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Questions and Answers
Within erythrocytes, which metabolic adaptation primarily sustains cellular energy requirements, and what critical enzymatic effector largely dictates its flux under hypoxic conditions?
Within erythrocytes, which metabolic adaptation primarily sustains cellular energy requirements, and what critical enzymatic effector largely dictates its flux under hypoxic conditions?
- Pentose phosphate pathway, regulated by glucose-6-phosphate dehydrogenase activity.
- Oxidative phosphorylation, modulated by cytochrome c oxidase efficacy.
- Beta-oxidation, controlled by carnitine palmitoyltransferase I activity.
- Anaerobic glycolysis, influenced primarily by phosphofructokinase-1 kinetics. (correct)
Given the exclusive reliance of erythrocytes on anaerobic glycolysis, how would a deficiency in pyruvate kinase most directly manifest clinically, and what compensatory mechanisms might be observed?
Given the exclusive reliance of erythrocytes on anaerobic glycolysis, how would a deficiency in pyruvate kinase most directly manifest clinically, and what compensatory mechanisms might be observed?
- Hemolytic anemia coupled with elevated levels of 2,3-bisphosphoglycerate (2,3-BPG). (correct)
- Thrombocytopenia caused by increased splenic sequestration.
- Methemoglobinemia due to impaired reduction of ferric iron.
- Erythrocytosis resulting from increased erythropoietin secretion.
Considering the absence of mitochondria in mature erythrocytes, if one were to introduce a synthetic organelle capable of oxidative phosphorylation, what immediate biochemical consequence would critically alter erythrocyte function?
Considering the absence of mitochondria in mature erythrocytes, if one were to introduce a synthetic organelle capable of oxidative phosphorylation, what immediate biochemical consequence would critically alter erythrocyte function?
- Enhanced pentose phosphate pathway activity, increasing NADPH production.
- Increased lactate production due to enhanced glycolytic flux.
- Suppression of glycolysis due to ATP production via oxidative phosphorylation. (correct)
- Decreased 2,3-bisphosphoglycerate (2,3-BPG) levels, raising hemoglobin's oxygen affinity.
If erythrocytes were engineered to express a functional urea cycle, how would this impact their bioenergetic profile, and what secondary metabolite accumulation or depletion would require careful monitoring?
If erythrocytes were engineered to express a functional urea cycle, how would this impact their bioenergetic profile, and what secondary metabolite accumulation or depletion would require careful monitoring?
In the context of severe hypophosphatemia, how is erythrocyte function compromised, and what specific glycolytic enzyme is most directly affected, potentially leading to hemolytic complications?
In the context of severe hypophosphatemia, how is erythrocyte function compromised, and what specific glycolytic enzyme is most directly affected, potentially leading to hemolytic complications?
Under what precise physiological conditions would the activity of glucose-6-phosphate dehydrogenase (G6PD) be maximally upregulated, considering both direct enzymatic regulation and longer-term gene expression modulation?
Under what precise physiological conditions would the activity of glucose-6-phosphate dehydrogenase (G6PD) be maximally upregulated, considering both direct enzymatic regulation and longer-term gene expression modulation?
In a cell undergoing simultaneous glycolysis and the hexose monophosphate shunt (HMS), how would a sudden, substantial increase in glycolytic flux most directly impact the HMS, considering shared intermediates and regulatory mechanisms?
In a cell undergoing simultaneous glycolysis and the hexose monophosphate shunt (HMS), how would a sudden, substantial increase in glycolytic flux most directly impact the HMS, considering shared intermediates and regulatory mechanisms?
If a researcher introduces a mutation in a cell line that completely disables the phosphopentose epimerase enzyme of the pentose phosphate pathway, what would be the most immediate and direct metabolic consequence, assuming glucose-6-phosphate dehydrogenase activity remains fully functional?
If a researcher introduces a mutation in a cell line that completely disables the phosphopentose epimerase enzyme of the pentose phosphate pathway, what would be the most immediate and direct metabolic consequence, assuming glucose-6-phosphate dehydrogenase activity remains fully functional?
How does insulin's influence on G6PD expression correlate with its broader effects on hepatic glucose metabolism, specifically concerning the balance between glycogenesis and the pentose phosphate pathway?
How does insulin's influence on G6PD expression correlate with its broader effects on hepatic glucose metabolism, specifically concerning the balance between glycogenesis and the pentose phosphate pathway?
Considering the regulatory role of NADPH in the hexose monophosphate shunt (HMS), what compensatory mechanism would a cell likely employ to maintain redox balance if a genetic mutation impairs the cell's ability to synthesize glutathione reductase?
Considering the regulatory role of NADPH in the hexose monophosphate shunt (HMS), what compensatory mechanism would a cell likely employ to maintain redox balance if a genetic mutation impairs the cell's ability to synthesize glutathione reductase?
Flashcards
Anaerobic Glycolysis
Anaerobic Glycolysis
Glycolysis that occurs without oxygen.
