PCB-treated Rats Research Articles

Influence of diet on the induction of hepatic ceroid pigment in rats by polychlorinated biphenyls

The effects of differences in diet composition on polychlorinated biphenyl (PCB) poisoning was studied in four groups of male Wistar rats fed two different diets for 30 days. In rats fed a commercial diet, normal growth was observed, whereas rats fed this diet with PCB added had markedly depressed growth. The growth of rats fed a synthetic diet was lower than that of the group fed commerical diet. The weight of the liver increased significantly in PCB-treated rats. In rats given PCB and fed a commercial diet, the liver showed prominent dark brown pigmentation which was identified histochemically as ceroid. The liver of rats given PCB and fed a synthetic diet had a pale yellow color due to an accumulation of lipids. Serum cholesterol was increased in both PCB-fed groups; serum triglyceride concentrations were increased only in rats given PCB and fed commercial diet. Liver linoleic acid concentrations in rats given PCB and fed a commercial diet, and the oleic acid concentrations in rats given PCB and fed a synthetic diet were elevated. Thus, the toxic manifestations of PCB in rats differ significantly when different dietary regimens are used.

Polychlorinated biphenyl-induced modification of lymphocyte response to plant mitogens in rats.

In PCB-treated rats total white cell and differential counts and lymphocyte proliferative response to PWM were unaltered. The lymphocyte response to PHA was increased in treated animals.

Enchanced in vitro hepatic glucuronidation of thyroxine in rats following cutaneous application or ingestion of polychlorinated biphenyls.

In rats four daily skin application of a 30% solution of a polychlorinated biphenyl (PCB) mixture in mineral oil or of a microscope immersion oil, containing 34% PCB, led to increases in liver weight, protein concentration of the 10 000 X g supernatant fluid of liver homogenates and the in vitro glucuronidation of thyroxine (T4) by the supernatant fluid, whether related to liver weight or to protein concentration in the reaction mixture. Similar effects occurred after feeding 250 ppm (mg/kg) of PCB in either Purina chow or a low-iodine diet for 11 days. It is concluded that increased hepatic T4 glucuronidation contributes to the enhanced biliary excretion of T4 previously observed in PCB-treated rats.

Effects of a polychlorinated biphenyl mixture (aroclor 1254) and DDT on biliary thyroxine excretion in rats.

Treatment of rats with a polychlorinated biphenyl mixture (Aroclor 1254; PCB) causeda 4- to 5-fold increase in the 3-hr biliary excretion of 125I-thyroxine (T4). In treated rats bile flow was increased and the 125I-T4 bile:plasma ratios (B/Pratios) and biliary clearance rate of plasma 125I-T4 were greatly elevated. The proportion of biliary 125I present as T4-glucuronide was larger in PCB-treated rats. PCB also elevated thyroid 13II uptake andreduced serum PBI concentrations. DDT did not affect the biliary excretion of 125I-T4, but did increase bile flow and the biliary clearance rate of plasma 125I-T4. It also caused a marginal elevation of B/P ratios and increased the proportion of biliary 125I present as T4-glucuronide slightly but significantly. DDT did not affect thyroid 13II uptake or serum PBI concentrations. The effects of PCB were similar to those of the polycyclic hydrocarbon-type of enzyme inducers. The results of DDT-treatment were similar to those produced by the phenobarbital type of inducer...