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735286 
Journal Article 
Abstract 
Effects of co-administration of polychlorinated biphenyls and the plasticizer di(2-ethylhexyl)phthalate on the liver and thyroid 
Ozalp, S; Weaver, R; Price, SC; Hinton, RH 
1987 
Yes 
Biochemical Society Transactions
ISSN: 0300-5127
EISSN: 1470-8752 
15 
452-453 
English 
The effect of combined dietary treatment with di(2-ethylhexyl)phthalate (117817) (DEHP) in doses of 2000 or 10,000 parts per million (ppm) and Aroclor (1336363) in doses of 25 to 150ppm on liver and thyroid structure and function of rats was evaluated by electron microscopy and by levels of thyroid hormones in the plasma and hepatic enzyme assays. Both Aroclor and DEHP reduced the levels of thyroxine (T4) in serum and induced hypertrophy of the Golgi apparatus, increased lysosomes, and degenerative mitochondrial changes in the thyroid. DEHP depressed and Aroclor induced liver glucuronyltransferase, while alpha-glycerophosphate-dehydrogenase was depressed by Aroclor and induced by DEHP. The effects of combined administration of low doses of the chemicals were not significantly different from those of the major compound given singly. The outcome of the combined administration of high doses of the compounds was dependent on the particular factor measured. Additive effects of liver weight and activity of glucose-6-phosphatase were seen on levels of T4 in the plasma and thyroid morphology. In contrast, only the levels of inducing agents influenced alpha-glycerophosphate-dehydrogenase and glucuronyltransferase. The level of triiodothyronine in the serum was depressed in all animals treated with DEHP in combination with Aroclor, while the single compounds failed to alter this parameter. The authors conclude that the only likely effect of combined exposure which is of toxicological concern is depression of triiodothyronine, which could result in clinical hypothyroidism. 
DCN-158318; Polychlorinated biphenyls; Phthalates; Laboratory animals; In vivo studies; Toxicology; Histopathology; Ultrastructure; Liver enzymes; Hepatotoxicity; Thyroid gland disorders 
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