Di-2-ethylhexyl phthalate induced oxidative damage involving FasL-associated apoptotic pathway in mouse spermatogenic GC-2spd cells

Di-2-ethylhexyl phthalate (DEHP) which belongs to phthalatic-acid esters, is a kind of harmful, global environmental pollutants. It is a known endocrine disrupting chemical and male reproductive toxicant. However, the mechanism by which DEHP exposure result in male reproductive toxicity is still unc...

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Bibliographic Details
Published in:Molecular & cellular toxicology 2016, 12(4), , pp.381-389
Main Authors: Tang, Xiao, Tong, Kun, Zhu, Lishan, Fu, Guoqing, Chang, Wei, Zhou, Ting, Zhang, Zhibing, Tong, Ling, Zhang, Ling, Shi, Yuqin
Format: Article
Language:English
Subjects:
Apoptosis
Biomedical and Life Sciences
Caspase
Caspase-3
Caspase-8
Cell Biology
Endocrine disruptors
Esters
FasL protein
Gene expression
Life Sciences
Malondialdehyde
mRNA
Original Paper
Oxidative stress
Peroxidase
Pharmacology/Toxicology
Pollutants
Protein expression
Rodents
Superoxide dismutase
Toxicity
생물학
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Summary:Di-2-ethylhexyl phthalate (DEHP) which belongs to phthalatic-acid esters, is a kind of harmful, global environmental pollutants. It is a known endocrine disrupting chemical and male reproductive toxicant. However, the mechanism by which DEHP exposure result in male reproductive toxicity is still unclear. To elucidate the productive toxicity mechanism of DEHP, we attemptted to investigate oxidative stress, apoptotic effects, mRNA and protein expression of apoptosis-associated genes including FasL, caspase-3, and caspase-8 in GC-2spd (mouse spermatogenic cells). The results showed that, with the increase of DEHP concentration, cell apoptosis rate increased; the activities of relation index of oxidative stress such as malondialdehyde (MDA), superoxide dismutase (SOD) and glutatione peroxidase (GSH-PX) changed significantly; the mRNA and protein expression levels of FasL, caspase-3, -8, altered obviously. These results suggested that DEHP could induce apoptosis of GC-2spd cells through oxidative stress and FasL-dependent pathway.
ISSN:1738-642X
2092-8467
DOI:10.1007/s13273-016-0042-x