Evaluation of toxicity of 4-octylphenol in TM4 Sertoli cells: an in vitro study. (13th October 2019)

• Record Type: Journal Article
• Authors: Zhang, Mingtian; Park, Hyun Jung; Seo, Sang-Ah; Seo, Hye-Ryoung; Song, Hyuk
• Is Part Of: Toxicology mechanisms and methods. Volume 29:Number 8(2019)
• Page Start: 623
• Page End: 631
• Publication Date: 2019-10-13
• Subjects: 4-Octylphenol -- TM4 Sertoli cells -- reproductive toxicity -- apoptosis -- mitochondria; Analytical toxicology -- Periodicals; Toxicology -- Periodicals; Toxicology -- Methodology -- Periodicals; 615.907
• DOI: 10.1080/15376516.2019.1646368
• Languages: English
• ISSNs: 1537-6516

Abstract

Abstract: The reproductive toxicity of 4-octylphenol (4-OP) has been studied in animals such as mouse and fish. In humans, the exposure of sperm to 4-OP has been shown to decrease motility and viability. In this study, we performed an in vitro assessment of the toxic effects of 4-OP on mouse TM4 Sertoli cells and investigated the underlying molecular mechanisms. TM4 cells were treated with four concentrations (0, 10, 30, and 50 µM) of 4-OP at the following time points: 24, 48, and 72 h. Cell viability and apoptosis assays were conducted following 4-OP exposure. We found that 4-OP significantly decreased cell viability in a concentration- and time-dependent manner, and increased apoptosis. Quantitative PCR analysis showed that the mRNA expression levels of BCL2 Associated X, Apoptosis Regulator (Bax) and BCL2 Antagonist/Killer (Bak) increased while that of BCL2 Apoptosis Regulator (Bcl-2) decreased in 4-OP-exposed cells compared with that in the controls. Western blotting revealed that 4-OP induced caspase-3 activity and Bad phosphorylation in a concentration- and time-dependent manner. Additionally, cytochrome C protein did not colocalize with mitochondrial marker dye by 24 h. Cytochrome c protein expression increased in a time-dependent manner upon exposure to 50 µM 4-OP. These results suggest that 4-OP induces mitochondria-mediated apoptosis through regulation of Bcl-2 family proteins and caspase-3 activation in male Sertoli cells.