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The pentose phosphate pathway generates NADPH and pentoses through oxidative and non-oxidative phases. It occurs prominently in tissues that require NADPH for fatty acid synthesis, cholesterol synthesis, steroid synthesis, and glutathione-mediated antioxidant defenses. A deficiency in glucose-6-phosphate dehydrogenase, which catalyzes the first step in the oxidative phase, can lead to hemolytic anemia upon exposure to oxidative drugs or foods like primaquine or fava beans due to the inability to generate sufficient NADPH for antioxidant defenses in red blood cells.
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Pentose phosphate pathway
The pentose phosphate pathway generates NADPH and pentoses through oxidative and non-oxidative phases. It occurs prominently in tissues that require NADPH for fatty acid synthesis, cholesterol synthesis, and antioxidant defenses. The pathway includes glucose-6-phosphate dehydrogenase, which is the first and rate-limiting step. Deficiency of this enzyme, as in G6PD deficiency, can lead to hemolytic anemia when exposed to oxidative drugs or foods due to impaired antioxidant activity in red blood cells. A case study describes a patient with G6PD deficiency who developed hemolytic anemia after treatment for malaria with the oxidative drug primaquine.
Pentose Phosphate Pathway
The pentose phosphate pathway generates NADPH and pentoses through oxidative and non-oxidative phases. It produces NADPH, an important cellular antioxidant, in tissues like liver and red blood cells. Glucose-6-phosphate dehydrogenase (G6PD) deficiency results in inadequate NADPH production and leads to hemolytic anemia upon exposure to oxidative drugs or foods. A case study describes a medical student with malaria treated with primaquine who developed hemolytic anemia due to his unknown G6PD deficiency.
Hmp shunt
The pentose phosphate pathway generates NADPH and ribose-5-phosphate. NADPH is important for protecting cells against reactive oxygen species through its role in reducing glutathione. The pathway occurs in two phases - an oxidative phase that produces ribose-5-phosphate and NADPH, and a non-oxidative phase that recycles pentose phosphates. A defect in glucose-6-phosphate dehydrogenase can cause hemolytic anemia by impairing the production of NADPH and the ability to detoxify reactive oxygen species. The entry of glucose-6-phosphate into the pathway is regulated by NADPH levels.
Hmp shunt
The document summarizes the hexose monophosphate pathway (HMP pathway), also known as the pentose phosphate pathway (PPP). The key points are:
1. The HMP pathway is an alternative glucose oxidation pathway to glycolysis that occurs in the cytosol and generates reducing equivalents in the form of NADPH as well as pentoses for nucleic acid synthesis.
2. Glucose-6-phosphate enters the oxidative phase of the pathway where it is dehydrogenated by G6PD, producing NADPH. It is then hydrolyzed and decarboxylated further producing a second NADPH molecule.
3. The non-oxidative phase interconverts
HMP Shunt | Hexose Monophosphate Pathway | Pentose Phosphate Pathway | Phosph...
This PPT contains HMP Shunt, Reactions of the pathway i.e. Oxidative & Non-oxidative. Glucose-6-Phosphate dehydrogenase (G6PD) deficiency, Regulation of Pathway, Significance of HMP shunt
Hmp shunt pathway
The pentose phosphate pathway occurs in the cytosol of cells and produces two molecules of NADPH for each glucose 6-phosphate molecule oxidized, without directly consuming or producing ATP. NADPH is important for processes like fatty acid synthesis in the liver and lactating mammary glands, and for maintaining glutathione levels in red blood cells. The pathway consists of oxidative and nonoxidative reactions, with the oxidative reactions producing pentose sugars and NADPH regulated by the enzyme G6PD.
Class 6 hmp pathway
Dr. Dhiraj J. Trivedi Biochemistry lectures for medical students
Professor, SDM College of Medical Sciences and Hospital, Dharwad, Karnataka, India.
Hexose monophosphate shunt
The document summarizes the pentose phosphate pathway, which oxidizes glucose-6-phosphate to generate pentose phosphates and the reducing agent NADPH. Rapidly dividing cells use pentoses for nucleic acid and coenzyme synthesis. Other tissues like the liver use the NADPH for fatty acid synthesis and reducing equivalents to counteract oxidative damage. The pathway contains an oxidative and nonoxidative phase, with the nonoxidative phase recycling pentoses back to glucose-6-phosphate to sustain the oxidative reactions. A mutation impairing this pathway causes Wernicke-Korsakoff syndrome due to NADPH and thiamine deficiencies. The pathway flux is regulated by cellular NADPH and NAD
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Pentose phosphate pathway
The pentose phosphate pathway generates NADPH and pentoses through oxidative and non-oxidative phases. It occurs prominently in tissues that require NADPH for fatty acid synthesis, cholesterol synthesis, and antioxidant defenses. The pathway includes glucose-6-phosphate dehydrogenase, which is the first and rate-limiting step. Deficiency of this enzyme, as in G6PD deficiency, can lead to hemolytic anemia when exposed to oxidative drugs or foods due to impaired antioxidant activity in red blood cells. A case study describes a patient with G6PD deficiency who developed hemolytic anemia after treatment for malaria with the oxidative drug primaquine.
