Low Dose of Nickel and Benzo [a] Anthracene in Rat-Diet, Induce Apoptosis, Fibrosis, and Initiate Carcinogenesis in Liver via NF- Ƙβ Pathway

This study was designed to evaluate the carcinogenic risk and other risks associated with long-term consumption of environmentally relevant dose of nickel and benzo [a] anthracene in rats. Thirty-six (36) male rats weighing between 80 and 100 g were assigned into 6 groups of 6 animals each; normal, nickel-, and benzo [a] anthracene-exposed groups for 12 and 24 weeks, respectively. Micronucleus and comet analyses were done in the blood, liver, and bone marrow. Liver function, redox, and inflammatory markers (AST, ALT, GGT, SOD, GSH, MDA, protein carbonyl, protein thiol, total protein, IL-10, 1L-1β, TNF-α, TGF-β NF-Ƙβ, and 8-oxodeoxyguansine) were analysed by standard methods. Immuno-histochemical quantification of Bax, Bcl2, and Erk 1/2 as well as mRNA expression of cyclin D1 was done in liver. From the results, weight gain was observed in varying degrees throughout the exposure period. The polychromatic erythrocytes/normochromatic erythrocytes ratio > 0.2 indicates no cytotoxic effects on the bone marrow. Percentage-MnPCE in blood significantly (p < 0.05) increased throughout exposure duration. Percentage tail DNA in blood was significantly (< 0.05) increased at weeks 20 and 24 in the exposed groups and in liver at weeks 12 (16.22 ± 0.47) and 24 (17.00 ± 0.36) of nickel-exposed rats. The aspartate amino transferase (AST):alanine amino transferase (ALT) ratio indicated fatty liver disease in the benzo [a] anthracene (0.90) and acute liver injury in the nickel (...
Source: Biological Trace Element Research - Category: Biology Authors: Source Type: research