FOOD SCIENCE ›› 2019, Vol. 40 ›› Issue (13): 130-136.doi: 10.7506/spkx1002-6630-20180614-242

• Nutrition & Hygiene • Previous Articles     Next Articles

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

LIU Xiaozhen, NIE Shaoping, YU Qiang, HUANG Danfei, XIE Mingyong   

  1. 1. Institute of Science and Technology Innovation, School of Chemical Engineering and Energy Technology, Dongguan University of Technology, Dongguan 523808, China; 2. State Key Laboratory of Food Science and Technology, Nanchang University, Nanchang 330047, China
  • Online:2019-07-15 Published:2019-07-23

Abstract: Objective: The aim of this study was to explore the effect of N-acetyl-cysteine (NAC) on nonylphenol (NP)-induced oxidative stress and cell apoptosis in TM4 mouse Sertoli cells. Methods: The cells were divided into 4 groups: control group, NP group (20 μmol/L NP), NP + NAC group (sequential treatment with 5 mmol/L NAC for 4 h followed by 20 mmol/L NP for 24 h), NAC group (sequential treatment with 5 mmol/L NAC for 4 h followed by normal cell culture medium). Cell survival rate was monitored by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay, and reactive oxygen species (ROS) generation and cell apoptosis were analyzed by flow cytometry. Caspase-3 activity, superoxide dismutase (SOD) activity, catalase (CAT) activity, and malondialdehyde (MDA) content were measured by assay kits. The 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 rate significantly (P < 0.05), induced reactive oxygen species (ROS) generation, increased SOD and CAT activities, and decreased MDA content in Sertoli TM4 cells. Additionally, NP induced cell apoptosis, increased caspase-3 activity, and activated the ERK/JNK signaling pathways. Compared with the NP group, NAC pretreatment attenuated ROS production, reduced SOD and CAT activities and increased MDA content. Moreover, NAC blocked cell apoptosis, increased caspase-3 activity, and activated the ERK/JNK signal pathways. Conclusion: NAC attenuated NP-induced damage in mouse Sertoli TM4 cells, which may be related to the ability of NAC to attenuate NP-induced oxidative stress and cell apoptosis and block the activation of the ERK and JNK signaling pathways.

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

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