An in vivo study on the effects of hexavalent chromium contaminated drinking water on rat livers

In industrial areas chromium compounds are widespread in soil, sediments and ground-water, mostly as result of hazardous disposal practices. In the case of aquatic systems the contamination with chromium is chiefly resulting from chromium contaminated industrial and domestic wastewater effluents. It is known that the valence state of chromium depends on the pH and the redox potential and, thus, in an aquifer under high oxidative conditions and neutral pH the hexavalent chromium [Cr(VI)] species predominates. Epidemiological animal studies have established that Cr(VI) compounds are toxic, and carcinogenic and, in spite of the protective mechanisms, long term exposures to particulate Cr(VI) compounds if often related to an increased risk. of respiratory tract cancer in humans. Although some authors claim that Cr(VI) compounds also injure the gastrointestinal system this issue is object of debate. The controversy around the theme incited us to carried out a study on which human exposure to highly Cr(VI)-contaminated drinking water was mimicked by exposing along 9 weeks male Wistar rats (6) to Cr(VI)-contaminated water (Cr(VI) concentration 20 ppm). The purpose of this study was to evaluate the possible health effects resulting from ingestion of an highly Cr(VI)-contaminated drinking water. To this end the liver of Cr(VI)-exposed rats and control rats was subject to a careful raicroscopic and histological examination, and the expression of genes related to apoptosis (caspases 3 and 8, and Tp53) as well as of Tgf-beta was assessed by RT-PCR on the liver of both control rats and Cr(VI)-exposed rats. The increased expression of all the genes related to apoptosis and of Tgf-beta and the concomitant observed alterations on cell and tissue morphology, decreased cell size, inflammatory infiltration, and fibrosis following Cr(VI) ingestion do, in fact, suggest that ingestion of water contaminated with high levels of Cr(VI) caused liver injury, and that there is an ongoing growth/repair process mediated by the growth factor Tgf-beta.