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• W2892086057 abstract "The acute administration of AsIII or AsV to rats produced in liver a decrease in the saturation of tryptophan pyrrolase (TP) accompanied by dose-related increases in aminolevulinate synthetase (ALAS) and oxygenase (HO) activities and corresponding decreases in P-450 concentration. The relationship between synthesis and degradation was changed as a result of As treatment. The magnitude of these effects was related to the oxidation state of As, AsIII being more potent than AsV. These results support the contention that the saturation of TP is sensitive to treatments that modify liver concentration. However, it remains to be stablished which parameter, saturation of TP or ALA synthetase activity reflect more accurately changes in the free heme pool size. The increase in oxygenase produced by As in liver appears to be mediated by a mechanism largely or entirely independent of heme. There were indications that the inhibition of P-450- dependent monooxygenases reflects a selective effect of As on certain P-450 isoforms. Although only the higher doses of As were able to affect testicular metabolism, the general effect was similar to that observed in liver. AsV affected renal ALAS, HO and P-450 at doses which were ineffective in liver and testis. The main effects of continuous exposure to As III were : 1) an initial decrease in the degree of saturation of TP which remained constant during the period of treatment and 2) an initial increase in ALA synthetase which after 10 days of exposure was reduced to a 30% increase. No significant effects on oxygenase or P-450 concentration were observed. These observations were interpreted as indicative that a new balance between synthesis and degradation had been reached and that an adaptive response to the toxic effects of AsIII was taking place. Se produced effects on TP, ALAS and HO similar to those produced by As, but it was more potent than either AsIII or AsV. Se appears to be unusual in that it increases HO without reducing P-450 concentration. Se also appears to be the first element reported to increase epoxide hydrolase (EH) activity, as yet there is no evidence to explain how or why Se induces EH. It appears that Se has a dual effect on As-induced hepatoxicity. On the one hand it has additive effects in reducing the saturation of TP, and on the other it seems to protect against the decrease in P-450 levels produced by AsIII." @default.
• W2892086057 created "2018-09-27" @default.
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• W2892086057 date "1986-01-01" @default.
• W2892086057 modified "2023-09-27" @default.
• W2892086057 title "Some hepatic and extrahepatic effects of arsenic and selenium on heme metabolism." @default.
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