Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.3.5.1 (succinate dehydrogenase)
 8,177 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The expression of a number of enzymes involved in drug metabolism, membrane function etc. was compared in hyperplastic and neoplastic lesions of the rat bladder and in human bladder tumours. Transitional cell carcinomas (TCC) in both rat and Man were characterized by decreased alkaline phosphatase (ALP) and increased gamma-glutamyl transpeptidase (GGT), beta-glucuronidase (beta-G1), succinate dehydrogenase (SD) and glucose-6-phosphate dehydrogenase (G6PD) activities. In addition, binding for antibodies specific for different cytochrome P-450 species (UT50, PB3a, MC1, MC2) and microsomal epoxide hydrolase (mEHb) was elevated in both murine and human tumours. Comparison of the enzyme phenotype in hyperplastic lesions induced by freeze ulceration or uracil administration with that in preneoplastic papillary or nodular hyperplasia (PNH) and TCC suggested, however, that most of the alteration in enzyme content or activity was non-specific and related to requirements for epithelial cell proliferation. On the other hand, the decreased ALP, and increased GGT and beta-G1 activity appeared more directly related to neoplastic transformation. The results suggested that qualitative differences exist between reactive hyperplasia and preneoplastic or neoplastic lesions in the urinary bladder. The finding of increased cytochrome P-450, in clear contrast to the reduction characteristic of preneoplastic hepatic lesions, may be important with regard to the observed difference in neoplastic transformation between the bladder and liver in response to drug metabolising enzyme inducers.
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PMID:Comparison of enzyme phenotypes in human bladder tumours and experimentally induced hyperplastic and neoplastic lesions of the rat urinary bladder. A combined histochemical and immunohistochemical approach. 256 27

Adult male rats were exposed to 0.5% manganese as MnCl2 in their drinking water for 1, 4, or 6 weeks. Manganese content was measured in brain, liver, kidney, and intestine. Peak manganese concentrations were found in all tissues after one week exposure. Hepatic aryl hydrocarbon hydroxylase, ethoxycoumarin O-deethylase, and epoxide hydrase activities increased after one week manganese exposure, while intestinal and renal activities decreased. The activities returned nearly to the control level at six weeks of exposure. The UDPglucuronosyltransferase activity increased in the liver, kidney, and intestinal mucosa after one week exposure, decreasing thereafter nearly to the control level. In the brain, most significant changes were found after six weeks exposure when the succinate dehydrogenase activity decreased. The results suggest an adaptation to manganese absorption during continuous exposure. The biotransformation enzymes respond first to manganese exposure followed by neurochemical changes in the central nervous system.
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PMID:Neurochemical and biotransformational enzyme responses to manganese exposure in rats. 678 83