decreased capacity for sperm production induced by perinatal bisphenol a exposure is associated with an increased inflammatory response in the offspring of c57bl6 male mice many previous studies have indicated the adverse effects of bisphenol a bpa on sperm production and quality however the mechanisms underlying bpa male reproductive toxicity have yet to be elucidated the main purpose of this study was to investigate the effect of perinatal exposure to bpa on the spermatogenic capacity of male offspring and to explore the possible influence of inflammatory responses in bpa reproductive toxicity twentyone pregnant c57bl6mice were randomly divided into three groups a control group a group receiving 02 gml lbpa and a group receiving 2 gml of bpa hbpa all via drinking water from gestational day 6 to the end of lactation after weaning one male mouse was randomly selected from each group n 7group these three mice were fed a normal diet and drinking water for 1 month levels of serum testosterone t and tumor necrosis factor tnf were then measured in all mice sperm count and the proportion of sperm malformation were also determined the levels of tolllike receptor 4 tlr4 nuclear factor nfb and aryl hydrocarbon receptor ahr protein expression in the testis tissue were determined analysis showed that the proportion of sperm malformation increased in the lbpa and hbpa groups p 005 sperm count significantly decreased only in the hbpa group p 005 while the levels of serum tnf increased in the lbpa and hbpa groups p 005 levels of serum t decreased significantly in the hbpa group compared with controls p 005 levels of tlr4 and nfb protein expression in the testis were significantly higher in the lbpa and hbpa groups p 005 or p 001 while ahr protein expression was higher and seminiferous tubules in the testis showed more damage in the hbpa group compared to controls p 005 and p 001 respectively our results showed that perinatal exposure to low or high doses of bpa decreased the capacity for spermatogenesis in male offspring which may be associated with an inflammatory response activated by the tlr4 nfb and ahr signaling pathways in the testis