Hypoxia-Induced Oxidative Stress in Health Disorders

Chronic hypoxia has been shown to promote a large number of pathologies such as hypertension, cardiovascular and metabolic disorders, and respiratory diseases. The oxidative stress that occurs during intermittent or continuous cellular hypoxia is likely involved in all these diseases. Indeed, the reactive species were demonstrated to inhibit active substances, modulate the signaling of intracellular pathways, and mediate enzymes activation, which are known to play a critical role in the geneses and/or the outcomes of these pathologies. The four review articles of this special issue describe the current knowledge regarding the role of oxidative stress in ischemic retinopathy, pulmonary diseases, and infertile testis and discuss a new model of yeast to study hypoxia-induced oxidative stress. In addition, the two original research articles presented in this issue further expand the understanding of the redox biology in the context of pulmonary arterial hypertension and impaired spermatogenesis induced by hypoxia. The review article by S.-Y. Li et al. presents the underlying mechanisms involved in the hypoxia/ischemia-induced oxidative damage in diabetic retinopathy and retinopathy of prematurity. In particular, the authors have discussed the effect of therapeutic strategies of antioxidants treatment such as administration of catalase and superoxide dismutase, vitamin E, and lutein and inhibition of NADPH oxidase or similar signaling pathways in these retinal ischemic diseases. The extensive review by O. F. Araneda and M. Tuesta reports recent in vitro and in vivo experimental evidence that shows the implied mechanisms in pulmonary redox state by hypoxia via the increase of ROS generation in mito-chondria, as from activation of NADPH oxidase, xanthine oxidase/reductase, and nitric oxide synthase enzymes, as well as throughout inflammatory process. Then, the role and impact of enzymatic and nonenzymatic antioxidant in the modulation of the pathways involved in the physiopatholog-ical response to hypoxia are extensively discussed. In a last part, the authors report the evolution of the two most studied makers of oxidative stress (exhaled nitric oxide for humans and pulmonary content of malondialdehydes for animals) in the lung in response to hypoxic exposure. The paper of J. G. Reyes et al. synthesizes the current state of knowledge of the physiology of the testicles under pathologic hypoxic conditions that lead to reduced sper-matogenesis. The molecular events triggered by all causes of hypoxia in the testis share common mechanistic pathways involving ROS generated by mitochondrial dysfunction and activation of enzymes such as xanthine oxidase or the inducible nitric oxide synthase. The recent …