Background: Phthalates are used as plasticizers in Polyvinyl chloride (PVC) plastics. The essential trace element selenium (Se) is the critical component of cellular antioxidant defense. It participates in the cellular antioxidant defense and helps in protection and repair of DNA and apoptosis. Objectives: the aim of this study was to assess the influence of di (2-ethylhexyl) phthalate (DEHP) on the male reproductive system in newborn and pubertal rats and to evaluate the effect of association between it and selenium on the development of male reproductive system. Design: forty adult pregnant female albino rats were utilized in this work (mating was performed and pregnancy was detected by daily vaginal swab). These animals were allocated randomly into four main groups. Group I (control group) received corn oil. Group ΙΙ: received diphthalates (DEHP) (150 mg/kg) by gavage daily from day 6 of gestation. Group IΙΙ: received sodium selenate (0.16mg/kg) from day 6 of gestation. Group IV: received (diphthalates (DEHP) 150 mg/kg + sodium selenate 0.16 mg/kg), daily from day 6 of gestation .After labour, the mother and the pups were categorized into 3 groups (a, b, c) according to the age of scarifying of the male newborn rats (postnatal day (PND) 1, PND21 “the age of weaning" and PND35 day which is the age of puberty). At the end of every stage of the experiment, 24 hours after the last administration, all animals were sacrificed and the testes were dissected out and subjected to histopathological, immunohistochemistry, and morphometrical examination. Results: Administration of DEHP at a dose of 150 mg/kg induced several histopathological changes in testes of albino rats as sloughed germinal epithelium and apoptosis of epithelial cells of seminiferous tubules in addition to delayed puberty. It significantly reduced tubular diameter and tubular epithelial height. The addition of selenium partially improved the state of apical processes of Sertoli cells as evidenced by vimentin immunohistochemistry. It also reduced the degree of apoptosis as evidenced by caspase-3 immunohistochemistry in addition to the improvement of tubular epithelial height. Conclusion: Exposure to DEHP led to pronounced testicular damage and impaired spermatogenesis in newborn and pubertal male rats. Recommendations: Many alternatives should be developed to improve the safety profile of the plasticizer or prevent its release from P-PVC devices especially medical ones.