[Effect of the early postnatal induction of microsomal enzymes on their activity and the cholesterol content in the blood of adult mice from a hypercholesteremic line].
Activity of microsomal enzymes and the patterns of cholesterol metabolism were studied in mice of WSR/y strain, characterized by spontaneous development of atherosclerosis within the later periods of life, after early postnatal administration of an inductor of the enzymes 3-acetate-16 alpha-isothiocyanopregnenolone (ATCP). Administration of ATCP into newborn mice of SWR/y strain, from the 2nd up to 16th day after birth, led to a stable increase in activity of arylhydrocarbonate hydroxylase (an enzyme participating in unspecific metabolism of drugs), which was observed during the whole experimental period (4 months). The treatment with ATCP caused also a distinct increase in activity of cholesterol-7 alpha-hydroxylase (a key enzyme of cholesterol biotransformation and elimination) as well as a considerable decrease in content of cholesterol and lipoprotein atherogenic fractions in blood serum. The rate of cholesterol biosynthesis was similar both in mice treated with ATCP and in the control animals.
D000367:Age Factors; D000818:Animals; D000831:Animals, Newborn; D001189:Aryl Hydrocarbon Hydroxylases / Q000096:biosynthesis; D002784:Cholesterol / Q000097:blood*; D002790:Cholesterol 7-alpha-Hydroxylase / Q000096:biosynthesis; D004789:Enzyme Activation / Q000187:drug effects; D004790:Enzyme Induction / Q000187:drug effects; D006937:Hypercholesterolemia / Q000201:enzymology*; D051379:Mice; D008810:Mice, Inbred C57BL; D008815:Mice, Inbred Strains; D008862:Microsomes, Liver / Q000201:enzymology*; D011284:Pregnenolone / Q000031:analogs & derivatives / Q000494:pharmacology
D011284:Pregnenolone; D002784:Cholesterol; D001189:Aryl Hydrocarbon Hydroxylases; D002790:Cholesterol 7-alpha-Hydroxylase
Vliianie ranneĭ postnatal'noĭ induktsii mikrosomal'nykh fermentov na ikh aktivnost' i soderzhanie kholesterina v krovi vzroslykh mysheĭ giperkholesterinemicheskoĭ linii.