Mitochondria absence in RBCs
Mitochondria absence in RBCs
Red blood cells lack this organelle.
Energy pathway in RBCs
Energy pathway in RBCs
The sole pathway for energy production in RBCs.
Location of Anaerobic Glycolysis
Location of Anaerobic Glycolysis
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Role of Anaerobic Glycolysis in RBCs
Role of Anaerobic Glycolysis in RBCs
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What is HMS?
What is HMS?
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ATP in HMS
ATP in HMS
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Rate-limiting enzyme in HMS
Rate-limiting enzyme in HMS
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Insulin's effect on G6PD
Insulin's effect on G6PD
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HMS timing
HMS timing
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Study Notes
- Circulatory System Biochemistry Lecture 8
Anaerobic Glycolysis
- Serves as the exclusive energy production pathway within red blood cells (RBCs). This is due to the absence of mitochondria.
- Defects in glycolytic enzymes can lead to hemolytic anemia.
Hexose Monophosphate Shunt (Pentose Phosphate Pathway)
- Functions as a parallel pathway to glycolysis, operating concurrently.
- Does not directly consume or produce ATP. NADPH is created however.
Regulation of HMS (Hexose Monophosphate Shunt)
- Glucose-6-phosphate dehydrogenase (G6PD) acts as the rate-limiting enzyme.
- Insulin enhances the gene expression for G6PD.
Products of HMS and Their Importance
- Ribose-5-P: Plays a role in synthesis of nucleotides.
- It is converted via multiple steps to glycolytic intermediates.
NADPH
- Crucial in lipid biosynthesis, particularly in the liver, adipose tissue, mammary gland, and for cholesterol and steroid hormone production.
- Hydrogen Peroxide Reduction (Role in Erythrocytes): Hydrogen peroxide (H2O2) is dangerous to the cell.
- As a reactive oxygen species (ROS), hydrogen peroxide can oxidize lipids or cell membranes, leading to hemolysis.
- Glutathione peroxidase is an antioxidant enzyme that protects the body from hydrogen peroxide by using glutathione.
- Glutathione peroxidase includes selenium.
- Role in Invading Bacteria: HADPH Dehydrogenases reduce oxygen, turning it into peroxide, that helps kill bacteria.
Further Degradation of Peroxide After Bacteria are Killed
- Catalase splits peroxide into water and oxygen.
- Glutathione peroxidase converts peroxide into water.
Dismutase
- Dismutase converts to oxygen:
Role in Nitric Oxide Synthesis
- Functions: Nitric oxide (NO) acts as a vasodilator and neurotransmitter.
- Prevents platelet aggregation and aids in macrophage function.
- It has a very short half-life in tissues approximately 3-10 seconds.
- Nitric oxide reacts with O2, converting into nitrates and nitrites.
- Synthesis of nitric oxide requires arginine, O2, and NADPH by nitric.
Role in Cytochrome P450 Mono-oxygenase System
- Serves as the primary system for detoxification of harmful.
- Monooxygenase provides one oxygen to form hydroxyl, also hydrogen is obtained from NADPH
G6PD Deficiency (Favism)
- An X-linked, recessive hereditary defect in the G6PD gene.
- It is the most common enzyme abnormality especially in the middle east.
- Inability to detoxify oxidizing agents leads to the hemolysis of RBCs, resulting in increased unconjugated bilirubin.
Symptoms of G6PD Deficiency
- Hemolytic anemia
- Neonatal jaundice(present 1–4 days after birth.)
- Resistance to malaria
Pathogenesis of G6PD Deficiency
- A decrease in G6PD activity results in lower NADPH levels affecting glutathione. This causes damage the lipids in the RBC membrane, leading to hemolysis.
- A lack of protection against peroxides.
- ROS can oxidize proteins including hemoglobin.
- Denatured hemoglobin forms insoluble masses or Heinz bodies.
- Macrophages remove damaged RBCs in the spleen and liver.
Precipitating Factors in G6PD Deficiency
- A) Oxidant drugs: Antibiotics, Antimalarials, and Antipyretics
- B) Favism
- C) Infection
Uronic Acid Pathway
- The goal: Glucuronic acid production is obtained.
- UDP-glucose acts as the active form of glucose.
- The eventual product of glucuronic acid metabolism is D-xylulose 5-phosphate. It enters the pentose phosphate pathway.
- The glycolytic intermediates glyceraldehyde 3-phosphate and fructose 6-phosphate are produced.
Importance of Uronic Acid Pathway
- Glucuronic acid helps remove drugs, hormones, food preservatives and bilirubin via detoxification.
- Facilitates the synthesis of GAGS and proteoglycans.
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Description
Explore the intricacies of biochemistry within the circulatory system. Learn about anaerobic glycolysis in red blood cells, the hexose monophosphate shunt, its regulation, and vital products like Ribose-5-P and NADPH. Understand NADPH's crucial role in lipid biosynthesis and hydrogen peroxide reduction.