Pentose Phosphate Pathway
The pentose phosphate pathway generates NADPH and pentoses through oxidative and non-oxidative phases. It produces NADPH, an important cellular antioxidant, in tissues like liver and red blood cells. Glucose-6-phosphate dehydrogenase (G6PD) deficiency results in inadequate NADPH production and leads to hemolytic anemia upon exposure to oxidative drugs or foods. A case study describes a medical student with malaria treated with primaquine who developed hemolytic anemia due to his unknown G6PD deficiency.
Hmp shunt
The pentose phosphate pathway generates NADPH and ribose-5-phosphate. NADPH is important for protecting cells against reactive oxygen species through its role in reducing glutathione. The pathway occurs in two phases - an oxidative phase that produces ribose-5-phosphate and NADPH, and a non-oxidative phase that recycles pentose phosphates. A defect in glucose-6-phosphate dehydrogenase can cause hemolytic anemia by impairing the production of NADPH and the ability to detoxify reactive oxygen species. The entry of glucose-6-phosphate into the pathway is regulated by NADPH levels.
Hmp shunt
The document summarizes the hexose monophosphate pathway (HMP pathway), also known as the pentose phosphate pathway (PPP). The key points are:
1. The HMP pathway is an alternative glucose oxidation pathway to glycolysis that occurs in the cytosol and generates reducing equivalents in the form of NADPH as well as pentoses for nucleic acid synthesis.
2. Glucose-6-phosphate enters the oxidative phase of the pathway where it is dehydrogenated by G6PD, producing NADPH. It is then hydrolyzed and decarboxylated further producing a second NADPH molecule.
3. The non-oxidative phase interconverts
HMP Shunt | Hexose Monophosphate Pathway | Pentose Phosphate Pathway | Phosph...
This PPT contains HMP Shunt, Reactions of the pathway i.e. Oxidative & Non-oxidative. Glucose-6-Phosphate dehydrogenase (G6PD) deficiency, Regulation of Pathway, Significance of HMP shunt
Hmp shunt pathway
The pentose phosphate pathway occurs in the cytosol of cells and produces two molecules of NADPH for each glucose 6-phosphate molecule oxidized, without directly consuming or producing ATP. NADPH is important for processes like fatty acid synthesis in the liver and lactating mammary glands, and for maintaining glutathione levels in red blood cells. The pathway consists of oxidative and nonoxidative reactions, with the oxidative reactions producing pentose sugars and NADPH regulated by the enzyme G6PD.
Class 6 hmp pathway
Dr. Dhiraj J. Trivedi Biochemistry lectures for medical students
Professor, SDM College of Medical Sciences and Hospital, Dharwad, Karnataka, India.
Hexose monophosphate shunt
The document summarizes the pentose phosphate pathway, which oxidizes glucose-6-phosphate to generate pentose phosphates and the reducing agent NADPH. Rapidly dividing cells use pentoses for nucleic acid and coenzyme synthesis. Other tissues like the liver use the NADPH for fatty acid synthesis and reducing equivalents to counteract oxidative damage. The pathway contains an oxidative and nonoxidative phase, with the nonoxidative phase recycling pentoses back to glucose-6-phosphate to sustain the oxidative reactions. A mutation impairing this pathway causes Wernicke-Korsakoff syndrome due to NADPH and thiamine deficiencies. The pathway flux is regulated by cellular NADPH and NAD
Class 6 hmp pathway
The pentose phosphate pathway, also known as the hexose monophosphate shunt, generates NADPH and pentoses through oxidative and non-oxidative phases. It occurs mainly in the liver, erythrocytes, and adipose tissue. The oxidative phase produces NADPH and pentoses, while the non-oxidative phase interconverts the pentoses. The pathway provides reducing power for biosynthesis and maintains glutathione levels, protecting red blood cells from oxidative damage. Deficiencies in this pathway can cause hemolytic anemia and other conditions.
Hmp shunt
The pentose phosphate pathway (PPP), also known as the phosphogluconate pathway or hexose monophosphate shunt, is an alternative glucose metabolism pathway to glycolysis that occurs in the cytoplasm. It has two major functions: generating reducing potential in the form of NADPH for biosynthesis, and synthesizing ribose 5-phosphate for nucleotide biosynthesis. The pathway occurs in two phases - an oxidative phase that generates NADPH and a non-oxidative phase that interconverts five carbon sugars. It is important for tissues that require NADPH for reductive biosynthesis like fatty acids, steroids, and glutathione maintenance.
