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- W2410737400 abstract "Previously, we have shown the close association between hepatic concentrations of N1-acetylspermidine and the radical-producing potency of several drugs. Since vitamin E, superoxide dismutase (SOD), and reduced glutathione (GSH) are known to scavenge free radicals, in this study we tested the effect of alpha-tocopherol, one of the most potent vitamin E isomers, and SOD on the lipopolysaccharide (LPS)-induced increase in hepatic concentrations of N1-acetylspermidine. The LPS-induced increase in hepatic N1-acetylspermidine was more than twice as great in vitamin E-deficient mice as in vitamin E-supplemented mice. Pretreatment with alpha-tocopherol suppressed the LPS-induced increase in hepatic N1-acetylspermidine in vitamin E-deficient mice. Alpha-tocopherol and SOD given to mice maintained on a usual diet likewise suppressed the LPS-induced increase in hepatic N1-acetylspermidine and putrescine. The hepatic concentrations of alpha-tocopherol and GSH were lower in LPS-treated mice than in control animals. Diethyldithiocarbamate, an inhibitor of SOD, and diisopropylidene (phorone), a GSH-depleting agent, enhanced the LPS-induced increase in hepatic N1-acetylspermidine. These results suggest that the LPS-induced hepatic increase in N1-acetylspermidine is connected with radical-induced injury in vivo and that superoxide anion is produced in the liver of LPS-treated mice." @default.
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- W2410737400 date "1991-03-01" @default.
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- W2410737400 title "Alpha-tocopherol and superoxide dismutase suppress and diethyldithiocarbamate and phorone enhance the lipopolysaccharide-induced increase in N1-acetylspermidine concentrations in mouse liver." @default.
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