to manage PKU and avoid complications.
Phenylketonuria
Phenylketonuria (PKU) is a genetic disorder caused by mutations in the PAH gene that result in deficient phenylalanine hydroxylase enzyme activity. This prevents the breakdown of the essential amino acid phenylalanine, causing it to accumulate to toxic levels and cause neurological damage if left untreated. Symptoms of PKU include intellectual disability, seizures, and behavioral issues. Treatment involves a lifelong low-phenylalanine diet to control blood phenylalanine levels, as well as enzyme replacement or gene therapies currently under investigation.
Background Phenylketonuria is an inherited disease which re.pdf
Background: Phenylketonuria is an inherited disease which results from the lack of the enzyme
phenylalanine hydroxylase (PAH). The PAH enzyme catalyzes the first step in the degradation of
phenylalanine, as shown in Figure 30.1. In the phenylketonuric patient, phenylalanine accumulates
which is eventually transaminated to phenylpyruvate, a phenylketone compound. Excess
phenylpyruvate accumulates in the blood and urine and has the effect of causing mental
retardation if untreated. Screening programs identify PKU babies at birth, and treatment consists
of a low phenylalanine diet until maturation of the brain is completed. The structure and
biochemical properties of the PAH enzyme have been well-studied.The gene for PAH has been
isolated and has been localized to chromosome 12. The PAH enzyme is a protein 451 amino
acids in length with a molecular weight of 51,900 daltons. More than 60 different mutant genes
giving rise to nonfunctional PAH proteins have been identified in PKU patients.
Question:Kinetic data in which PAH activity is compared with and without preincubation with
phenylalanine is shown in Figure 30.3. Give a structural basis for the interpretation of these data.
Figure 30.1. Phenylalanine and tyrosine meravurior. an essential cofactor for phenylalanine
hydroxylase. 95Figure 30.1. Phenylalanine and tyrosmio ..... an essential cofactor for
phenylalanine hydroxylase. 95.
Background Phenylketonuria is an inherited disease which re.pdf
Background: Phenylketonuria is an inherited disease which results from the lack of the enzyme
phenylalanine hydroxylase (PAH). The PAH enzyme catalyzes the first step in the degradation of
phenylalanine, as shown in Figure 30.1. In the phenylketonuric patient, phenylalanine accumulates
which is eventually transaminated to phenylpyruvate, a phenylketone compound. Excess
phenylpyruvate accumulates in the blood and urine and has the effect of causing mental
retardation if untreated. Screening programs identify PKU babies at birth, and treatment consists
of a low phenylalanine diet until maturation of the brain is completed. The structure and
biochemical properties of the PAH enzyme have been well-studied.The gene for PAH has been
isolated and has been localized to chromosome 12. The PAH enzyme is a protein 451 amino
acids in length with a molecular weight of 51,900 daltons. More than 60 different mutant genes
giving rise to nonfunctional PAH proteins have been identified in PKU patients.
Question:Kinetic data in which PAH activity is compared with and without preincubation with
phenylalanine is shown in Figure 30.3. Give a structural basis for the interpretation of these data.
Figure 30.1. Phenylalanine and tyrosine meravurior. an essential cofactor for phenylalanine
hydroxylase. 95Figure 30.1. Phenylalanine and tyrosmio ..... an essential cofactor for
phenylalanine hydroxylase. 95.
Recommended
Phenylalanine & tyrosine.pptx
This document summarizes the catabolism of phenylalanine and tyrosine. It discusses that phenylalanine is an essential amino acid that is converted to tyrosine. Tyrosine can then be incorporated into proteins or used to synthesize important compounds like catecholamines, thyroid hormones, and melanin. It also describes disorders that can occur if there are defects in the metabolic pathways of phenylalanine and tyrosine, including phenylketonuria (PKU), tyrosinemia types 1 and 2, and albinism. PKU is caused by a deficiency of phenylalanine hydroxylase and causes accumulation of phenylalanine that can lead to intellectual disability if left untreated.
Catabolism of phenylalanine and tyrosine and their metabolic disorders by BNP...
Catabolism of phenylalanine and tyrosine and their metabolic disorders by BNP...College of pharmaceutical sciences
Decarboxylation is the reaction by which CO2 is removed from the COOH group of an amino acid as a result an amine is formed. The reaction is catalyzed by the enzyme decarboxylase, which requires pyridoxal-P (B6-PO4) as coenzyme. Tissues like liver, kidney, brain possess the enzyme decarboxylase and also by microorganisms of intestinal tract. The enzyme removes CO2 from COOH and converts the amino acid to corresponding amine.