Pentose phosphate pathway (Hexose Monophosphate Pathway)
Pentose phosphate pathway is an alternative pathway to glycolysis and TCA cycle for oxidation of glucose. It is a shunt of glycolysis. It is also known as hexose monophosphate (HMP) shunt or phosphogluconate pathway. It occurs in cytoplasm of both prokaryotes and eukaryotes. While it involves oxidation of glucose, its primary role is anabolic rather than catabolic. It is an important pathway that generates precursors for nucleotide synthesis and is especially important in red blood cells (erythrocytes).
HEXOSE MONOPHOSPHATE SHUNT
The document summarizes the hexose monophosphate pathway (HMP pathway), also known as the pentose phosphate pathway. It has three main functions: 1) supply NADPH, 2) convert hexoses to pentoses, and 3) enable complete oxidation of pentoses. NADPH functions as an electron donor in biosynthetic reactions, unlike NADH which generates ATP. The pathway occurs in the cytosol and is important in tissues that synthesize fatty acids and steroids, as it provides the required NADPH. Glucose utilization via this pathway varies between tissues and is higher in liver, adipose tissue, and erythrocytes. Deficiencies in enzymes in this pathway can cause
6 hmp+glucuronic
The pentose phosphate shunt, also known as the hexose monophosphate shunt (HMP shunt), is a metabolic pathway that generates NADPH and pentoses through oxidative and non-oxidative phases. It occurs mainly in the liver, adipose tissue, mammary glands, adrenal cortex, and red blood cells. The HMP shunt is a source of ribose-5-phosphate for nucleotide biosynthesis and NADPH, which is used for fatty acid synthesis and antioxidant defenses through glutathione reduction. It helps maintain red blood cell integrity by protecting hemoglobin and preventing hemolysis.
hmp-shunt
The hexose monophosphate (HMP) pathway, also known as the pentose phosphate pathway or PP pathway, functions to produce NADPH and ribose-5-phosphate. It occurs in the cytoplasm and is divided into oxidative and non-oxidative phases. The oxidative phase produces NADPH through irreversible reactions, while the non-oxidative phase produces ribose-5-phosphate through reversible reactions. NADPH is important for reducing glutathione and eliminating hydrogen peroxide, while ribose-5-phosphate contributes to nucleic acid synthesis. Deficiencies in glucose-6-phosphate dehydrogenase, an enzyme in the oxidative phase of the HMP pathway, can cause hemolytic anemia by inhibiting the production
Hmp shunt
The HMP shunt is an alternative pathway to glycolysis and the TCA cycle that oxidizes glucose. It is more anabolic in nature and responsible for biosynthesis of NADPH and pentoses (riboses) which are used to produce important biological molecules like DNA, RNA, fatty acids, and steroids. The HMP shunt involves 4 steps - 1) glucose-6-phosphate is converted to 6-phospho-glucono-δ-lactone producing NADPH, 2) hydrolysis of 6-phospho-glucono-δ-lactone to 6-phosphogluconate, 3) dehydrogenation and decarboxylation of 6-phosphog
Hmp shunt pathway
The HMP shunt, also known as the pentose phosphate pathway or phosphogluconate pathway, is an alternative pathway to glycolysis and the TCA cycle for glucose oxidation. It is more anabolic in nature and concerned with biosynthesis of NADPH and pentoses. The pathway occurs in the cytosol of tissues involved in biosynthesis like the liver, adipose tissue, and erythrocytes. It is significant in generating NADPH and pentoses like ribose-5-phosphate. NADPH is important for biosynthesis of fatty acids, steroids, and antioxidant defense while pentoses are precursors for nucleic acid synthesis. Regulation involves inhibition of the first step by NADPH. Genetic deficiencies can
HMP shunt
The pentose phosphate pathway generates NADPH and pentose sugars. It has both an oxidative and non-oxidative phase. In the oxidative phase, glucose-6-phosphate is oxidized to produce NADPH. In the non-oxidative phase, 5-carbon sugars are converted into 3 and 6 carbon sugars through a series of isomerization, epimerization, and transketolase reactions. The pathway is important as it provides NADPH for biosynthetic reactions and pentose sugars for nucleotide synthesis. A defect in glucose-6-phosphate dehydrogenase can lead to insufficient NADPH and glutathione, resulting in hemolytic anemia due to oxidative damage of red blood cells.
