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Chronic ethanol consumption affects glutathione status in rat liver.
TLDR
Chronic ethanol consumption by well-nourished rats for 6 wk increased enzyme activities related to the recycling and utilization of glutathione in the liver, suggesting an enhancement in the activities of the hepatic antioxidative defense system may be one of the protective mechanisms of the body against oxidative tissue damage caused by ethanol-induced free radicals.
Metabolism of retinol and retinoic acid by human liver cytochrome P450IIC8.
TLDR
Metabolism of two physiologic substrates by a human liver cytochrome P450 related to a group of "constitutive" rodent P450s believed to participate in the metabolism of endogenous compounds is shown for the first time.
Interaction of ethanol with β‐carotene: Delayed blood clearance and enhanced hepatotoxicity
TLDR
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.
Retinol forms retinoic acid via retinal.
TLDR
The results of this study indicate that retinal is an obligatory intermediate in the hepatic production of retinoic acid fromretinol and that cytosolic and microsomal retinol dehydrogenases play a key role in this process.
Increased hepatic retinal dehydrogenase activity after phenobarbital and ethanol administration.
TLDR
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.
Ultraviolet light-induced reductions in plasma carotenoid levels.
TLDR
It was concluded that UV treatment can reduce plasma carotenoid levels in vivo after repeated irradiation in human subjects.
Glutathione recycling is attenuated by acute ethanol feeding in rat liver.
TLDR
It is suggested that acute ethanol administration causes the oxidative tissue damage by CYP II E1-associated radical generation and the decreased radical scavenging function due to the reduced activities of hepatic glutathione recycling system such as GPx and GR.
Attenuation of alcohol‐induced hepatic fibrosis by polyunsaturated lecithin
TLDR
Results indicate that some component of lecithin exerts a protective action against the fibrogenic effects of ethanol, and that the polyunsaturated phospholipids themselves might be responsible for the protective effect.
NAD+-dependent retinol dehydrogenase in liver microsomes.
TLDR
A microsomal NAD+-dependent retinol dehydrogenase is being described with optimal activity at physiological pH which may contribute to hepatic Retinol depletion, especially in view of the insensitivity of the enzyme to ethanol inhibition.
Increased vitamin A in esophagus and other extrahepatic tissues after chronic ethanol consumption in the rat.
TLDR
Significant increases of retinoids were also found in lungs, trachea, kidneys, and testes, but not in the eyes, which suggests that chronic ethanol consumption may be associated with some mobilization of vitamin A from the liver to other organs.
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