Lead-induced oxidative stress contributes to the pathogenesis of lead poisoning. Considering the antioxidant properties of allicin, the objective of this study was to evaluate the efficacy of allicin in preventing lead-induced oxidative damage in the liver, kidney, brain, and gill of the common carp. Fish were divided randomly into five groups, depending on the combination of lead acetate and allicin treatments. The oxidative stress was measured by the malondialdehyde (MDA) level, reduced glutathione (GSH) content, and by enzymatic activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) in tissue homogenates. Lead acetate exposure (7.0 mgL−1, 10 days) caused a significant decrease in GSH concentration in the liver, kidney, and brain; SOD activity in the liver, kidney, and gill; and GPx activity in the liver and brain. MDA content in the liver, kidney, brain, and gill showed a significant increase following lead acetate treatment compared with the normal control group. Administration of allicin was markedly effective in decreasing lead-induced lipid peroxidation and increasing the cellular antioxidant enzyme activities and GSH levels. These results suggest that allicin can modulate lead-induced oxidative stress and might have some therapeutic and prophylactic effects on lead poisoning.

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