Phenylalanine is an essential, aromatic amino acid. The need for phenylalanine becomes minimal, if adequate tyrosine is supplied in the food. This is called the sparing action of tyrosine on phenylalanine.
Tyrosine is an aromatic amino acid. It is synthesized from phenylalanine, and so is a non-essential amino acid. The need for phenylalanine becomes minimal, if adequate tyrosine is supplied in the food. This is called the sparing action of tyrosine on the phenylalanine.
Seven amino acids produce acetyl CoA or acetoacetate and therefore are categorized as ketogenic. Of these, isoleucine, threonine, and the aromatic amino acids (phenylalanine, tyrosine, and tryptophan) are converted to compounds that produce both glucose and acetyl CoA or acetoacetate. Leucine and lysine do not produce glucose; they produce acetyl CoA and acetoacetate.
The name phenylketonuria is coined due to the fact that the metabolite phenylpyruvate is a keto acid (C6H5CH2−CO−COO−) excreted in urine in high amounts.
Phenylalanine cannot be converted to tyrosine. So, phenylalanine accumulates. Phenylalanine level in blood is elevated.Metabolism part i
The document discusses drug biotransformation and metabolism. It notes that biotransformation typically makes drugs more polar to enhance excretion, and may decrease or increase drug effects or toxicity. Drug metabolism mainly occurs in the liver, and can result in pharmacological inactivation, equal activity, or toxicological activation of metabolites. Phase I reactions include oxidation, reduction, and hydrolysis. Phase II involves conjugating metabolites to make them inactive and excretable, such as glucuronidation, acetylation, glycine addition, or sulfation.
keto.pptx
Phenylketonuria (PKU) is an inherited disorder that causes the body to be unable to break down an amino acid called phenylalanine. If left untreated, it can cause intellectual disabilities and other neurological problems. There are different types of PKU depending on severity. It is caused by mutations that impact the phenylalanine hydroxylase enzyme needed to metabolize phenylalanine. Symptoms usually appear between 3-6 months of age if untreated. Diagnosis involves newborn blood tests and managing PKU involves a lifelong low-phenylalanine diet to control symptoms and prevent complications.
Phenylketonuria Ppt
Phenylketonuria (PKU) is a genetic disorder caused by a mutation that prevents the breakdown of phenylalanine. This allows phenylalanine levels to accumulate in the blood and brain, which can cause intellectual disabilities if left untreated. The condition is usually diagnosed via newborn screening, which tests for high phenylalanine levels. Treatment requires a lifelong low-phenylalanine diet to prevent cognitive issues and other health problems associated with elevated phenylalanine. Strict dietary control is necessary to manage PKU and avoid complications.
Phenylketonuria
Phenylketonuria (PKU) is a genetic disorder caused by mutations in the PAH gene that result in deficient phenylalanine hydroxylase enzyme activity. This prevents the breakdown of the essential amino acid phenylalanine, causing it to accumulate to toxic levels and cause neurological damage if left untreated. Symptoms of PKU include intellectual disability, seizures, and behavioral issues. Treatment involves a lifelong low-phenylalanine diet to control blood phenylalanine levels, as well as enzyme replacement or gene therapies currently under investigation.
Background Phenylketonuria is an inherited disease which re.pdf
Background: Phenylketonuria is an inherited disease which results from the lack of the enzyme
phenylalanine hydroxylase (PAH). The PAH enzyme catalyzes the first step in the degradation of
phenylalanine, as shown in Figure 30.1. In the phenylketonuric patient, phenylalanine accumulates
which is eventually transaminated to phenylpyruvate, a phenylketone compound. Excess
phenylpyruvate accumulates in the blood and urine and has the effect of causing mental
retardation if untreated. Screening programs identify PKU babies at birth, and treatment consists
of a low phenylalanine diet until maturation of the brain is completed. The structure and
biochemical properties of the PAH enzyme have been well-studied.The gene for PAH has been
isolated and has been localized to chromosome 12. The PAH enzyme is a protein 451 amino
acids in length with a molecular weight of 51,900 daltons. More than 60 different mutant genes
giving rise to nonfunctional PAH proteins have been identified in PKU patients.
Question:Kinetic data in which PAH activity is compared with and without preincubation with
phenylalanine is shown in Figure 30.3. Give a structural basis for the interpretation of these data.
