Q.28 The amino acid in renal tubular cells that forms ammonia,
which is finally excreted as NH4+ is:
- Aspartate
- Glutamate
- Asparagine
- Glutamine
Glutamine is the primary amino acid in renal tubular cells that generates ammonia (NH₄⁺) for excretion, aiding acid-base balance during acidosis.
Option Analysis
Renal ammoniagenesis occurs mainly in proximal tubule cells, where glutamine is deaminated to form NH₄⁺, which is secreted into urine with new bicarbonate generation.
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Aspartate – Incorrect. Aspartate participates in urea cycle/malate-aspartate shuttle but lacks key enzymes (e.g., no direct glutaminase pathway) for major NH₃ production in kidneys.
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Glutamate – Incorrect as primary source. Glutamate is an intermediate from glutamine hydrolysis via glutaminase (producing glutamate + NH₄⁺); glutamate dehydrogenase then yields more NH₄⁺, but glutamine is the initial substrate.
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Asparagine – Incorrect. Asparagine can be hydrolyzed to aspartate + NH₃ via asparaginase, but this pathway is minor in kidneys compared to glutamine’s dominant role.
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Glutamine – Correct. Taken up by proximal tubules (via SNAT3/B⁰AT1), glutamine is metabolized by phosphate-dependent glutaminase (to glutamate + NH₄⁺) and glutamate dehydrogenase (to α-KG + NH₄⁺), yielding 2 NH₄⁺ per glutamine for luminal secretion.
The amino acid in renal tubular cells that forms ammonia (NH₄⁺) is glutamine, crucial for excreting acid and regenerating bicarbonate during metabolic acidosis. This SEO guide targets “amino acid in renal tubular cells” key phrase, analyzing the MCQ options for biology/physiology exam prep like GATE Life Sciences.
Glutamine’s Role in Renal Ammoniagenesis
Proximal tubule cells extract glutamine from blood, hydrolyzing it via glutaminase (glutamine → glutamate + NH₄⁺) and glutamate dehydrogenase (glutamate → α-KG + NH₄⁺), producing 2 NH₄⁺ and 2 HCO₃⁻ per molecule. NH₄⁺ exits luminally via NHE3/Rhcg, buffering urine pH and enabling ~50-100% increased excretion in acidosis.
Why Not Other Amino Acids?
Aspartate/glutamate act downstream or in minor pathways; asparaginase from asparagine is negligible. Glutamine provides >90% of renal NH₃, upregulated 2-3x in acidosis via enzyme induction.
Key Pathways Comparison
Amino Acid Enzyme/Pathway NH₄⁺ Yield in Kidney Primary Role Glutamine Glutaminase + GDH High (2/mol) Main ammoniagenesis Glutamate GDH only Moderate (intermediate) Secondary Aspartate None direct Low Urea cycle link Asparagine Asparaginase Minimal Negligible Master glutamine as the key player for renal acid-base homeostasis in exams.
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