Abstract: ObjectiveTo explore the influences of di-(2-ethylhexyl)phthalate (DEHP) and its principle metabolite mono
(2-ethylhexyl)phthalate (MEHP) on spermatogenic cell apoptosis in young male Wistar rats.MethodsNinety-eight2-week-old
male Wistar rats were randomly divided into14equal groups to receive daily intragastric administration of0.2ml/kg normal
saline for3weeks (normal control),100mg/kg cyclophosphamide (CTX) for1week (positive control),100, 200, and 300mg/kg
DEHP or MEHP for1week, or100mg/kg DEHP or MEHP for1, 2, and 3weeks. After the treatments, the pathological changes
of the testicular tissues were examined, spermatogenic cell apoptosis was detected, and serum sex hormones levels were
measured using TUNEL assay or radioimmunoassays.ResultsCTX, DEHP, and MEHP all caused shrinkage, development
retardation and quantitative reduction of spermatogenic cells with and mitochondrial swelling vacuolar changes. The damage
of spermatogenic cells increased significantly with the increment of DEHP and MEHP doses and exposure time. Both DEHP
and MEHP treatments resulted in significantly increased cell apoptosis index (AI) in close correlation with the exposure doses
and duration (P<0.01). DEHP and MEHP treatments also significantly increased serum levels of follicle stimulating hormone
and luteinizing hormone and decreased testosterone levels in a dose- and time-dependent manner (P<0.05).ConclusionDEHP
and MEHP can induce obvious apoptosis of spermatogenic cells in young male rats with a dose- and time-dependent effect.