Chloroacetonitrile reduces rat prenatal bone length and induces oxidative stress, apoptosis, and DNA damage in rat fetal liver.

One of the disinfection byproducts of chlorinating drinking water is chloroacetonitrile (CAN). Thirty-six female rats were used and distributed equally into four groups. The low dose treated group received CAN at a dose of 5.5 mg/kg body weight/day (1/40 LD50 ) orally from the 6th to 12th day of gestation. The high dose treated group received 11 mg/kg body weight/day (1/20 LD50 ) of CAN orally for the same period, the vehicle control group received 1 mL of corn oil, and the water control group received 1 mL of distilled water orally for the same period. High dose exposure to CAN significantly reduced gravid uterine weight, fetal body weights, and length, and caused obvious skeletal deformities, weak mineralization. Fetal tibial growth plates displayed histopathologic changes. Induced oxidative stress and redox imbalance in fetal liver tissues was evidenced by significantly decreased in catalase and superoxide dismutase activity, and elevated malondialdehyde levels. Histopathological, glycogen content changes, and DNA damage were observed in the fetal liver of high dose treated group. Additionally, administration of high dose of CAN induced apoptosis, evidenced by increased caspase-3 concentration in fetal liver. Thus, extensive exposure to CAN induces poor pregnancy outcomes. CAN levels in water should be monitored regularly.