Cigarette smoke exposure alters [14c]arachidonic acid metabolism in aortas and platelets of rats fed various levels of selenium and vitamin e

M. A. Valentovic, C. Gairola, W. C. Lubawy

Research output: Contribution to journalArticle

8 Scopus citations

Abstract

Tats were placed on a basal diet supplemented with 0,0.03, or 3 ppm selenium and 0 or 20 ppm vitamin E (or 41-43 wk. Selenium deficiency decreased hepatic glutathione peroxidase activity and lowered both aortic prostacyclin (PGI2) and platelet thromboxane (TXA2) production compared to selenium- and vitamin E-supplemented animals. Vitamin E deficiency increased hepatic lipid peroxidation and decreased aortic PGI2synthesis. Rats exposed daily for 31-32 wk to fresh smoke from a UK 2R1 reference cigarette had carboxyhemoglobin levels of 0.75 + 0.12 and 4.73 ± 0.12% in sham- and smoke-exposed groups, respectively. Animals chronically exposed to cigarette smoke displayed a nearly twofold increase in pulmonary aryl hydrocarbon hydroxylase activity. Smoke exposure produced a 26-33% decrease in aortic PCI, synthesis compared to shams in the Se2E20, Se0 03E20, and Se3E0groups. Smoking also increased platelet thromboxane 91% and 98%. in the Se003E10and S3E0groups compared to shams. It is concluded that cigarette-smoke exposure and selenium or vitamin E deficiency alter aortic PGI, and platelet TXA1production.

Original languageEnglish
Pages (from-to)493-502
Number of pages10
JournalJournal of Toxicology and Environmental Health
Volume15
Issue number3-4
DOIs
StatePublished - 1 Jan 1985

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