GSTA2 overexpression alleviates bis (2-ethylhexyl) phthalate (DEHP)-induced male reproductive disorders by inhibiting oxidative stress-mediated cell apoptosis via the activated PI3K/AKT signaling pathway.

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Tác giả: Qian Dou, Zonggang Feng, Bin Hao, Genhong Mao, Lei Wei, Hu Zhao, Xinghua Zhao

Ngôn ngữ: eng

Ký hiệu phân loại:

Thông tin xuất bản: Ireland : Molecular and cellular endocrinology , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 496700

Male reproductive disorders are responsible for approximately 50% of infertility cases. Bis (2-ethylhexyl) phthalate (DEHP) is a common environmental pollutant known for its reproductive toxicity. Oxidative stress is a key mechanism in response to DEHP exposure. Glutathione S-transferase A2 (GSTA2), a member of the glutathione S-transferase family, has the capacity to detoxify environmental toxins. However, its role in regulating DEHP-induced male reproductive disorders remains unexplored. Next, male mice aged 3 weeks were orally administered with DEHP (500 mg/kg/day) for 14 days to induce male reproductive disorders. We observed a decrease in the GSTA2 expression in the testicular tissues of DEHP-treated mice. To investigate the role of GSTA2 in DEHP exposure, lentiviral vectors carrying GSTA2 sequences (1 × 10
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