BCHM 210 Midterm: Transporting Ammonia

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ceriseminnow432

18 Feb 2019

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The ammonium ion is incorporated into glutamate and glutamine: glutamate is synthesized from ammonia and -ketoglutarate in a reaction catalyzed by glutamate dehydrogenase using nadph as a reductant. Nh4 glu + nadp+ + h2o: the reaction proceeds through a protonated schiff base, the enzyme binds -ketoglutarate in a way that the hydride is transferred to form the l isomer (s absolute) of glutamate. Recall that naturally occuring amino acids in proteins are l. Now that we have the ammonium ion from the nitrogenase component, we have to incorporate it into glutamate and glutamine. Remember, glutamate dehydrogenase is a reversible reaction. In the biosynthetic direction, the nh4 reacts with a-kg and nadph; nadph gets oxidized to nadp+ and the product gets reduced to glutamate. Schiffman"s base is created in both the degradation reaction and synthetic reaction. Since the glutamate is a chiral molecule, you can get d-amino acids or l-amino acids. Naturally occurring amino acids in proteins are l-amino acids.

Related Questions

Question 1: Why do you think that the adding of sodium acetoacetate resulted in a 50% decrease in renal ammonia production?

Question 2: Explain how ketone bodies depress renal ammoniogenesis by preventing the transformation of glutamine and glutamate into Î±-ketoglutarate in the mitochondria of the renal tubular cell.

Excerpt:

Infusion of ketone bodies to ammonium chloride-loaded acidotic dogs was found to induce significant reduction in urinary excretion of ammonia. This effect could not be attributed to urinary pH variations. Total ammonia production by the left kidney was measured in 25 animals infused during 90 min with the sodium salt of D,L-Î²-hydroxybutyric acid adjusted to pH 6.0 or 4.2. Ketonemia averaged 4.5 mM/liter. In all experiments the ammonia content of both urine and renal venous blood fell markedly so that ammoniogenesis was depressed by 60% or more within 60 min after the onset of infusion. Administration of equimolar quantities of sodium acetoacetate adjusted to pH 6.0 resulted in a 50% decrease in renal ammonia production. Infusion of ketone bodies adjusted to pH 6.0 is usually accompanied by a small increase in extracellular bicarbonate (3.7 mM/liter). However infusion of D,L-sodium lactate or sodium bicarbonate in amounts sufficient to induce a similar rise in plasma bicarbonate resulted in only a slight decrement in ammonia production (15%). The continuous infusion of 5% mannitol alone during 90-150 min failed to influence renal ammoniogenesis.

Infusion of pure sodium-free Î²-hydroxybutyric acid prepared by ion exchange (pH 2.2) resulted in a 50% decrease in renal ammoniogenesis in spite of the fact that both urinary pH and plasma bicarbonate fell significantly. During all experiments where ketones were infused, the renal extraction of glutamine became negligible as the renal glutamine arteriovenous difference was abolished. Renal hemodynamics did not vary significantly. Infusion of Î²-hydroxybutyrate into the left renal artery resulted in a rapid decrease in ammoniogenesis by the perfused kidney. The present study indicates that ketone bodies exert their inhibitory influence within the renal tubular cell. Since their effect is independent of urinary or systemic acid-base changes, it is suggested that they depress renal ammoniogenesis by preventing the transformation of glutamine and glutamate into Î±-ketoglutarate in the mitochondria of the renal tubular cell.

orangeguinea-pig426

Please help me answer the questions below in reference to the reading below as well:

