Di-(2-ethylhexyl) phthalate exacerbates abnormalities of testicular development in F1 males via inhibition the Wnt/β-catenin signaling pathway

Li, Nan; Sun, De-Ming; Chang, Yong-Zhang; Li, Xue-Nan; Li, Jin-Long; Wang, Tian-Qi

doi:10.1016/j.envpol.2023.123170

Environmental Pollution

2024

DOI: 10.1016/j.envpol.2023.123170

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Di-(2-ethylhexyl) phthalate exacerbates abnormalities of testicular development in F1 males via inhibition the Wnt/β-catenin signaling pathway

Nan Li,

De-Ming Sun,

Yong-Zhang Chang

et al.

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Cited by 3 publications

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Metabolic and neurodevelopmental effects of the environmental endocrine disruptor di-2-ethylhexyl phthalate: a review

Wang,

Liu,

Ding

et al. 2024

Environ Chem Lett

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Metabolic and neurodevelopmental effects of the environmental endocrine disruptor di-2-ethylhexyl phthalate: a review

Wang,

Liu,

Ding

et al. 2024

Environ Chem Lett

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Multiomics Profiling Uncovers Curdione-Induced Reproductive Toxicity in HTR-8/SVneo Cells

Wu,

Chen,

Lin

et al. 2024

Heliyon

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Mechanism of mitochondrial oxidative phosphorylation disorder in male infertility

Meng,

Liu,

Qin

et al. 2024

Chinese Medical Journal

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Male infertility has become a global concern, accounting for 20–70% of infertility. Dysfunctional spermatogenesis is the most common cause of male infertility; thus, treating abnormal spermatogenesis may improve male infertility and has attracted the attention of the medical community. Mitochondria are essential organelles that maintain cell homeostasis and normal physiological functions in various ways, such as mitochondrial oxidative phosphorylation (OXPHOS). Mitochondrial OXPHOS transmits electrons through the respiratory chain, synthesizes adenosine triphosphate (ATP), and produces reactive oxygen species (ROS). These mechanisms are vital for spermatogenesis, especially to maintain the normal function of testicular Sertoli cells and germ cells. The disruption of mitochondrial OXPHOS caused by external factors can result in inadequate cellular energy supply, oxidative stress, apoptosis, or ferroptosis, all inhibiting spermatogenesis and damaging the male reproductive system, leading to male infertility. This article summarizes the latest pathological mechanism of mitochondrial OXPHOS disorder in testicular Sertoli cells and germ cells, which disrupts spermatogenesis and results in male infertility. In addition, we also briefly outline the current treatment of spermatogenic malfunction caused by mitochondrial OXPHOS disorders. However, relevant treatments have not been fully elucidated. Therefore, targeting mitochondrial OXPHOS disorders in Sertoli cells and germ cells is a research direction worthy of attention. We believe this review will provide new and more accurate ideas for treating male infertility.

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Di-(2-ethylhexyl) phthalate exacerbates abnormalities of testicular development in F1 males via inhibition the Wnt/β-catenin signaling pathway

Cited by 3 publications

References 35 publications

Metabolic and neurodevelopmental effects of the environmental endocrine disruptor di-2-ethylhexyl phthalate: a review

Metabolic and neurodevelopmental effects of the environmental endocrine disruptor di-2-ethylhexyl phthalate: a review

Multiomics Profiling Uncovers Curdione-Induced Reproductive Toxicity in HTR-8/SVneo Cells

Mechanism of mitochondrial oxidative phosphorylation disorder in male infertility

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