Aim: Allylmercaptocaptopril (AMC) is a covalently bonded product of allicin and captopril has been evaluated for its anticataract activity against selenite induced cataract in experimental animals. We wanted to evaluate its anticataract potential in galactosemic cataract to elucidate biochemical mechanism to appraise its activity. Method: We examined the protective effect of AMC in both in vitro and in vivo models of galactose-induced cataract in rats and compared the effect with captopril. We evaluated the effect of both captopril and AMC on onset and maturation of cataract in galactosemic cataract. Result: AMC reduced the rat lens polyol level, the marker of osmotic stress induced by galactose when compared with galactose treated and captopril treated lens. Glucose-6-phosphate dehydrogenase, succinate dehydrogenase, lactate dehydrogenase activity and reduced glutathione level were decreased in the galactose treated group compared with normal lenses. AMC treatment significantly restored these biochemical levels compared with the galactose treated group. The second, in vivo phase of the study revealed that AMC treatment significantly delayed the onset and maturation of cataract in galactose treated rats compared to captopril treatment. Conclusion: These results support the view that AMC counteracts the effects of galactose in inducing cataract. The anticataract effects of AMC may be related to its intrinsic ability to protect and restore the activities of lens enzymes and the bioavailability of glutathione respectively.