Morteza Mirzaei - Department of Biology, Faculty of Sciences, University of Guilan, University Campus ۲, Rasht, Iran
Hamid Tebyanian - School of Dentistry, Baqiyatallah University of Medical Sciences, Tehran, Iran
Saeed Izadpanah - Applied Biotechnology Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran
Rezvan Seid Moradi - Applied Biotechnology Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran
Mona Rastegar Shariat Panahi - Applied Biotechnology Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran
Mehrdad Moosazadeh Moghaddam - Applied Biotechnology Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran
Ali Mohammad Latifi - Applied Biotechnology Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran

Today, the use of pesticides is an essential issue for health control. Organophosphorus insecticides are considered as the most widely used pesticides in the world and as they have the potential to eliminate pests, they can endanger human health by inhibiting acetylcholinesterase family enzymes. In this research, we aimed to study the effects of paraxon, most important metabolite of organophosphorus insecticide partion, on the viability, cytotoxicity, and apoptosis occurrence in the presence of butyrylcholinesterase (BCHE). In this study, the effects of the viability, cytotoxicity, and apoptosis of paraxon-induced PC۱۲ cells were investigated in the presence of butyrylcholinesterase (BCHE). The cell viability was assessed using MTT test. The cell cytotoxicity was calculated through Lactate Dehydrogenase (LDH) test. The caspase activity was used to measurement of caspase-۳ activity. Mitochondrial membrane potential (MMP) was studied by rhodamine۱۲۳ and also, TUNEL staining was performed to quantification of apoptosis index. Paraxon induced cell cytotoxicity and decrease cell viability of PC۱۲ cells and BCHE inhibited the paraxon function in a dose-dependent manner. Paraxon disrupted the MMP and increased the function of caspase but BCHE suppressed paraxon-induced apoptosis through inhibition of paraxon function. Treatment of PC۱۲ cell by paraxon increased cell death index. BCHE can use in treatment of poisoning with organophosphorus insecticides because of its potential to suppress the paraxon-induced cell death. BCHE inhibits the paraxon function in a dose-dependent manner.Today, the use of pesticides is an essential issue for health control. Organophosphorus insecticides are considered as the most widely used pesticides in the world and as they have the potential to eliminate pests, they can endanger human health by inhibiting acetylcholinesterase family enzymes. In this research, we aimed to study the effects of paraxon, most important metabolite of organophosphorus insecticide partion, on the viability, cytotoxicity, and apoptosis occurrence in the presence of butyrylcholinesterase (BCHE). In this study, the effects of the viability, cytotoxicity, and apoptosis of paraxon-induced PC۱۲ cells were investigated in the presence of butyrylcholinesterase (BCHE). The cell viability was assessed using MTT test. The cell cytotoxicity was calculated through Lactate Dehydrogenase (LDH) test. The caspase activity was used to measurement of caspase-۳ activity. Mitochondrial membrane potential (MMP) was studied by rhodamine۱۲۳ and also, TUNEL staining was performed to quantification of apoptosis index. Paraxon induced cell cytotoxicity and decrease cell viability of PC۱۲ cells and BCHE inhibited the paraxon function in a dose-dependent manner. Paraxon disrupted the MMP and increased the function of caspase but BCHE suppressed paraxon-induced apoptosis through inhibition of paraxon function. Treatment of PC۱۲ cell by paraxon increased cell death index. BCHE can use in treatment of poisoning with organophosphorus insecticides because of its potential to suppress the paraxon-induced cell death. BCHE inhibits the paraxon function in a dose-dependent manner.

PC۱۲ cells, Viability, Cytotoxicity, Apoptosis, Butyrylcholinesterase