Figure 30.1. Phenylalanine and tyrosine meravurior. an essential cofactor for phenylalanine
hydroxylase. 95Figure 30.1. Phenylalanine and tyrosmio ..... an essential cofactor for
phenylalanine hydroxylase. 95.
Background Phenylketonuria is an inherited disease which re.pdf
Background: Phenylketonuria is an inherited disease which results from the lack of the enzyme
phenylalanine hydroxylase (PAH). The PAH enzyme catalyzes the first step in the degradation of
phenylalanine, as shown in Figure 30.1. In the phenylketonuric patient, phenylalanine accumulates
which is eventually transaminated to phenylpyruvate, a phenylketone compound. Excess
phenylpyruvate accumulates in the blood and urine and has the effect of causing mental
retardation if untreated. Screening programs identify PKU babies at birth, and treatment consists
of a low phenylalanine diet until maturation of the brain is completed. The structure and
biochemical properties of the PAH enzyme have been well-studied.The gene for PAH has been
isolated and has been localized to chromosome 12. The PAH enzyme is a protein 451 amino
acids in length with a molecular weight of 51,900 daltons. More than 60 different mutant genes
giving rise to nonfunctional PAH proteins have been identified in PKU patients.
Question:Kinetic data in which PAH activity is compared with and without preincubation with
phenylalanine is shown in Figure 30.3. Give a structural basis for the interpretation of these data.
Figure 30.1. Phenylalanine and tyrosine meravurior. an essential cofactor for phenylalanine
hydroxylase. 95Figure 30.1. Phenylalanine and tyrosmio ..... an essential cofactor for
phenylalanine hydroxylase. 95.
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1) The document discusses different types of colloidal states including emulsions, which are liquids dispersed in other liquids, and gels, which are liquids dispersed in solids.
2) Emulsions are unstable and require an emulsifying agent like soap to create a stable emulsion by reducing the tendency of the dispersed liquid droplets to coalesce.
3) The addition of electrolytes can cause the precipitation of colloidal particles by neutralizing their charge through adsorption of oppositely charged ions according to Hardy-Schulze rule where precipitation increases with higher valent ions.B.Sc. I Year Physical Chemistry_Unit III_Colloidal State Part 1
B.Sc. I Year Physical Chemistry_Unit III_Colloidal State Part 1Department of Biochemistry, Veer Bahadur Singh Purvanchal Univarsity, Jaunpur
The document discusses colloidal states and defines colloids as systems with particle sizes between 10-2000 Angstroms. It notes that Thomas Graham first classified substances into crystalloids and colloids based on their ability to diffuse through membranes. Later, it was realized that any substance can be made colloidal by subdividing particles to the appropriate size range. The document then discusses various properties of colloidal solutions or sols, including kinetic, optical, electrical properties. It also covers concepts like protective action, stability of colloids, and Hardy-Schulze law which states that precipitation increases with ion valence.B.Sc. I Year Physical Chemistry_Unit III_A- Solid State
B.Sc. I Year Physical Chemistry_Unit III_A- Solid StateDepartment of Biochemistry, Veer Bahadur Singh Purvanchal Univarsity, Jaunpur
The document discusses key concepts regarding solid states and crystallography. It defines crystalline and amorphous solids, and describes the ordered crystal lattice structure of crystalline solids. It then outlines three fundamental laws of crystallography: 1) the law of constancy of interfacial angles, 2) Hauy's law of rationality of indices, and 3) the law of constancy of symmetry. The document also discusses techniques for determining crystal structures, including Bragg's law of diffraction and X-ray diffraction methods like the Laue method and powder method.B.Sc. I Year Physical Chemistry_Unit II_b_Lequid State
B.Sc. I Year Physical Chemistry_Unit II_b_Lequid StateDepartment of Biochemistry, Veer Bahadur Singh Purvanchal Univarsity, Jaunpur
This document provides information about liquid crystals and their structure and properties. It discusses different types of liquid crystals including thermotropic, lyotropic, and metallotropic phases. Thermotropic liquid crystals exhibit phase transitions based on temperature, while lyotropic phases transition based on both temperature and concentration. Common liquid crystal phases described include nematic, smectic, chiral, and discotic phases. The document also discusses the design of liquid crystalline materials and methods for analyzing mesophases including thermal optical microscopy and differential scanning calorimetry. Biological membranes are noted to exhibit lyotropic liquid crystalline properties.B.Sc. I Year Physical Chemistry_Unit II_a_Gaseous State
B.Sc. I Year Physical Chemistry_Unit II_a_Gaseous StateDepartment of Biochemistry, Veer Bahadur Singh Purvanchal Univarsity, Jaunpur
The document discusses key concepts in physical chemistry related to gaseous states including:
1) The postulates of the kinetic molecular theory of gases and deviations from ideal gas behavior.
