Transcriptomic profiling of testis exposure to low dose lead

Lead (Pb) is a common environmental pollutant. It has been demonstrated that long-term exposure to Pb at environmental levels may cause severe and irreversible damage to the male reproductive system. Of note, the impairments may originate from environmental Pb exposure at puberty. However, the underlying mechanisms remain unclear. In this study, we administrated male ICR mice with 200 mg/L Pb through the drinking water for 30-, 60-, 90-day from postnatal day 28. RNA sequencing was performed in the control group and 90-day Pb exposure group. It was found that Pb exposure induced testicular damage and poor sperm quality. Bioinformatic analysis and experimental verification showed that Pb exposure induces energy dysmetabolism and decreases glycolysis products in mice testicular tissue. The AMPK signaling pathway was found to be deactivated after Pb exposure. GLUT1, GLUT3, PFK1 and LDH, which play a critical role in the cell glycolysis process, also were decreased. Besides, the expression of CD147 was decreased and the location of CD147 was altered upon Pb exposure. Together, these findings indicated the implication of the AMPK signaling pathway in Pb exposure induced pubertal testicular and poor sperm quality by inhibiting cell glycolysis and disordering lactate transportation in Sertoli cells.