Lec07 hm ppath
The document summarizes key aspects of the pentose phosphate pathway (PPP). It describes the two main functions of the PPP as generating NADPH and producing ribose-5-phosphate. It also outlines the oxidative and nonoxidative branches of the PPP and explains how the pathway can operate in different modes depending on the cell's needs for NADPH, ribose-5-phosphate, or ATP. The document also discusses glucose-6-phosphate dehydrogenase deficiency and its implications.
Pentose Phosphate Pathway (Hexose Monophosphate Shunt)
The pentose phosphate pathway generates NADPH and ribose-5-phosphate. It occurs in the cytosol in two phases: an oxidative phase that produces NADPH and ribose-5-phosphate from glucose-6-phosphate, and a non-oxidative reversible phase. NADPH is used to produce fatty acids, amino acids, and reduced glutathione which protects cells from reactive oxygen species. A deficiency in glucose-6-phosphate dehydrogenase, which produces the first NADPH, can cause hemolytic anemia due to increased oxidative damage from a lack of protection against reactive oxygen species. The pathway is regulated by NADPH levels, with more NADPH production when NADPH is used in other pathways
Hexose Monophosphate Shunt
The Hexose Monophosphate Shunt (HMP shunt) is an alternative pathway to glucose oxidation that generates NADPH and pentose sugars rather than ATP. It occurs in the cytosol and is most active in tissues involved in lipid and steroid biosynthesis that require NADPH. The pathway has an oxidative phase that produces NADPH and a non-oxidative phase that regenerates pentose sugars. It is important because it provides precursors for nucleic acid synthesis and NADPH for lipid synthesis, steroidogenesis, and antioxidant defenses. Deficiencies in the pathway can cause hemolytic anemia or neurological disorders.
Bioprocess ppt
The document summarizes two types of fermentation: alcoholic fermentation and lactic acid fermentation. In alcoholic fermentation, yeast and microorganisms ferment glucose to ethanol and CO2 through glycolysis and subsequent conversion of pyruvate to acetaldehyde and ethanol. In lactic acid fermentation, when tissues cannot be supplied with oxygen, NAD+ is regenerated through the reduction of pyruvate to lactic acid by lactate dehydrogenase. Lactic acid fermentation allows extraction of some energy from glucose in the form of ATP.
Sacharidy3 11 angl
The document summarizes several metabolic pathways including:
1) The pentose phosphate pathway which generates NADPH and ribose-5-phosphate in the oxidative phase and converts intermediates to glycolysis in the nonoxidative phase.
2) Fructose metabolism which occurs mainly in the liver and bypasses regulation of glycolysis.
3) Galactose metabolism which is converted to glucose-1-phosphate in the liver.
Hexose Monophosphate Shunt Pathway - HMP Pathway
The HMP pathway, also known as the pentose phosphate pathway or phosphogluconate oxidative pathway, is an alternate pathway to glycolysis where glucose-6-phosphate is oxidized to produce NADPH and pentoses like ribose-5-phosphate. It occurs in the cytosol of liver, adipose tissue, adrenal cortex, and red blood cells. The pathway has two phases - an oxidative phase that generates NADPH and a non-oxidative phase that produces pentoses. Glucose-6-phosphate dehydrogenase, which catalyzes the first reaction of the oxidative phase, is regulated by NADPH levels. The uronic acid pathway is another oxidative pathway for glucose that produces glucuronic
Significance of HMP Pathway
The hexose monophosphate shunt pathway generates NADPH which is used for reductive biosynthesis of fatty acids, cholesterol, and steroids in the liver, adipose tissue, adrenal cortex, and mammary glands. NADPH is also used for free radical scavenging, maintaining red blood cell membrane integrity, preventing formation of met-hemoglobin, detoxification, preserving lens transparency, and bacterial killing by macrophages. The oxidative phase occurs in tissues that require NADPH for lipid and steroid synthesis, while the non-oxidative phase can occur in all tissues to produce ribose for DNA and RNA synthesis.
EMP vs ED vs HMP
Simply differentiated between Embden-Mayerhoff Pathway (EMP) and Entner–Doudoroff pathway (ED pathway) and Hexose Monophosphate (HMP) Pathway or Pentose Phosphate Pathway.
Hmp shunt seminar
The HMP shunt involves oxidative and non-oxidative phases, with the oxidative phase consisting of 4 steps to produce NADPH and pentose sugars, and the non-oxidative phase rearranging phosphates. The shunt provides reducing power in the form of NADPH for antioxidant functions like maintaining red blood cell integrity, and produces pentose sugars used for nucleotide synthesis. Clinical significance includes G6PD deficiency causing hemolytic anemia and favism when exposed to oxidative stress, as well as other conditions related to NADPH levels like methemoglobinemia and Wernicke-Korsakoff syndrome.
