Hypercholesterolemia and the regulation of adrenal steroidogenesis in 2,3,7,8-tetrachlorodibenzo-p-dioxin-treated rats

Toxicology and Applied Pharmacology
M J DiBartolomeisC R Jefcoate

Abstract

Plasma and adrenal cholesterol disposition have been examined to gain further insight into the mechanisms by which 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) treatment decreases the diurnal peak in plasma corticosterone concentrations. TCDD induces an increase in plasma cholesterol concentration that is nearly complete on Day 2, at least 2 days before the most pronounced increase in adrenal cholesterol concentration (Days 4-6). This adrenal increase involves both free cholesterol and cholesterol esters, in contrast to the response to dietary hypercholesterolemia where only cholesterol esters increase. Although adrenocorticotropin (ACTH) does not increase adrenal mitochondrial cholesterol in normal rats (cholesterol turnover is faster than cholesterol uptake), this response changes between Days 6 and 9 after TCDD treatment such that ACTH then stimulates accumulation of mitochondrial cholesterol. This additional cholesterol is fully available to cytochrome P-450SCC, as judged both by active cholesterol metabolism in isolated mitochondria and by increased cholesterol-P-450SCC complex formation. The accompanying in vivo suppression of the peak plasma corticosterone concentration suggests a TCDD-induced inhibition of cholesterol sid...Continue Reading

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Citations

Apr 6, 2004·Aquatic Toxicology·Neelakanteswar Aluru, Mathilakath M Vijayan
May 1, 1995·Environmental Health Perspectives·L J GuilletteH F Percival

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