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A D Rahimtula

Publications and source records attributed to A D Rahimtula.

53 records · Page 3Linked to original sources
PubMed1972

A novel olefinic rearrangement. The enzymic conversion of cholesta-7,9-dien-3 -ol into cholesta-8,14-dien-3 -ol.

1. [3alpha-(3)H]Cholesta-7,9-dien-3beta-ol is converted in high yield into cholesterol by a 10000g(av.) supernatant fraction of rat liver homogenate. 2. Incubation of cholesta-7,9-dien-3beta-ol with [4-(3)H]NADPH and rat liver microsomal fractions under anaerobic conditions resulted in (3)H being incorporated into the 14alpha-position of cholest-7-en-3beta-ol. 3. Under anaerobic conditions in the absence of NADPH cholesta-7,9-dien-3beta-ol was isomerized into cholesta-8,14-dien-3beta-ol by rat liver microsomal fractions.

Anaerobiosis↗
PubMed1970

The stereochemistry of hydrogen elimination from C-7 in cholesterol and ergosterol biosynthesis.

The synthesis of [7alpha-(3)H]lanosterol is described. It is shown that in the conversion of [7alpha-(3)H,26,27-(14)C(2)]lanosterol into cholesterol by a rat liver system, it is the 7beta-hydrogen atom that is predominantly removed. On the other hand, the conversion of doubly labelled lanosterol into ergosterol by whole yeast cells results in the loss of the 7alpha-hydrogen atom. These results therefore suggest that the C-7 hydrogen atoms with opposite stereochemistry are labilized by the rat liver and the yeast Delta(8)-Delta(7) steroid isomerases.

Animals↗
PubMed1969

The role of a cholesta-8,14-dien-3-beta-ol system in cholesterol biosynthesis.

The biosynthesis of cholesterol from squalene and tritiated water is described. Degradation of the cholesterol indicated that C-15 may be involved in cholesterol biosynthesis. In accordance with this view it is shown that in the conversion of [2RS-(3)H(2)]mevalonic acid into cholesterol one of the hydrogen atoms at C-15 is removed. A mechanism for the removal of the 14alpha-methyl group in steroid biosynthesis that involves the labilization of a C-15 hydrogen atom is outlined. In accordance with the requirement of this scheme it is shown that 4,4'-dimethyl-cholesta-8,14-dien-3beta-ol is converted into cholesterol.

Animals↗
PubMedDate not supplied

Mechanisms of petroleum hydrocarbon toxicity: functional changes in rat liver mitochondria after exposure to a Prudhoe Bay Crude Oil.

Administration of a Prudhoe Bay Crude Oil (PBCO) to rats (5 ml/kg/day for 2 days) resulted in a 30-35% inhibition of liver mitochondrial state 3 respiration with beta-hydroxybutyrate or succinate as substrates. beta-Hydroxybutyrate dehydrogenase, succinate dehydrogenase, NADH oxidase and succinate oxidase activities were also decreased in PBCO-treated rats. A significant increase in latent ATPase activity was also observed. Our results suggest that PBCO exerts its effects on liver mitochondria through the inhibition of beta-hydroxybutyrate- and succinate-supported electron transfer activities and by impairment of the mitochondrial membrane.

Animals↗
PubMedDate not supplied

Metabolism of 2,6-dimethylnaphthalene by rat liver microsomes and effect of its administration on glutathione depletion in vivo.

Metabolism of the environmental contaminant 2,6-dimethylnaphthalene (2,6-DMN) by rat liver microsomes and an NADPH-regenerating system led to the formation of three ring oxidation metabolites--2,6-dimethyl-3-naphthol, 2,6-dimethyl-3,4-naphthoquinone, and 3,4-dihydro-3,4-dihydroxy-2,6-dimethylnaphthalene--and one side chain oxidation metabolite--2-hydroxymethyl-6-methylnaphthalene. In addition, one metabolite remained unidentified. Pretreatment of rats with phenobarbital, 3-methylcholanthrene, Prudhoe Bay crude oil, or 2,6-DMN enhanced the rate of microsomal metabolism of 2,6-DMN 2-6-fold and significantly altered the metabolite profile. Liver microsomes from variously pretreated rats also enhanced the irreversible binding of 2,6-DMN[8-14C]N to microsomal protein. This binding to protein was inhibited by glutathione in a concentration-dependent manner. In vivo administration of 2,6-DMN to untreated rats led to a time-dependent depletion of hepatic glutathione levels. Both the rate and the extent of glutathione depletion were significantly enhanced in 3-methylcholanthrene-pretreated rats but not in phenobarbital-pretreated rats.

Animals↗