Transport and metabolism of glutamate by rat cerebellar mitochondria during ammonia toxicity.
Pathophysiological concentrations of ammonia, both in vivo and in vitro, suppressed the oxidation of glutamate by rat cerebellar mitochondria. The transport of glutamate into mitochondria was either unaltered or enhanced during hyperammonemic states. Activities of mitochondrial enzymes, aspartate aminotransferase, alanine aminotransferase, glutamate dehydrogenase, glutaminase, and GABA-transaminase were suppressed during hyperammonemic states. Suppression of 14CO2 production with (aminooxy)acetic acid but not with glutamic acid diethyl ester indicated that transamination but not oxidative deamination of glutamate plays a major role in glutamate oxidation during normal and hyperammonemic states.
Rao
V L
VL
Department of Animal Sciences, School of Life Sciences, University of Hyderabad, India.
Murthy
C R
CR
D000641:Ammonia / Q000097:blood / Q000633:toxicity*; D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D002245:Carbon Dioxide / Q000378:metabolism; D002250:Carbon Radioisotopes; D002531:Cerebellum / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D005971:Glutamates / Q000378:metabolism*; D018698:Glutamic Acid; D066298:In Vitro Techniques; D008928:Mitochondria / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar
D002250:Carbon Radioisotopes; D005971:Glutamates; D002245:Carbon Dioxide; D018698:Glutamic Acid; D000641:Ammonia