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Interaction of ethanol with β‐carotene: Delayed blood clearance and enhanced hepatotoxicity
It is concluded that β‐carotene must be administered cautiously in the presence of heavy alcohol consumption because of an associated exacerbation of the liver toxicity, and interference with the conversion of β‐ carotene to vitamin A is suggested.
Decreased hepatic vitamin A after drug administration in men and in rats.
In rats, two representative drugs (phenobarbital and methylcholanthrene) produced a significant depression of hepatic vitamin A, whereas plasma vitamin A levels remained normal, and the livers of drug-treated animals showed no abnormalities.
Increased hepatic retinal dehydrogenase activity after phenobarbital and ethanol administration.
Under conditions in which retinal dehydrogenase activity is rate-limiting for the metabolism of retinal to retinoic acid, its induction after phenobarbital or ethanol administration may contribute to hepatic vitamin A depletion.
Interaction of drugs and retinol.
In liver microsomes of ethanol-fed rats, retinol competitively inhibited the hydroxylation of aniline, the demethylation of dimethylnitrosamine, and the oxidation of ethanol to acetaldehyde, whereas
Potentiation of ethanol-induced hepatic vitamin A depletion by phenobarbital and butylated hydroxytoluene.
Administration of ethanol, phenobarbital or butylated hydroxytoluene (BHT) each resulted in significantly lower hepatic vitamin A than in untreated controls, and lung levels of retinol and retinyl esters were significantly higher in rats treated with ethanol, but remained unchanged in Rats treated with phenobarBital orbutylatedHydroxytolUene compared with control animals.
Interaction of ethanol with enflurane metabolism and toxicity: role of P450IIE1.
The results imply that ethanol-inducible P450IIE1 is the primary catalyst of hepatic EF bioactivation and that the increased bioactivation occurring in vivo secondary to chronic ethanol consumption is attendant with an increased incidence of EF hepatotoxicity.
Effects of vitamin A and ethanol on liver plasma membrane fluidity
It is concluded that liver plasma membranes contain a significant amount of vitamin A, that vitamin A supplementation increases membrane fluorescence polarization and that chronic ethanol administration can interfere with this effect.
Differential effects of retinoids and chronic ethanol consumption on membranes in rats.
Increased sialic acid concentration has been incriminated in the pathogenesis of tumor development, it may provide a mechanism whereby lowered hepatic vitamin A promotes carcinogenesis and retinoic acid feeding opposes this process.
The role of sphingosine -1 -phosphate in cardiac remodeling
The findings demonstrate that the S1P signaling machinery is increased in CF compared to CM and that CF may serve as a source of S1p in the heart, and the anti-S1P antibody reduces cardiac fibrosis in mice following MI.