Chronic exposure to Bisphenol A resulted in alterations of reproductive functions via immune defense, oxidative damage and disruption DNA/ histone methylation in male rare minnow Gobiocypris rarus

Bisphenol A (BPA) is a widely used chemical that represents a reproductive hazard in fish. However, the molecular pathways mediating reproductive toxicity under chronic BPA exposure remain unclear. To study the reproductive hazards associated with chronic BPA exposure, adult male rare minnows (Gobiocypris rarus) were treated with 15 mu g L - 1 and 225 mu g L - 1 BPA for 90 days. Results showed that chronic BPA treatment induced reproductive impairments with decreased fertilization capacity and movement time of sperm. Transcriptome analysis indicated 1421 transcripts that were differentially expressed in response to BPA exposure, which are involved in the biological process of oxidative stress, immune responses and DNA/histone methylation. BPA caused the oxidative stress via significantly increasing hydrogen peroxide (H2O2) levels and inhibiting the activities of antioxidant-related enzymes (Catalase, CAT). BPA caused an inflammatory response in the testes by significantly increasing IL-113 levels and inducing infiltration of inflammatory cells. Moreover, exposure to 15 mu g L - 1 BPA significantly decreased the genomic DNA methylation level. These data revealed that chronic BPA exposure had adverse effects on male reproduction. Oxidative stress, inflammatory response and DNA/histone methylation might account for the decreased sperm quality.

Automated summary

Chronic exposure to BPA in fish can impair male reproductive capacity, leading to decreased fertilization ability and motility of sperm. BPA induces oxidative stress, inflammatory response, and DNA/histone methylation, affecting the normal function of the reproductive system.