| Literature DB >> 27416487 |
Guoqing Fu1, Juan Dai2, Dayi Zhang3, Lishan Zhu1, Xiao Tang1, Ling Zhang1, Ting Zhou1, Peng Duan4, Chao Quan4, Zhibing Zhang1,5, Shizhen Song1, Yuqin Shi1.
Abstract
Di(2-ethylhexyl) phthalate (DEHP), a plasticizer of synthetic polymers, is a well-known endocrine disrupting chemical (EDC) and reproductive toxicant. Addressing the unclear mechanism of DEHP-induced reproductive dysfunction, this study used GC-2spd cells to investigate the molecular mechanism involved in the DEHP-induced toxicity in the male reproductive system. The results indicated that the apoptotic cell death was significantly induced by DEHP exposure over 100 μM. Furthermore, DEHP treatment could induce oxidative stress in GC-2spd cells involving in the decrease of superoxide dismutase (SOD) activity (200 μM) and glutathione peroxidase (GSH-Px) activity (50 and 100 μM). In addition, DEHP induction also caused the elevated ratios of Bax/Bcl-2, release of cytochrome c and decomposition of procaspase-3 and procaspase-9 in GC-2spd cells. Taken together, our work provided the evidence that DEHP exposure might induce apoptosis of GC-2spd cells via mitochondria pathway mediated by oxidative stress.Entities:
Keywords: Di(2-ethylhexyl) phthalate (DEHP); GC-2spd cells; apoptosis; mitochondrial pathway; oxidative stress
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Year: 2016 PMID: 27416487 PMCID: PMC5673478 DOI: 10.1002/tox.22304
Source DB: PubMed Journal: Environ Toxicol ISSN: 1520-4081 Impact factor: 4.119