Exposure to high concentrations of mercury is known to cause damage to the nervous system, kidney and liver in human beings [13–15]. It has been reported that mercury interferes with numerous cellular activities, such as cellular repair enzymes to enhance genotoxicity [60] and significantly decreased DNA repair efficiency with the duration of exposure [17]. Mercury compounds are known to be potent chemical agents that cause DNA damage in cells. Strand breaks in DNA, unlike the breaks caused by X-rays, cannot be easily repaired [61]. In the present study, it was found that fish exposed
even to sublethal concentration of Hg(II) resulted in a significant (p < 0.05, p < 0.001) increase in the frequency of chromosomal aberrations after all the exposure periods compared with the group I, but lower than the group II. As the exposure time increased, the percentage of aberrations per metaphase and percentage incidence of aberrant cells was also increased up to 72 h and then decreased subsequently (Table 2). Single-strand breaks may arise directly from
the binding of mercury with DNA. Inorganic mercury was found to be teratogenic [18] and mutagenic [19] in the killfish, Fundulus heteroclitus. In another study, mercury was found to induce significant cytogenetic damage in terms of micronuclei in hepatocytes of salmonid rainbow trout, Oncorhynchus mykiss [62] and, in renal erythrocytes of European minnow Phoxinus phoxinus and mollie Poecilia latipinna [63]. All mercury compounds interfere with thiol metabolism, causing inhibition or inactivation of proteins containing thiol ligands and ultimately leading to mitotic disturbances