2) Critical phenomena and real gas behavior based on the van der Waals equation of state including relationships between critical constants and van der Waals constants.
3) Maxwell's distribution of molecular velocities and concepts like root mean square, average, and most probable velocities.Prabhakar Singh- IV_SEM-CELL GROWTH IN CULTURES
Prabhakar Singh- IV_SEM-CELL GROWTH IN CULTURESDepartment of Biochemistry, Veer Bahadur Singh Purvanchal Univarsity, Jaunpur
The document summarizes key aspects of cell growth in culture, including the typical growth cycle phases (lag, log, plateau), plating efficiency, cell synchronization techniques, cellular senescence, and methods to measure cell growth and senescence. Specifically, it describes:
1) The growth cycle phases - lag (adaptation), log (exponential growth), and plateau (confluence with reduced growth).
2) Plating efficiency is a measure of colony formation from single cells and survival at low densities.
3) Cell synchronization techniques make cells progress through the cell cycle simultaneously to study progression.
4) Senescent cells stop dividing after 30-60 population doublings and can be identified by assays likePrabhakar Singh- IV_SEM-Basic Techniques of Mammalian cell culture in vitro
Prabhakar Singh- IV_SEM-Basic Techniques of Mammalian cell culture in vitroDepartment of Biochemistry, Veer Bahadur Singh Purvanchal Univarsity, Jaunpur
This document discusses techniques for primary cell culture, including mechanical disaggregation, enzymatic disaggregation using trypsin or collagenase, and the primary explant technique. It provides details on each technique, such as how tissues are chopped or sliced, the use of enzymes at different temperatures, and factors that promote efficient development of primary cultures. The document also covers criteria for cell separation methods, cell differentiation, methods of cell transformation, and characteristics of transformed cells.Prabhakar Singh- IV_SEM-ANIMAL CELL CULTURE MEDIA
Prabhakar Singh- IV_SEM-ANIMAL CELL CULTURE MEDIADepartment of Biochemistry, Veer Bahadur Singh Purvanchal Univarsity, Jaunpur
1. Cell culture media must provide nutrients to support cell growth, maintain physiological pH and osmolality, and be sterile and isotonic. Early media used natural fluids but now artificial media are more common.
2. Complete media contain defined components like amino acids, vitamins, salts, glucose and organic supplements as well as serum which provides growth factors and nutrients. Different cell types require different optimized media.
3. Key properties of good culture media include maintaining pH of 7.0-7.4, appropriate levels of oxygen, carbon dioxide, and temperature usually 37°C. Osmolality is typically 260-320 mosm/kg to match cells.Prabhakar Singh- IV_SEM-Paper_Unit I Disorders of carbohydrate metabolism- P...
Prabhakar Singh- IV_SEM-Paper_Unit I Disorders of carbohydrate metabolism- P...Department of Biochemistry, Veer Bahadur Singh Purvanchal Univarsity, Jaunpur
The document discusses disorders of carbohydrate and lipid metabolism. It begins by defining diabetes mellitus as a metabolic disease characterized by hyperglycemia. It then describes the two main types: insulin-dependent diabetes mellitus (IDDM), which results from destruction of insulin-producing beta cells and requires insulin treatment; and non-insulin dependent diabetes mellitus (NIDDM), which is more common and often associated with obesity. It further discusses disorders like glycogen storage diseases, pentosuria, galactosemia, and regulation of blood glucose levels. Lipid disorders like hyperlipidemia are also briefly mentioned.Prabhakar singh iv sem-disorder of lipids
Prabhakar singh iv sem-disorder of lipidsDepartment of Biochemistry, Veer Bahadur Singh Purvanchal Univarsity, Jaunpur
This document discusses disorders of lipids and lipoproteins. It begins by defining lipoproteins as complexes of lipids and proteins that transport lipids in circulation, including chylomicrons, VLDL, LDL, HDL, and fatty acid-albumin complexes. It then discusses the classification and metabolism of lipoproteins, focusing on the role of LCAT and HDL in reverse cholesterol transport. The document goes on to summarize disorders related to sphingomyelins, glycolipids, cerebrosides, cholesterol, fatty liver, and ketone bodies.Prabhakar singh iv sem-paper v-maple syrup urine disease, sickle cell anemia
Prabhakar singh iv sem-paper v-maple syrup urine disease, sickle cell anemia Department of Biochemistry, Veer Bahadur Singh Purvanchal Univarsity, Jaunpur
