Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.1.1.37 (malate dehydrogenase)
 4,591 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute renal failure was induced in male rats by the subcutaneous injectioon of 4 mg HgC12 per kg body weight. Enzyme activities of the proximal tubule were studied histochemically at six time intervals from 15 min to 24 h. The enzyme studied were alkaline phosphatase, 5'-nucleotidase, acid phosphatase, alpha-glycerophosphate dehydrogenase (NAD-independent), malic dehydrogenase, succinic dehydrogenase, latic dehydrogenase, glucose-6-phosphate dehydrogenase and glucose-6-phosphatase. Decreases in activity were observed for alkaline phosphatase and 5'-nucleotidase after 15 min. Acid phosphatase was decreased after 30 min. These three enzymes returned to control levels after 3 h, but malic dehydrogenase and alpha-glycerophosphate dehydrogenase were decreased at this time interval. Succinic dehydrogenase was first decreased after 6 h. The earliest morphological changes detectable by light microscopy were observed in pars recta tubules in the medullary rays after 6 h, a time when all enzymes studied showed widespread decreased activity throughout the proximal tubule. After 24 h, the pars convoluta appeared morphologically normal but the pars recta was necrotic and exhibited calcification, whereas enzyme activity was decreased (absent in some cases) in both pars convoluta and pars recta. These results support the hypothesis that Hg++, when given in a sublethal dose, is associated with early histochemical changes in the brush border of the proximal tubule, which may be related to early changes in sodium reabsorption and to the subsequent development of acute renal failure. The observation that changes in plasma membrane-associated enzymes occur early and prior to alterations in enzymes of mitochondria and the endoplasmic reticulum suggests that Hg++ interacts initially with the plasma membrane.
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PMID:Studies on the pathophysiology of acute renal failure. II. A histochemical study of the proximal tubule of the rat following administration of mercuric chloride. 18 27

1. Coupled mitochondria were isolated from exponentially growing Physarum polycephalum. 2. Activity of malate dehydrogenase (oxalacetate reduction) was 10.9 mumol/min/mg protein; the apparent Km was 64 microM. 3. The activity of NADP-isocitric dehydrogenase (IDH) was 110 nmol/min/mg with apparent Km of 35 microM. 4. NAD-IDH showed allosteric properties with AMP as a positive modulator. The apparent Km for the unmodulated activity, 2 mM, was decreased to 0.95 mM by 0.13 mM AMP. 5. Succinic dehydrogenase activity was estimated as three times higher than that of alpha-glycerophosphate dehydrogenase. 6. Mitochondria contained significant amounts of phenolic compounds. Protein estimation by the Bradford method is recommended.
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PMID:Activity of some dehydrogenase enzymes in mitochondria from Physarum polycephalum. 31 27

Zinc content of testes, bones, esophagus, kidneys, and muscles was decreased, whereas iron content was increased in the testes of zinc-deficient rats compared to restrictedly fed control rats. Histochemical enzyme determinations revealed reduced activities of certain enzymes in the testes, bones, esophagus, and kidneys. In the testes, lactic dehydrogenase (LDH), malic dehydrogenase (MDH), alcohol dehydrogenase (ADH), and NADH diaphorase; in the bones, LDH, MDH, ADH, and alkaline phosphatase; in the esophagus, MDH, ADH, and NADH diaphorase; and in the kidneys, MDH and alkaline phosphatase were decreased in zinc-deficient rats compared to restrictedly fed controls. Succinic dehydrogenase (SDH) revealed no significant changes under the conditions of our experiments in various groups of rats that were investigated. In a "repleted" group of rats, content of zinc in testes and bones increased significantly, compared to the deficient group. The iron content of the testes decreased after repletion with zinc. In the testes, bones, esophagus, and kidneys, the activities of various enzymes increased after repletion with zinc. Inasmuch as the major manifestations of zinc deficiency syndrome in the rat include growth retardation, testicular atrophy, and esophageal parakeratosis, our results suggest that the content of zinc in the above tissues most likely controls the physiological processes through the formation of zinc-dependent enzymes.
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PMID:Studies on zinc deficiency: changes in trace elements and enzyme activities in tissues of zinc-deficient rats. 429 21