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• Nutrition and Hygiene •     Next Articles

N-Acetyl-cysteine Attenuated Nonylphenol Induced Cell Damage in Mouse Sertoli TM4 Cells

  

  • Received:2018-06-14 Revised:2019-03-08 Online:2019-07-15 Published:2019-07-23

Abstract: Objective: The aim of this study was to explore the effects of N-Acetyl-cysteine (NAC) on nonylphenol (NP) induced oxidative stress and cell apoptosis. Methods: Mouse Sertoli TM4 cells were divided into 4 groups: Control group, NP group (20 μmol/L), NP + NAC group (5 mmol/L NAC pretreated 4 h, then NP treated 24 h), NAC group (5 mmol/L NAC treated 4 h, then treated as Control group). Cell survival was monitored by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay, reactive oxygen species (ROS) generation and cell apoptosis were analyzed by flow cytometric. Caspase-3 activity, superoxide dismutase (SOD) activity, catalase (CAT) activity, and maleic dialdehyde (MDA) content were measured by assay kits. Protein phosphorylation of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) was detected by western blot assay. Results: Compared with the Control group, NP decreased cell survival, induced ROS generation, increased SOD and CAT activities, decreased MAD content in Sertoli TM4 cells. Additionally, NP induced cell apoptosis, increased caspase-3 activity, and activated ERK/JNK pathways. Compared with NP group, NAC pretreatment attenuated NP decreased cell survival rate, induced ROS generation, increased SOD and CAT activities, and NP decreased MAD content. Moreover, NAC blocked NP induced cell apoptosis, increased caspase-3 activity, and activated ERK/JNK pathways. Conclusion: NAC attenuated NP induced cell damage in mouse Sertoli TM4 cells, which was related with NAC attenuated NP induced oxidative stress and cell apoptosis, and blocked the activation of ERK and JNK pathways.

Key words: nonylphenol, Sertoli TM4 cells, N-Acetyl-cysteine, cell apoptosis, oxidative stress

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