1. The document discusses two metabolic disorders: Maple Syrup Urine Disease and Sickle Cell Anemia.
2. Maple Syrup Urine Disease is caused by a defect in the enzyme branched chain D-keto acid dehydrogenase, resulting in a buildup of amino acids and their keto acids in the blood and urine. This gives the urine a distinctive maple syrup smell.
3. Sickle Cell Anemia results from a genetic mutation that causes hemoglobin to polymerize and distort red blood cells into a sickle shape under conditions of low oxygen. The polymerization occurs due to sticky patches that form on the deoxygenated hemoglobin, binding it together into long fibers.Prabhakar singh iv sem-paper-disorders of liver and kidney
Prabhakar singh iv sem-paper-disorders of liver and kidneyDepartment of Biochemistry, Veer Bahadur Singh Purvanchal Univarsity, Jaunpur
This document discusses disorders of the liver and kidney, including jaundice and fatty liver. It provides details on normal and abnormal liver and kidney functions. Specifically, it describes obstructive jaundice, which is caused by a blockage in the bile duct, leading to increased conjugated bilirubin and alkaline phosphatase in the serum. It also discusses inulin and its use in measuring glomerular filtration rate (GFR), which is considered the gold standard for kidney function assessment. Inulin is uniquely filtered by the kidneys but not secreted or reabsorbed, allowing accurate measurement of GFR.Prabhakar singh iv sem-unit iii- diagnostic enzymes
Prabhakar singh iv sem-unit iii- diagnostic enzymesDepartment of Biochemistry, Veer Bahadur Singh Purvanchal Univarsity, Jaunpur
This document discusses several diagnostic enzymes used in biochemical testing and disease diagnosis. It provides details on SGPT and SGOT which are used to diagnose liver damage. It also discusses aldolase which can indicate muscle or liver damage if elevated. Higher levels of aldolase may be due to various health conditions affecting the liver, muscles, or other tissues. The document also summarizes information about cholinesterase which is involved in the metabolism of certain anesthetics, and may be deficient in some people, increasing risks. Finally, it briefly mentions several other diagnostic enzymes including lactate dehydrogenase, creatine phosphokinase, alkaline phosphatase, and alcohol dehydrogenase.Prabhakar singh iv sem-function test of kidney and pancreas
Prabhakar singh iv sem-function test of kidney and pancreasDepartment of Biochemistry, Veer Bahadur Singh Purvanchal Univarsity, Jaunpur
1. The document discusses the functions of the kidney and pancreas, including homeostasis, excretion of waste, hormone production, and digestion.
2. Tests of pancreatic function include measuring the enzymes amylase and lipase in serum, which are elevated in conditions like pancreatitis.
3. Pancreatitis is inflammation of the pancreas often caused by gallstones or alcohol and presents with abdominal pain and problems with fat digestion. It can damage pancreatic tissue.Prabhakar singh iv sem-abnormalities in nitrogen metabolism
Prabhakar singh iv sem-abnormalities in nitrogen metabolismDepartment of Biochemistry, Veer Bahadur Singh Purvanchal Univarsity, Jaunpur
Hyperuricemia, or high levels of uric acid in the blood, can be caused by increased production of uric acid, decreased excretion by the kidneys, or a combination of both. Symptoms include fatigue, nausea, and joint pain. Treatment depends on the underlying cause but may include medications to decrease uric acid production or improve kidney excretion, as well as lifestyle changes like diet modification. Blood urea nitrogen (BUN) is a measure of kidney function, as the kidneys filter waste products from the bloodstream. Elevated BUN can indicate kidney dysfunction, while low BUN may point to liver disease. Nitrogen balance measures the difference between nitrogen intake through food and nitrogen lost from theMore from Department of Biochemistry, Veer Bahadur Singh Purvanchal Univarsity, Jaunpur (20)