Infusion of ketone bodies to ammonium chloride-loaded acidotic dogs was found to induce significant reduction in urin#ary excretion of ammonia. This effect could not be attributed to urinary pH variations. (1) Total ammonia production by the left kidney was measured in 25 animals infused during 90 min with the sodium salt of D,L-Î²-hydroxybutyric acid adjusted to pH 6.0 or 4.2. Ketonemia averaged 4.5 mM/liter. (2) . In all experiments the ammonia content of both urine and renal venous blood fell markedly so that ammoniogenesis was depressed by 60% or more within 60 min after the onset of infusion. (3). Administration of equimolar quantities of sodium acetoacetate adjusted to pH 6.0 resulted in a 50% decrease in renal ammonia production. (4) Infusion of ketone bodies adjusted to pH 6.0 is usually accompanied by a small increase in extracellular bicarbonate (3.7 mM/liter). However infusion of D,L-sodium lactate or sodium bicarbonate in amounts sufficient to induce a similar rise in plasma bicarbonate resulted in only a slight decrement in ammonia production (15%). The continuous infusion of 5% mannitol alone during 90-150 min failed to influence renal ammoniogenesis. (5) Infusion of pure sodium-free Î²-hydroxybutyric acid prepared by ion exchange (pH 2.2) resulted in a 50% decrease in renal ammoniogenesis in spite of the fact that both urinary pH and plasma bicarbonate fell significantly. (6) During all experiments where ketones were infused, the renal extraction of glutamine became negligible as the renal glutamine arteriovenous difference was abolished. Renal hemodynamics did not vary significantly. Infusion of Î²-hydroxybutyrate into the left renal artery resulted in a rapid decrease in ammoniogenesis by the perfused kidney. (7) The present study indicates that ketone bodies exert their inhibitory influence within the renal tubular cell. Since their effect is independent of urinary or systemic acid-base changes, it is suggested that they depress renal ammoniogenesis by preventing the transformation of glutamine and glutamate into Î±-ketoglutarate in the mitochondria of the renal tubular cell. (8)

QUESTION 1: Why do you think that infusion of pure sodium-free Î²-hydroxybutyric acid prepared resulted in a 50% decrease in renal ammoniogenesis in spite of the fact that both urinary pH and plasma bicarbonate fell significantly.

QUESTION 2:

Why do you think that infusion of Î²-hydroxybutyrate into the left renal artery resulted in a rapid decrease in ammoniogenesis by the perfused kidney.

beigeimpala281

Please help me answer the questions below in reference to the reading below as well:

Infusion of ketone bodies to ammonium chloride-loaded acidotic dogs was found to induce significant reduction in urin#ary excretion of ammonia. This effect could not be attributed to urinary pH variations. (1) Total ammonia production by the left kidney was measured in 25 animals infused during 90 min with the sodium salt of D,L-Î²-hydroxybutyric acid adjusted to pH 6.0 or 4.2. Ketonemia averaged 4.5 mM/liter. (2) . In all experiments the ammonia content of both urine and renal venous blood fell markedly so that ammoniogenesis was depressed by 60% or more within 60 min after the onset of infusion. (3). Administration of equimolar quantities of sodium acetoacetate adjusted to pH 6.0 resulted in a 50% decrease in renal ammonia production. (4) Infusion of ketone bodies adjusted to pH 6.0 is usually accompanied by a small increase in extracellular bicarbonate (3.7 mM/liter). However infusion of D,L-sodium lactate or sodium bicarbonate in amounts sufficient to induce a similar rise in plasma bicarbonate resulted in only a slight decrement in ammonia production (15%). The continuous infusion of 5% mannitol alone during 90-150 min failed to influence renal ammoniogenesis. (5)

Infusion of pure sodium-free Î²-hydroxybutyric acid prepared by ion exchange (pH 2.2) resulted in a 50% decrease in renal ammoniogenesis in spite of the fact that both urinary pH and plasma bicarbonate fell significantly. (6) During all experiments where ketones were infused, the renal extraction of glutamine became negligible as the renal glutamine arteriovenous difference was abolished. Renal hemodynamics did not vary significantly. Infusion of Î²-hydroxybutyrate into the left renal artery resulted in a rapid decrease in ammoniogenesis by the perfused kidney. (7) The present study indicates that ketone bodies exert their inhibitory influence within the renal tubular cell. Since their effect is independent of urinary or systemic acid-base changes, it is suggested that they depress renal ammoniogenesis by preventing the transformation of glutamine and glutamate into Î±-ketoglutarate in the mitochondria of the renal tubular cell. (8)

Question 1: Why do you think that the ammonia content of both urine and renal venous blood fell markedly so that ammoniogenesis was depressed by 60% or more within 60 min after the onset of infusion?

Question 2: Why do you think that the adding of sodium acetoacetate resulted in a 50% decrease in renal ammonia production?

Question 3: Why do you think that infusion of ketone bodies adjusted is usually accompanied by a small increase in extracellular bicarbonate, but infusion of sodium lactate or sodium bicarbonate in amounts sufficient to induce a similar rise in plasma bicarbonate results in only a slight decrement in ammonia production (15%)?

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BCHM 210 Midterm: Transporting Ammonia

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