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Quinalphos (QNP), an organophosphate insecticide, is known to induce genotoxic and cytotoxic effects in non-target organisms. This study evaluated the impact of subacute QNP exposure on chromosomal stability, DNA integrity, and apoptosis-related gene expression in bone marrow cells of male Swiss albino mice, and assessed the genoprotective potential of piperine (PIP), a bioactive compound from Piper nigrum. Mice were allocated into six groups: control (2% gum acacia), QNP I (0.375 mg/kg b.w.), QNP II (0.75 mg/kg b.w.), PIP alone (10 mg/kg b.w.), QNP I + PIP, and QNP II + PIP. All treatments were administered orally for 28 days. Genotoxicity was evaluated using micronucleus, chromosomal aberration, and alkaline comet assays. QNP caused a significant, dose-dependent increase in micronucleated erythrocytes, chromosomal aberrations, and DNA strand breaks, along with suppression of erythropoiesis. It also upregulated pro-apoptotic Bax and downregulated anti-apoptotic Bcl-2 mRNA expression, indicating activation of the mitochondrial apoptotic pathway. Co-administration of piperine significantly reduced genotoxic alterations, though it did not fully restore Bax/ Bcl-2 balance. These findings suggest that piperine exerts protective effects against QNP-induced genetic damage and apoptotic dysregulation.
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Singh et al. (2026) studied this question.