The Effect of Cobalt Chloride and Chromium Chloride on Development of Mouse Liver during Pregnancy

Cobalt (Co2+) is required as an essential trace element to a variety of metabolic functions such as the synthesis of vitamin B12 in mammals. It was proven that cobalt passes through the placenta to the fetus. Cobalt possesses toxic effect on embryo. Also, Chromium (Cr3+) as an essential element for both animal and human nutrition has antioxidative capacity. In this study we examined the effects of exposure to cobalt chloride and chromium chloride on development of mouse liver during pregnancy. Methods: Pregnant mice received intraperitoneally injection of cobalt chloride and chromium chloride at the concentrations of Co10, Co40, Cr 50, Co10 Cr50, Co40 Cr50 mg/Kg bw on day 14 pregnancy. A group did not receive any treatment and served as control group. After pups delivery, female pups were sacrificed on days 21 and 60 (P21 and P60) and then liver were removed, weighed and examined. Results: Cobalt chloride groups (10 and 40 mg/kg bw) caused a significant decrease in body and liver weights at P21 and P60 (p<0.05(. Light microscope investigations showed that only Co40 mg/Kg bw decreased number of uninucleate hepatocytes and increased number of binucleate hepatocytes and kupffer cells at P21 and P60 (p<0.05(. In addition, size of hepatocyte and their nuclear increased at P21 and P60 only after exposure to Co40 mg/Kg bw (p<0.05(. Co-administration of Co40 mg/Kg bw and Cr 50 mg/Kg bw to mice showed mild histological changes at P21 and P60. Histologically, the Co40 mg/Kg bw administration induced degenerative and developmental changes such as congestion of central vein, fatty changes and pyknotic nuclei in the liver of mice at P21 and P60. Conclusion: Comparative pathology of treated groups show that cobalt chloride in high concentrations affects the development of liver and appears that chromium chloride ameliorates cobalt chloride hepatotoxicity but are not completely protective.