Hmp shunt
The document summarizes the pentose phosphate pathway (PPP), also known as the phosphogluconate pathway or hexose monophosphate shunt. It has two main functions: providing NADPH and producing pentoses. The PPP occurs mainly in the liver, lactating mammary glands, and other tissues. It has an oxidative and non-oxidative phase and involves enzymes that oxidize glucose-6-phosphate to produce NADPH and pentose phosphates through a series of reactions. Deficiencies in enzymes in this pathway can cause hemolytic anemia, neurological disorders, and other conditions.
15 pentose
The pentose phosphate pathway generates NADPH and pentose sugars. Glucose-6-phosphate enters the pathway and is oxidized by glucose-6-phosphate dehydrogenase, producing 6-phosphogluconolactone. This is hydrolyzed to 6-phosphogluconate by 6-phosphogluconolactonase. 6-Phosphogluconate dehydrogenase further oxidizes this to ribulose-5-phosphate, producing NADPH. Ribulose-5-phosphate can be converted to other 5-carbon sugars like ribose-5-phosphate. Transketolase and transaldolase reactions interconvert pentose and triose phosphates to regenerate ribulose
Pentose phosphate pathway summary
The document discusses the pentose phosphate pathway, also known as the hexose monophosphate shunt or phosphogluconate pathway, which has two stages - an oxidative linear portion and a cyclic portion that generate NADPH and pentoses like ribose-5-phosphate.
Carbohydrate Mechanism
1. Glycolysis breaks down glucose into pyruvate, producing a small amount of ATP. Pyruvate can then enter the mitochondria for further processing.
2. In the mitochondria, pyruvate is converted into acetyl-CoA by the pyruvate dehydrogenase complex, producing NADH.
3. Acetyl-CoA then enters the citric acid cycle, where it is further oxidized, producing more NADH and FADH2. The electrons from these are transferred to the electron transport chain to produce large amounts of ATP through oxidative phosphorylation.
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Class 6 hmp pathway
The pentose phosphate pathway, also known as the hexose monophosphate shunt, generates NADPH and pentoses through oxidative and non-oxidative phases. It occurs mainly in the liver, erythrocytes, and adipose tissue. The oxidative phase produces NADPH and pentoses, while the non-oxidative phase interconverts the pentoses. The pathway provides reducing power for biosynthesis and maintains glutathione levels, protecting red blood cells from oxidative damage. Deficiencies in this pathway can cause hemolytic anemia and other conditions.
Hmp shunt
The pentose phosphate pathway (PPP), also known as the phosphogluconate pathway or hexose monophosphate shunt, is an alternative glucose metabolism pathway to glycolysis that occurs in the cytoplasm. It has two major functions: generating reducing potential in the form of NADPH for biosynthesis, and synthesizing ribose 5-phosphate for nucleotide biosynthesis. The pathway occurs in two phases - an oxidative phase that generates NADPH and a non-oxidative phase that interconverts five carbon sugars. It is important for tissues that require NADPH for reductive biosynthesis like fatty acids, steroids, and glutathione maintenance.
Pentose phosphate pathway (Hexose Monophosphate Pathway)
Pentose phosphate pathway is an alternative pathway to glycolysis and TCA cycle for oxidation of glucose. It is a shunt of glycolysis. It is also known as hexose monophosphate (HMP) shunt or phosphogluconate pathway. It occurs in cytoplasm of both prokaryotes and eukaryotes. While it involves oxidation of glucose, its primary role is anabolic rather than catabolic. It is an important pathway that generates precursors for nucleotide synthesis and is especially important in red blood cells (erythrocytes).
HEXOSE MONOPHOSPHATE SHUNT
The document summarizes the hexose monophosphate pathway (HMP pathway), also known as the pentose phosphate pathway. It has three main functions: 1) supply NADPH, 2) convert hexoses to pentoses, and 3) enable complete oxidation of pentoses. NADPH functions as an electron donor in biosynthetic reactions, unlike NADH which generates ATP. The pathway occurs in the cytosol and is important in tissues that synthesize fatty acids and steroids, as it provides the required NADPH. Glucose utilization via this pathway varies between tissues and is higher in liver, adipose tissue, and erythrocytes. Deficiencies in enzymes in this pathway can cause
6 hmp+glucuronic
The pentose phosphate shunt, also known as the hexose monophosphate shunt (HMP shunt), is a metabolic pathway that generates NADPH and pentoses through oxidative and non-oxidative phases. It occurs mainly in the liver, adipose tissue, mammary glands, adrenal cortex, and red blood cells. The HMP shunt is a source of ribose-5-phosphate for nucleotide biosynthesis and NADPH, which is used for fatty acid synthesis and antioxidant defenses through glutathione reduction. It helps maintain red blood cell integrity by protecting hemoglobin and preventing hemolysis.
