Long Exposure Of Automobile Exhaust Source PM_2.5 Leads To Male Reproductive Dysfunction Experimental Study In Animal

ObjectiveTo explore the effects of chronic PM2.5 (Particulate Matter 2.5, PM2.5) exposure on fertility function of Sprague Dawley (SD) male rats through establishing long term PM2.5 exposure model.MethodsForty-five male SD rats (80-94g,28 days old) were randomly assigned to three groups:saline control group, PM2.5 low dose group (2μg/100g.d) and PM2.5 high dose group (16μg/100g.d), and intratracheal instillation with 0.9% saline or PM2.5 respectively every day for sustaining 60 days.24h after the last exposure, the rats get mating experiments and other were sacrificed and the epididymis were removed for sperm count and deformity detection, the testis were removed for pathological examination and biochemical examination for cx43 protein expression.Western-blot experiments detect the superoxide dismutase expression level in testicular tissue, and then testicular tissue sections immunohistoehemistry analysis the location of p-AKT, as well as detected p-AKT, PI3K expression by Western blot.ResultsCompared with the normal group, the conception rate was lower, the sperm count and quality was significantly decreased, connexin43 expression was decreased in testis after PM2.5 exposure, and testicular blood-testis barrier damage,the histological structure of seminiferous tubule was disordered, the sperm count in testicular lumen decreased and part of the secondary spermatocyte falls off testicular.After PM2.5 exposure, PI3K/AKT signaling pathway is activated in testis, the production of reactive oxygen species increased. Correspondingly, the SOD1 expression was increased obviously in low dose group and increased slightly in high dose group.ConclusionLong exposure with the automobile exhaust source PM2.5 affected the integrity of blood testosterone barrier, destroyed the stability of spermatogenic microenvironment, spermatogenic cell developed abnormally, then caused the number of sperm decreased and the quality reduced, and ultimately led to reproductive function damage.Long exposure with the automobile exhaust source PM2.5 leading to increased production of reactive oxygen species by activating PI3K/AKT signaling pathway, Sertoli cell dysfunction then damage to the blood-testis barrier.