B.Sc. I Year Physical Chemistry_Unit_Computer Applications
B.Sc. I Year Physical Chemistry_Unit_Computer Applications
B.Sc. I Year Physical Chemistry_Unit-IV_B. Chemical Kinetics_Catalysis
B.Sc. I Year Physical Chemistry_Unit-IV_B. Chemical Kinetics_Catalysis
B.Sc. I Year Physical Chemistry_Unit-IV_A. Chemical Kinetics_Part 3
B.Sc. I Year Physical Chemistry_Unit-IV_A. Chemical Kinetics_Part 3
B.Sc. I Year Physical Chemistry_Unit-IV_A. Chemical Kinetics_Part II
B.Sc. I Year Physical Chemistry_Unit-IV_A. Chemical Kinetics_Part II
B.Sc. I Year Physical Chemistry_Unit-IV_A. Chemical Kinetics
B.Sc. I Year Physical Chemistry_Unit-IV_A. Chemical Kinetics
B.Sc. I Year Physical Chemistry_Unit III_Part 2_Colloidal State
B.Sc. I Year Physical Chemistry_Unit III_Part 2_Colloidal State
B.Sc. I Year Physical Chemistry_Unit III_Colloidal State Part 1
B.Sc. I Year Physical Chemistry_Unit III_Colloidal State Part 1
B.Sc. I Year Physical Chemistry_Unit III_A- Solid State
B.Sc. I Year Physical Chemistry_Unit III_A- Solid State
B.Sc. I Year Physical Chemistry_Unit II_b_Lequid State
B.Sc. I Year Physical Chemistry_Unit II_b_Lequid State
B.Sc. I Year Physical Chemistry_Unit II_a_Gaseous State
B.Sc. I Year Physical Chemistry_Unit II_a_Gaseous State
Prabhakar Singh- IV_SEM-Basic Techniques of Mammalian cell culture in vitro
Prabhakar Singh- IV_SEM-Basic Techniques of Mammalian cell culture in vitro
Prabhakar Singh- IV_SEM-Paper_Unit I Disorders of carbohydrate metabolism- P...
Prabhakar Singh- IV_SEM-Paper_Unit I Disorders of carbohydrate metabolism- P...
Prabhakar singh iv sem-paper v-maple syrup urine disease, sickle cell anemia
Prabhakar singh iv sem-paper v-maple syrup urine disease, sickle cell anemia
Prabhakar singh iv sem-paper-disorders of liver and kidney
Prabhakar singh iv sem-paper-disorders of liver and kidney
Prabhakar singh iv sem-unit iii- diagnostic enzymes
Prabhakar singh iv sem-unit iii- diagnostic enzymes
Prabhakar singh iv sem-function test of kidney and pancreas
Prabhakar singh iv sem-function test of kidney and pancreas
Prabhakar singh iv sem-abnormalities in nitrogen metabolism
Prabhakar singh iv sem-abnormalities in nitrogen metabolism
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- 1. TEJASVI NAVADHITAMASTU “Let our (the teacher and the taught) learning be radiant” Let our efforts at learning be luminous and filled with joy, and endowed with the force of purpose Paper XII: CLINICAL AND DIAGNOSTIC BIOCHEMISTRY Dr. Prabhakar Singh. D.Phil. Biochemistry Department of Biochemistry, VBSPU, Jaunpur Unit II: Inborn Errors of metabolism – Phenylketonuria, alkaptonuria, albinism, tyrosinosis,
- 2. PHENYLKETONURIA Phenylalanine (Phe, F) and tyrosine (Tyr, Y) are structurally related aromatic amino acids. Phenylalanine is an essential amino acid while tyrosine is non-essential. Besides its incorporation into proteins, the only function of phenylalanine is its conversion to tyrosine. For this reason, ingestion of tyrosine can reduce the dietary requirement of phenylalanine. This phenomenon is referred to as ‘sparing action’ of tyrosine on phenylalanine The enzyme phenylalanine hydroxylase is present in the liver. In the conversion of phenylalanine to tyrosine, the reaction involves the incorporation of one atom of molecular oxygen (O2) into the para position of phenylalanine while the other atom of O2 is reduced to form water. It is the tetrahydrobiopterin that supplies the reducing equivalents which, in turn, are provided by NADPH. Due to a defect in phenylalanine hydroxylase, the conversion of phenylalanine to tyrosine is blocked resulting in the disorder phenylketonuria (PKU) The name phenylketonuria is coined due to the fact that the metabolite phenylpyruvate is a Keto acid (C6H5CH2 CO COO–) excreted in urine in high amounts
- 5. ALKAPTONURIA (Black urine disease) OCHRONOSIS
- 7. TYROSINOSIS: Degradation Of Tyrosine Disorder
- 10. ALBINISM