hmp-shunt
The hexose monophosphate (HMP) pathway, also known as the pentose phosphate pathway or PP pathway, functions to produce NADPH and ribose-5-phosphate. It occurs in the cytoplasm and is divided into oxidative and non-oxidative phases. The oxidative phase produces NADPH through irreversible reactions, while the non-oxidative phase produces ribose-5-phosphate through reversible reactions. NADPH is important for reducing glutathione and eliminating hydrogen peroxide, while ribose-5-phosphate contributes to nucleic acid synthesis. Deficiencies in glucose-6-phosphate dehydrogenase, an enzyme in the oxidative phase of the HMP pathway, can cause hemolytic anemia by inhibiting the production
Hmp shunt
The HMP shunt is an alternative pathway to glycolysis and the TCA cycle that oxidizes glucose. It is more anabolic in nature and responsible for biosynthesis of NADPH and pentoses (riboses) which are used to produce important biological molecules like DNA, RNA, fatty acids, and steroids. The HMP shunt involves 4 steps - 1) glucose-6-phosphate is converted to 6-phospho-glucono-δ-lactone producing NADPH, 2) hydrolysis of 6-phospho-glucono-δ-lactone to 6-phosphogluconate, 3) dehydrogenation and decarboxylation of 6-phosphog
Hmp shunt pathway
The HMP shunt, also known as the pentose phosphate pathway or phosphogluconate pathway, is an alternative pathway to glycolysis and the TCA cycle for glucose oxidation. It is more anabolic in nature and concerned with biosynthesis of NADPH and pentoses. The pathway occurs in the cytosol of tissues involved in biosynthesis like the liver, adipose tissue, and erythrocytes. It is significant in generating NADPH and pentoses like ribose-5-phosphate. NADPH is important for biosynthesis of fatty acids, steroids, and antioxidant defense while pentoses are precursors for nucleic acid synthesis. Regulation involves inhibition of the first step by NADPH. Genetic deficiencies can
HMP shunt
The pentose phosphate pathway generates NADPH and pentose sugars. It has both an oxidative and non-oxidative phase. In the oxidative phase, glucose-6-phosphate is oxidized to produce NADPH. In the non-oxidative phase, 5-carbon sugars are converted into 3 and 6 carbon sugars through a series of isomerization, epimerization, and transketolase reactions. The pathway is important as it provides NADPH for biosynthetic reactions and pentose sugars for nucleotide synthesis. A defect in glucose-6-phosphate dehydrogenase can lead to insufficient NADPH and glutathione, resulting in hemolytic anemia due to oxidative damage of red blood cells.
Lec07 hm ppath
The document summarizes key aspects of the pentose phosphate pathway (PPP). It describes the two main functions of the PPP as generating NADPH and producing ribose-5-phosphate. It also outlines the oxidative and nonoxidative branches of the PPP and explains how the pathway can operate in different modes depending on the cell's needs for NADPH, ribose-5-phosphate, or ATP. The document also discusses glucose-6-phosphate dehydrogenase deficiency and its implications.
Pentose Phosphate Pathway (Hexose Monophosphate Shunt)
The pentose phosphate pathway generates NADPH and ribose-5-phosphate. It occurs in the cytosol in two phases: an oxidative phase that produces NADPH and ribose-5-phosphate from glucose-6-phosphate, and a non-oxidative reversible phase. NADPH is used to produce fatty acids, amino acids, and reduced glutathione which protects cells from reactive oxygen species. A deficiency in glucose-6-phosphate dehydrogenase, which produces the first NADPH, can cause hemolytic anemia due to increased oxidative damage from a lack of protection against reactive oxygen species. The pathway is regulated by NADPH levels, with more NADPH production when NADPH is used in other pathways
Hexose Monophosphate Shunt
The Hexose Monophosphate Shunt (HMP shunt) is an alternative pathway to glucose oxidation that generates NADPH and pentose sugars rather than ATP. It occurs in the cytosol and is most active in tissues involved in lipid and steroid biosynthesis that require NADPH. The pathway has an oxidative phase that produces NADPH and a non-oxidative phase that regenerates pentose sugars. It is important because it provides precursors for nucleic acid synthesis and NADPH for lipid synthesis, steroidogenesis, and antioxidant defenses. Deficiencies in the pathway can cause hemolytic anemia or neurological disorders.
Bioprocess ppt
The document summarizes two types of fermentation: alcoholic fermentation and lactic acid fermentation. In alcoholic fermentation, yeast and microorganisms ferment glucose to ethanol and CO2 through glycolysis and subsequent conversion of pyruvate to acetaldehyde and ethanol. In lactic acid fermentation, when tissues cannot be supplied with oxygen, NAD+ is regenerated through the reduction of pyruvate to lactic acid by lactate dehydrogenase. Lactic acid fermentation allows extraction of some energy from glucose in the form of ATP.
