Effects Of Pregnancy And Lactation Bisphenol A Exposure Spermatogenesis Function In Offspring Male Mice And Its Mechanism

Object: To explore the effect of pregnancy and lactation bisphenol A(BPA)exposure on spermatogenesis function in offspring male mice and to explore the possible influence of inflammatory responses in BPA reproductive toxicity.Material: Twenty-one pregnant C57BL/6 mice were randomly divided into three groups: a control group,a group receiving 0.2 μg/mL and a group receiving 2 μg/mL of BPA via drinking water from gestational day 6 to the end of lactation respectively.The time of sperm malformation were determined in male offspring(seven males were selected for each group)fed by normal feed for one month after wearn.Levels of serum testosterone(T)and tumor necrosis factor-α(TNF-α)were then measured in all mice.The levels of toll like receptor-4(TLR-4),nuclear factor-κB(NF-κB)and aryl hydrocarbon receptor(AhR)protein expression in the testis tissue were determined.Result: Compared with the control group,the rates of sperm malformation significantly increased in offspring of 0.2 μg/mL and 2 μg/mL BPA groups(P<0.05).Sperm count significantly decreased only in the HBPA group(P<0.05)while the levels of serum TNF-α increased in the 0.2 μg/mL and 2 μg/mL BPA groups(P<0.05).Levels of serum T decreased significantly in the 2 μg/mL BPA group,compared with controls(P<0.05).The levels of TLR4 and NF-κB protein expression in the testis were significantly higher in 0.2 μg/mL and 2 μg/mL BPA groups(P<0.05 or P<0.01),while AhR protein expression was higher,and seminiferous tubulesin the testis showed more damage,in 2 μg/mL BPA groups group compared to controls(P<0.05 and P<0.01,respectively).Conclusion: Exposure to BPA during pregnancy and lactation can cause decreased reproductive function in male offspring,which may be related to BPA damage to testicular tissue and lower serum testosterone levels;The mechanism of BPA injured reproductive function may be associated with an inflammatory response activated by the TLR4/ NF-κB and AhR signaling pathways in the testis.