Lactational exposure of phthalate causes long-term disruption in testicular architecture by altering tight junctional and apoptotic protein expression in Sertoli cells of first filial generation pubertal Wistar rats. (June 2015)

• Record Type: Journal Article
• Authors: Sekaran, S; Balaganapathy, P; Parsanathan, R; Elangovan, S; Gunashekar, J; Bhat, FA; Jagadeesan, A
• Is Part Of: Human & experimental toxicology. Volume 34:Number 6(2015:Jun.)
• Page Start: 575
• Page End: 590
• Publication Date: 2015-06
• Subjects: Apoptosis -- biochemical analysis -- phthalate -- testicular architecture -- tight junctional proteins; Toxicology -- Periodicals; 615.9
• DOI: 10.1177/0960327114555926
• Languages: English
• ISSNs: 0960-3271

Abstract

Di(2-ethylhexyl) phthalate (DEHP) is a ubiquitous environmental contaminant and a well-known endocrine disruptor (ED) that interferes with the reproductive function in both humans and animals. This study aimed to find out the impact of lactational exposure of DEHP in testes of first filial generation (F1 ) progeny male rat postnatal day (PND)-60. Lactating dams were orally treated with DEHP (0, 1, 10 and 100 mg/kg body weight/day, respectively) from the PND-1 to PND-21. Rats were killed at PND 60. Testes were removed and used for histological analysis and for isolation of Sertoli cells (SCs). The histoarchitecture of DEHP-treated rats showed disturbed testicular structure. DEHP-treated rats also showed increased oxidative stress by decreasing antioxidant levels in the SCs; it disrupted SC tight junctional proteins occludin, claudin, junctional adhesion molecule, zona occludens protein-1 (ZO-1), zona occludens protein-2 (ZO-2), and afadin-6 (AF-6), increased apoptosis by altering the apoptotic genes Bax, cytochrome c, caspase-8, -9, -3 and antiapoptotic gene Bcl-2 . It is concluded that early postnatal exposure to DEHP disturbs histoarchitecture of testis and SC function in pubertal Wistar rats.