4-[1-ethyl-1-methylhexy]-phenol Induces Apoptosis and Interrupts Ca2+ Homeostasis via ROS Pathway in Sertoli TM4 cells

Biological effect of an individual nonylphenol (NP) isomer extremely relies upon the side chain structure. This research was designed to evaluate the impact of NP isomer, 4-[1-ethyl-1-methylhexy]-phenol (NP 65 ), on Sertoli cells in vitro . Sertoli TM4 cells were exposed to various concentration (0, 0.1, 1, 10, or 20 μM) of NP 65 for 24 h, and the outcomes indicated that treatment of NP 65 induced reactive oxygen species (ROS) generation, oxidative stress as well as apoptosis for Sertoli TM4 cells. In addition, it was found that NP 65 exposure affected homeostasis of Ca 2+ in Sertoli TM4 cells by increasing cytoplasm [Ca 2+ ]i, inhibiting Ca 2+ -ATPase activity and decreasing cAMP concentration. Pretreatment with ROS scavenger, N-acetylcysteine (NAC), attenuated NP 65 -induced oxidative stress as well as apoptosis for TM4 cells. Furthermore, NAC blocked NP 65 -induced disorders of Ca 2+ homeostasis by attenuating the growth of intracellular [Ca 2+ ]i and the inhibition of Ca 2+ -ATPase and cAMP activities. Thus, we have demonstrated that NP 65 induced apoptosis as well as acted as a potent inhibitor of Ca 2+ -ATPase activity and resulted in disorder of Ca 2+ homeostasis in Sertoli TM4 cells, ROS participated in the process. Our results supported the view that oxidative stress acted an essential role within the development of apoptosis and Ca 2+ overload in TM4 cells as a consequence of NP 65 stimulation.