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β‐benzene hexachloride induces apoptosis of rat sertoli cells through generation of reactive oxygen species and activation of JNKs and FasL
β‐benzene hexachloride (β‐BHC), the major metabolite of benzene‐hexachloride (BHC), is a weak estrogen‐like chemical. It is a known persistent organic pollutant and male reproductive toxicant. However, the mechanism by which β‐BHC exposure causes male reproductive toxicity remains unknown. In the present study, rat Sertoli cells were used to investigate the molecular mechanism involved in β‐BHC‐induced toxicity in male reproductive system. The results indicated that β‐BHC exposure at over 30 μM showed the induction of apoptotic cell death. β‐BHC could induce elevation in reactive oxygen species (ROS) generation, increase in the leakage rate of LDH and MDA level, and decrease in SOD activity. In addition, there was an increase in the cellular levels of phospho‐JNKs and FasL in the β‐BHC‐induced apoptosis; and a significant reduction of procaspase‐3 and ‐8 was observed over 30‐μM β‐BHC treatment. The translocation of NF‐κB enhanced with the increase of concentration of β‐BHC. Furthermore, NAC administration, a scavenger of ROS, reversed β‐BHC‐induced apoptosis effects via inhibition of JNKs activation, FasL expression, and NF‐κB translocation. These results lead us to speculate that ROS generation may play a critical role in the initiation of β‐BHC‐induced apoptosis by activation of the JNKs, translocation of NF‐κB, expression of FasL, and further activation of caspase cascade. © 2009 Wiley Periodicals, Inc. Environ Toxicol 26: 124–135, 2011.
β‐benzene hexachloride induces apoptosis of rat sertoli cells through generation of reactive oxygen species and activation of JNKs and FasL
β‐benzene hexachloride (β‐BHC), the major metabolite of benzene‐hexachloride (BHC), is a weak estrogen‐like chemical. It is a known persistent organic pollutant and male reproductive toxicant. However, the mechanism by which β‐BHC exposure causes male reproductive toxicity remains unknown. In the present study, rat Sertoli cells were used to investigate the molecular mechanism involved in β‐BHC‐induced toxicity in male reproductive system. The results indicated that β‐BHC exposure at over 30 μM showed the induction of apoptotic cell death. β‐BHC could induce elevation in reactive oxygen species (ROS) generation, increase in the leakage rate of LDH and MDA level, and decrease in SOD activity. In addition, there was an increase in the cellular levels of phospho‐JNKs and FasL in the β‐BHC‐induced apoptosis; and a significant reduction of procaspase‐3 and ‐8 was observed over 30‐μM β‐BHC treatment. The translocation of NF‐κB enhanced with the increase of concentration of β‐BHC. Furthermore, NAC administration, a scavenger of ROS, reversed β‐BHC‐induced apoptosis effects via inhibition of JNKs activation, FasL expression, and NF‐κB translocation. These results lead us to speculate that ROS generation may play a critical role in the initiation of β‐BHC‐induced apoptosis by activation of the JNKs, translocation of NF‐κB, expression of FasL, and further activation of caspase cascade. © 2009 Wiley Periodicals, Inc. Environ Toxicol 26: 124–135, 2011.
β‐benzene hexachloride induces apoptosis of rat sertoli cells through generation of reactive oxygen species and activation of JNKs and FasL
Shi, Yuqin (author) / Song, Yang (author) / Wang, Yuping (author) / Wang, Yinan (author) / Liang, Xianmin (author) / Hu, Yafei (author) / Yu, Haige (author) / Guan, Xia (author) / Cheng, Jin (author) / Yang, Kedi (author)
Environmental Toxicology ; 26 ; 124-135
2011-04-01
12 pages
Article (Journal)
Electronic Resource
English