Firpronil induced spermotoxicity is associated with oxidative stress, DNA damage and apoptosis in male rats

• We investigated the spermotoxic potential of fipronil in male rats.
• It caused serious disturbance in seminal attributes.
• It caused oxidative stress, DNA damage and apoptosis of spermatozoa in dose dependent manner.
• It caused histopathological changes in testes.

The present study is the first to investigate and characterize the fipronil (FPN) induced spermotoxicity in male rats. Male rats were orally given FPN (2.5, 5.0 and 10 mg/kg/day) for 4 weeks. Epididymal sperms were collected and remaining testis was processed for histopathological evaluation. FPN treatment significantly reduced sperm density, motility, viability and per cent intact acrosome along with concomitant increase in spermatozoa abnormalities. Exposure of FPN caused excessive ROS generation, lipid peroxidation and alteration in mitochondrial membrane potential leading to apoptosis of spermatozoa in dose dependent manner. Higher FPN doses (5 and 10 mg/kg) markedly reduced the DNA integrity of spermatozoa. These data suggest that FPN causes male reproductive toxicity through oxidative stress induced DNA damage and apoptosis of spermatozoa.

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