Preprint Article Version 1 This version is not peer-reviewed

Reproductive Toxicity of 4-Octylphenol Induced Mitochondria-Mediated Apoptosis in Male Mouse-Specific Niche Cells

Version 1 : Received: 16 October 2018 / Approved: 16 October 2018 / Online: 16 October 2018 (08:35:47 CEST)

How to cite: Zhang, M.; Park, H.J.; Hong, K.; Park, C.; Song, H. Reproductive Toxicity of 4-Octylphenol Induced Mitochondria-Mediated Apoptosis in Male Mouse-Specific Niche Cells. Preprints 2018, 2018100342 (doi: 10.20944/preprints201810.0342.v1). Zhang, M.; Park, H.J.; Hong, K.; Park, C.; Song, H. Reproductive Toxicity of 4-Octylphenol Induced Mitochondria-Mediated Apoptosis in Male Mouse-Specific Niche Cells. Preprints 2018, 2018100342 (doi: 10.20944/preprints201810.0342.v1).

Abstract

The toxic effects of 4-octylphenol (4-OP) have been studied in species such as mouse and fish; however, the toxic effects of 4-OP in male specific niche cells has not been researched. In this study, we investigated the molecular mechanism of toxicity of 4-OP in mouse TM4 Sertoli cells. TM4 cells were treated with four concentrations (0, 10, 30, and 50 µM/mL) of 4-OP at time points 24, 48, and 72 h. Cell viability and apoptosis assay was conducted following exposure. 4-OP significantly decreased cell viability in a concentration- and time-dependent manner, and increased apoptosis. Quantitative PCR analysis showed that Bad, Bax, and Bak mRNA expression levels were higher in exposed cells than in the control, but Bcl-2 expression was decreased. Western blotting revealed that 4-OP induced activities of caspase-3 and phosphorylation of Bad in a concentration- and time-dependent manner. Additionally, cytochrome C protein did not colocalize with mitochondria marker dye by 24 h. Cytochrome c protein expression increased in a time-dependent manner with 50 µM/mL. These results suggest that 4-OP induces mitochondria-mediated apoptosis by regulation of Bcl-2 family proteins and caspase-3 activation in male Sertoli cells.

Subject Areas

4-octylphenol; male sertoli cells; reproductive toxicity; apoptosis; mitochondria

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