Effects of vitamin A and/or thyroidectomy on liver microsomal enzymes and their induction in 2,3,7,8-tetrachlorodibenzo- p -dioxin-treated rats
Toxicology, ISSN: 0300-483X, Vol: 46, Issue: 1, Page: 107-117
1987
- 14Citations
- 8Captures
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Article Description
Vitamin A and thyroid hormone status have been shown previously to alter the toxicity of 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD) in rats. In the present study, we have examined the effects of a vitamin A-excess and a vitamin A-deficient diet on thyroid hormone levels, on selected drug-metabolizing enzymes in liver microsomes, and on their inducibility by TCDD in male Sprague-Dawley rats. Except for a slight increase in serum T 3 levels, none of these end points was affected by feeding rats the vitamin A-deficient diet. In contrast, excess dietary vitamin A caused a decrease in serum thyroxine (T 4 ) and triiodothyronine (T 3 ) levels, although the levels of T 3 remained in the euthyroid range (60–80 ng/dl). The concentration of liver microsomal cytochromes P -450 and b 5 and the basal activity of benzo[ a ]pyrene hydroxylase and 7-ethoxyresorufin O -de-ethylase were unaffected by excess dietary vitamin A. This result is consistent with our previous observation that the basal activity of these enzymes is dependent more on T 3 than on T 4 levels. Vitamin A excess markedly suppressed the activity of liver microsomal UDP-glucuronosyl transferase toward 1-naphthol. However, no such enzyme suppression was observed in thyroidectomized rats. This suggests that the suppressive effect of vitamin A on UDP-glucuronosyl transferase activity may be dependent on T 3. Neither vitamin A nor thyroid status had any major effect on the inducibility of UDP- glucuronosyl transferase and cytochrome P -450-dependent enzyme activities by TCDD. However, vitamin A and TCDD had a nearly additive effect on suppression of serum T 4. It is concluded that liver microsomal enzyme induction is not associated with the modulatory effect of vitamin A and thyroid hormones on the toxicity of TCDD.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/0300483X87901429; http://dx.doi.org/10.1016/0300-483x(87)90142-9; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0023239778&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/3116724; http://linkinghub.elsevier.com/retrieve/pii/0300483X87901429; http://api.elsevier.com/content/article/PII:0300483X87901429?httpAccept=text/xml; http://api.elsevier.com/content/article/PII:0300483X87901429?httpAccept=text/plain; https://linkinghub.elsevier.com/retrieve/pii/0300483X87901429; http://dx.doi.org/10.1016/0300-483x%2887%2990142-9; https://dx.doi.org/10.1016/0300-483x%2887%2990142-9
Elsevier BV
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