Biochemical and histocytochemical studies on response of ammonia-producing enzymes for nh4cl-induced acidosis.
Author(s) -
Shinichi Seyama,
Soichi Iijima,
Nobuhiko Katunuma
Publication year - 1977
Publication title -
journal of histochemistry and cytochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.971
H-Index - 124
eISSN - 1551-5044
pISSN - 0022-1554
DOI - 10.1177/25.6.18540
Subject(s) - acidosis , convoluted tubule , glutamate dehydrogenase , medicine , glutaminase , tubule , endocrinology , proximal tubule , chemistry , metabolic acidosis , enzyme , distal convoluted tubule , kidney , mitochondrion , biochemistry , biology , glutamine , amino acid , glutamate receptor , nephron , receptor
NH4Cl-induced acidosis in rats resulted in renal enlargement and increase in activities of phosphate-dependent glutaminase and glutamic dehydrogenase. The renal enlargement was associated with protein synthesis but not deoxyribonucleic acid synthesis. In control rats histochemical activity of glutamic dehydrogenase was seen dominantly in the proximal straight tubule. In acidotic rats high activity was noted in the proximal convoluted tubule as well as in the proximal straight tubule. By electron microscopy reaction product was in mitochondria. The results suggest that urine ammonia is produced in mitochondria of epithelial cells in the proximal straight tubule in both normal and acidotic rats. Increased enzyme activity in acidotic rats is largely associated with epithelial cells of the proximal convoluted tubule.
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