Sacharidy3 11 angl
The document summarizes several metabolic pathways including:
1) The pentose phosphate pathway which generates NADPH and ribose-5-phosphate in the oxidative phase and converts intermediates to glycolysis in the nonoxidative phase.
2) Fructose metabolism which occurs mainly in the liver and bypasses regulation of glycolysis.
3) Galactose metabolism which is converted to glucose-1-phosphate in the liver.
Hexose Monophosphate Shunt Pathway - HMP Pathway
The HMP pathway, also known as the pentose phosphate pathway or phosphogluconate oxidative pathway, is an alternate pathway to glycolysis where glucose-6-phosphate is oxidized to produce NADPH and pentoses like ribose-5-phosphate. It occurs in the cytosol of liver, adipose tissue, adrenal cortex, and red blood cells. The pathway has two phases - an oxidative phase that generates NADPH and a non-oxidative phase that produces pentoses. Glucose-6-phosphate dehydrogenase, which catalyzes the first reaction of the oxidative phase, is regulated by NADPH levels. The uronic acid pathway is another oxidative pathway for glucose that produces glucuronic
Significance of HMP Pathway
The hexose monophosphate shunt pathway generates NADPH which is used for reductive biosynthesis of fatty acids, cholesterol, and steroids in the liver, adipose tissue, adrenal cortex, and mammary glands. NADPH is also used for free radical scavenging, maintaining red blood cell membrane integrity, preventing formation of met-hemoglobin, detoxification, preserving lens transparency, and bacterial killing by macrophages. The oxidative phase occurs in tissues that require NADPH for lipid and steroid synthesis, while the non-oxidative phase can occur in all tissues to produce ribose for DNA and RNA synthesis.
EMP vs ED vs HMP
Simply differentiated between Embden-Mayerhoff Pathway (EMP) and Entner–Doudoroff pathway (ED pathway) and Hexose Monophosphate (HMP) Pathway or Pentose Phosphate Pathway.
Hmp shunt seminar
The HMP shunt involves oxidative and non-oxidative phases, with the oxidative phase consisting of 4 steps to produce NADPH and pentose sugars, and the non-oxidative phase rearranging phosphates. The shunt provides reducing power in the form of NADPH for antioxidant functions like maintaining red blood cell integrity, and produces pentose sugars used for nucleotide synthesis. Clinical significance includes G6PD deficiency causing hemolytic anemia and favism when exposed to oxidative stress, as well as other conditions related to NADPH levels like methemoglobinemia and Wernicke-Korsakoff syndrome.
Hmp shunt
The document summarizes the pentose phosphate pathway (PPP), also known as the phosphogluconate pathway or hexose monophosphate shunt. It has two main functions: providing NADPH and producing pentoses. The PPP occurs mainly in the liver, lactating mammary glands, and other tissues. It has an oxidative and non-oxidative phase and involves enzymes that oxidize glucose-6-phosphate to produce NADPH and pentose phosphates through a series of reactions. Deficiencies in enzymes in this pathway can cause hemolytic anemia, neurological disorders, and other conditions.
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The pentose phosphate pathway generates NADPH and pentose sugars. Glucose-6-phosphate enters the pathway and is oxidized by glucose-6-phosphate dehydrogenase, producing 6-phosphogluconolactone. This is hydrolyzed to 6-phosphogluconate by 6-phosphogluconolactonase. 6-Phosphogluconate dehydrogenase further oxidizes this to ribulose-5-phosphate, producing NADPH. Ribulose-5-phosphate can be converted to other 5-carbon sugars like ribose-5-phosphate. Transketolase and transaldolase reactions interconvert pentose and triose phosphates to regenerate ribulose
Pentose phosphate pathway summary
The document discusses the pentose phosphate pathway, also known as the hexose monophosphate shunt or phosphogluconate pathway, which has two stages - an oxidative linear portion and a cyclic portion that generate NADPH and pentoses like ribose-5-phosphate.
Carbohydrate Mechanism
1. Glycolysis breaks down glucose into pyruvate, producing a small amount of ATP. Pyruvate can then enter the mitochondria for further processing.
2. In the mitochondria, pyruvate is converted into acetyl-CoA by the pyruvate dehydrogenase complex, producing NADH.
3. Acetyl-CoA then enters the citric acid cycle, where it is further oxidized, producing more NADH and FADH2. The electrons from these are transferred to the electron transport chain to produce large amounts of ATP through oxidative phosphorylation.
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The document discusses carbohydrate metabolism, specifically glucose metabolism and the pathways involved in glucose oxidation and storage. It covers the following key points:
1) Glycolysis and the citric acid cycle are the two major pathways for glucose oxidation and energy production. Glycolysis occurs in the cytoplasm and citric acid cycle in the mitochondria.
