Assessment of genotoxicity of aluminium acetate in bone marrow, male germ cells and fetal liver cells of Swiss albino mice.

Aluminium acetate (AA) has many pharmaceutical applications, which necessitates a thorough evaluation of its toxicity. Dose- and time-dependent genotoxic effects of AA were investigated in Swiss albino mice after exposure via intraperitoneal (i.p.) injection, by employing assays to detect chromosomal aberrations (CA) and micronuclei (MN) in bone marrow, MN in fetal liver, and abnormalities in sperm. Animals were treated with single doses of 50, 100 and 150mg/kg body weight (bw), and with daily doses of 50mg/kg bw for seven consecutive days, in order to study the effects of acute and cumulative doses, respectively. Post-treatment sampling was done at 24, 48 and 72h for bone-marrow CA and MN tests, to study time-dependent effects. Both single and repeated exposures of AA induced chromosomal aberrations, which were dose and time-dependent. The MN test failed to demonstrate genotoxicity after the single-dose exposures, indicating that a higher threshold dose is required for MN induction. Repeated treatment of AA, however, induced MN formation even at the low dose (P<0.05), reflecting genotoxicity following chronic/sub-chronic exposure. A significant reduction in mitotic index and in the P/N (polychromatic/normochromatic erythrocytes) ratio suggests that AA also has a mitodepressive effect in bone-marrow cells. AA-induced germinal genotoxicity was evident from a significant and dose-dependent increase in the percentage of abnormal spermatozoa and a reduction in sperm count. Transplacental exposure of AA resulted in the dose-dependent increase in the frequency of micronucleated erythrocytes in the developing fetus. Thus, the current in vivo study revealed genotoxic effects of AA both on somatic and germ cells of Swiss albino mice.