enzymes found in the mucous membrane antioxidant defense system, that catalyse nucleophilic attack by reduced glutathione (gsh) on non-polar compounds that contain an electrophilic carbon and nitrogen. these inhibition mechanisms generates free radicals that causes peroxidation from the lipids in the mucous membrane leading to increased peroxidized erythrocyte lipids, a reaction that proceeds by a free radical chain reaction mechanism that result in oxidative stress. the oxidative stress on the mucous membrane causes the dissociation of the gstp-jnk complex, oligomerization of gstp and induction of the jnk pathway, resulting in apoptosis or inflammation of the bronchioles and pulmonary alveolus in mild cases. on migrating to the bloodstream, nitrogen dioxide poisoning results in an irreversible inhibition of the erythrocyte membrane acetylcholinesterase which may lead to muscular paralysis, convulsions, bronchoconstriction, the narrowing of the airways in the lungs (bronchi and bronchioles) and death by asphyxiation. it also causes a decrease in glucose-6-phosphate dehydrogenase which may results in glucose-6-phosphate dehydrogenase deficiency known as favism, a condition that predisposes to hemolysis (spontaneous destruction of red blood cells). acute and chronic exposure also reduces glutathione reductase, an enzyme that catalyzes the reduction of glutathione disulfide (gssg) to the sulfhydryl form glutathione (gsh), which is a critical molecule in resisting oxidative stress and maintaining the reducing environment of the cell. reproductive effects exposure to nitrogen dioxide has a significant effect on the male reproductive system by inhibiting the production of sertoli cells, the "nurse" cells of the testicles that are part of a seminiferous tubule and help in the process of spermatogenesis. these effects consequently retard the production of sperm cells. the effects of nitrogen dioxide poisoning on female reproduction may be linked with the effects of oxidative stress on female reproduction. nitrogen dioxide poisoning disrupts the balance of reactive oxygen species (ros), which results in oxidative stress, leading to significant effects on the female reproductive lifespan. ros play a significant role in body physiology, from oocyte production, development and maturation to fertilization, development of the embryo and gestation. exposure to nitrogen dioxide causes ovulation-induced oxidative damage to the dna of ovarian epithelium. there is a growing body of literature on the pathological effects of ros on female reproduction as evidenced by free-radical-induced birth defects, abortions, hydatidiform moles and pre-eclampsia. ros also play a significant role in the etiopathogenesis of endometriosis, a disease in which tissue that normally grows inside the uterus grows outside of it. oxidative stress causes defective placentation, which is likely to lead to placental hypoxia, shortage of oxygen in the placental as well as reperfusion injury resulting from ischemia, which may lead to endothelial cell dysfunction. increased oxidative stress caused by nitrogen dioxide poisoning may result in ovarian epithelium inflammation and potentially to cancer in the most severe cases.