2) Glycolysis converts glucose to pyruvate, producing a small amount of energy. Pyruvate can then enter the citric acid cycle or be converted to lactate.
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- 1. Pentose Phosphate Pathway Generation of NADPH and Pentoses
- 2. Overview Function NADPH production • Reducing power carrier • Synthetic pathways • Role as cellular antioxidants Ribose synthesis • Nucleic acids and nucleotides
- 3. Characteristics: Tissue Distribution Demand for NADPH Biosynthetic pathways • FA synthesis (liver, adipose, mammary) • Cholesterol synthesis (liver) • Steroid hormone synthesis (adrenal, ovaries, testes) Detoxification (Cytochrome P-450 System) – liver Reduced glutathione as an antioxidant (RBC) Generation of superoxide (neutrophils)
- 4. Characteristics: Oxidative and Non-oxidative Phases Oxidative phases Reactions producing NADPH Irreversible Non-oxidative phases Produces ribose-5-P Reversible reactions feed to glycolysis
- 5. NADPH producing reactions Glucose-6-P dehydrogenase 6-P-gluconate dehydrogenase
- 6. The Pentose Phosphate Pathway: Non-oxidative phases
- 7. Regulation Glucose-6-P dehydrogenase First step Rate limiting Allosteric Regulation Feedback inhibited by NADPH Inducible enzyme Induced by insulin
- 8. Role of NADPH in the RBC Production of superoxide Hb-Fe2+-O2 -> Hb-Fe3+ + O2 -. • Spontaneous rxn, 1% per hour O2 -. + 2H2O -> 2H2O2 Both O2 -. & H2O2 can produce reactive free radical species, damage cell membranes, and cause hemolysis
- 9. Detoxification of Superoxide Anion and Hydrogen Peroxide Antioxidant enzymes Superoxide dismutase Glutathione peroxidase Glutathione reductase
- 10. Case Study 21 yo male medical student with malaria Treated with primaquine Four days later: Black colored urine Low RBC count Elevated reticulocyte count RBC with Heinz bodies Low hemoglobin Elevated serum bilirubin Pt recovered in a few days
- 11. G6PDH Deficiency and Hemolytic Anemia Most common genetic enzymopathy 400 hundred variants of G6PDH deficiency Mediterranean, Asian, African descent • 400 million people affected worldwide • 50% of Kurdish men • 10-14% of African-American men with G6PD deficiency
- 12. Worldwide distribution of G6PD deficiency: 1995
- 13. G6PD Deficiency Distribution of G6PD deficiency coincides prevalence of malaria G6PD deficiency may impart some degree of malaria resistance Also sickle cell anemia
- 14. Genetics Recessive sex-linked mutation X-chromosome Rare in females (two X-chromosomes) Homozygous mutation: high hemolysis and anemia Heterozygous mutation: Normally asymptomatic • unless exposed to drugs (primaquine, anti-malarial drug) or compounds (fava bean) that produce superoxide or hydrogen peroxide
- 15. Inheritance of G6PD Deficiency
- 16. G6PD Deficiency Exposure to anti-malarial drugs (Primaquine) results in increased cellular production of superoxide and hydrogen peroxide (Primaquine sensitivity) Other chemicals known to increase oxidant stress Sulfonamides (antibiotic) Asprin and NSAIDs Quinadine and quinine Napthlane (mothballs) Fava beans (vicine & isouramil)
- 17. Fava Beans Grown worldwide Important in Middle East High in protein Frost resistant perennial Genetically modified fava bean being developed Low in vicine and isouramil Favism
- 18. Case Study 21 yo male medical student with malaria Treated with primaquine Four days later: Black colored urine Low RBC count Elevated reticulocyte count RBC with Heinz bodies Low hemoglobin Elevated serum bilirubin Pt recovered in a few days
- 19. Symptoms Black colored urine Hemolysis may result in urinary excretion of hemoglobin Low RBC count & low hemoglobin Result of high rate of hemolysis Elevated bilirubin Catabolism of heme
- 20. RBCs with Heinz Bodies Precipitation of hemoglobin due to disulfide bond formation between Hb molecues Upper photo shows distorted RBCs with large Heinz bodies Bottom photo shows RBC stained with methylene blue
- 21. Elevated Reticulocytes A RBC containing granules or filaments representing an immature stage in cell development Normally constitutes 1% of circulating RBCs Reticulocytosis Elevation of reticulocytes Indicative of active erthropoiesis in red bone marrow
- 22. Defective G6PDH Results in enzyme with unstable structure Patient with 10% of normal activity Enough to generate NADPH under normal condition Newly made RBCs have normal 6PDH activity Patients recover quickly (8 days)