Naserzadeh, P., Hosseini, M., Mohammadzadeh Asl, B., Pourahmad, J. (2015). Toxicity Mechanisms of Cigarette Smoke on Mouse Fetus Mitochondria. Iranian Journal of Pharmaceutical Research, 14(supplement), 131-138.
Parvaneh Naserzadeh; Mir-Jamal Hosseini; Baharak Mohammadzadeh Asl; Jalal Pourahmad. "Toxicity Mechanisms of Cigarette Smoke on Mouse Fetus Mitochondria". Iranian Journal of Pharmaceutical Research, 14, supplement, 2015, 131-138.
Naserzadeh, P., Hosseini, M., Mohammadzadeh Asl, B., Pourahmad, J. (2015). 'Toxicity Mechanisms of Cigarette Smoke on Mouse Fetus Mitochondria', Iranian Journal of Pharmaceutical Research, 14(supplement), pp. 131-138.
Naserzadeh, P., Hosseini, M., Mohammadzadeh Asl, B., Pourahmad, J. Toxicity Mechanisms of Cigarette Smoke on Mouse Fetus Mitochondria. Iranian Journal of Pharmaceutical Research, 2015; 14(supplement): 131-138.
Toxicity Mechanisms of Cigarette Smoke on Mouse Fetus Mitochondria
1Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran, P. O. Box: 14155-6153
2Zanjan Applied Pharmacology Research Center, Zanjan University of Medical sciences, Zanjan, Iran.
3School of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran
Abstract
Maternal smoking has been recognized as a common cause of low birth weight, preterm birth and the decrease of gestational age period. Unfortunately, there is an increasing interest within public especially woman in Iran in the tobacco products consumption. On the other hand, the deleterious effect of maternal smoking on human fetus in pregnancy period especially in the first trimester encouraged us to investigate toxicity mechanisms of cigarette smoke on mouse fetus mitochondria. For this purpose different concentrations of standardized cigarette smoke extract (1, 10 and 100%) were administrated on mitochondria isolated from fetus of NMRI mice on the 15 day of gestation. Our results showed a significant increase in ROS formation, lipid peroxidation, mitochondrial membrane potential collapse, mitochondrial swelling and finally a decrease in ATP concentration in the CSE-treated isolated fetus mitochondria. Our results suggest that CSE-induced embryo toxicity is the result of disruptive effect on mitochondrial respiratory chain that leads to ROS formation, lipid peroxidation, mitochondrial MMP decline and decrease of ATP level which starts apoptosis signaling.
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