Within the lethal dose range, 8.70 mmol/ml ethanol (EtOH, LD50 = 226 mmol/kg) and 6.86 mmol/ml styrene (ST, LD50 = 77.4 mmol/kg) had an additive effect in rats. A four-week pretreatment with 1/10 of the LD50 of the corresponding combination partner did not modify the lethal dose effect of the subsequently administered substance (EtOH or ST). Subchronical treatment with EtOH and ST had an additive effect, too but produced no cumulative effect in relation to lethality. Unlike EtOH, subchronical treatment with ST caused severe symptoms of illness, decrease in body weight and liver lesions. Histological examination at the combined application of EtOH plus ST showed no evidence of qualitatively or intensified effects. Subchronic administration of 1/10 of the LD50-ies of EtOH and ST produced in rats more pronounced histological liver changes than single application of the corresponding LD16-ies. Except for ATP'ase activity, histochemical reactions following EtOH or ST application showed minimal quantitative differences.

Male albino rats were orally treated in a single dose with 40 mg allyl alcohol/kg or 50 mg 4,4'-methylenedianilline/kg, or 100 mg 1,1,2,2-tetrachloroethane/kg, or 400 mg carbon tetrachloride/kg, or 800 mg chloroforme/kg, immediately after-wards exposed to increased temperature (35 degrees C, 50% RH, 4 h), and examined 20--22 hours later. Under these conditions, only carbon tetrachloride led to a more intensified changes manifesting themselves in changes of the serum enzymes LAP, ALAT, and GLDH, as well as in liver histology. The liver lesions, caused by the substances mentioned, reacted to an additional thermal strain in a comparable manner as the LD50-values determined under identical exposure conditions. The temperature-dependent enhancement of the carbon tetrachloride hepatotoxicity is ascribed to an intensification of liver peroxidation processes due to increased core temperature.