Trichloroethylene toxicity in mice: a biochemical, hematological and pathological assessment.

Oral administration of trichloroethylene (TCE; 0, 500, 1000 and 2000 mg/kg/day) to male mice once daily, 5 days a week for a period of 28 days, caused a significant increase in liver weight, degeneration/necrosis of hepatocytes and characteristics proliferation of endothelial cells of hepatic sinusoids. Increase in kidney weight, glomerular nephrosis, degeneration/desquamation of tubular epithelium and characteristic amyloid deposition in glomeruli were observed only in the group of mice treated with 2000 mg/kg TCE. These changes occurred concurrently with a significant increase in total protein and free sulphydryl contents, elevated activities of acid phosphatase and catalase and decreased activity of delta-aminolevulinic acid dehydratase (delta-ALAD) indicating the sensitivity of liver and kidney as target tissues in TCE-toxicity. Hematological studies showed a significant increase in RBC counts and a reduction in WBC counts without any statistically significant change in the hemoglobin, urea nitrogen, creatinine and uric acid levels in the blood of TCE-exposed mice. A dose-related increase in cell density and acid phosphatase activity with a parallel significant decrease in the activity of delta-ALAD were observed in the bone marrow, which appear to be responsible for hematological alterations in TCE-exposed mice. The results suggest that early metabolic, pathological and hematological perturbations following a short-term exposure of TCE in mice, can provide the basis for its documented potential for chronic effects like blood dyscrasia and cancer.