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Oxidative stress condition arises during imbalance between oxidants and antioxidants of diverse origin damaging both structure and function of tissues. Oxidative stress has been suggested as a cofactor during Human Immunodeficiency Virus Infection course involved in many aspects of disease pathogenesis as viral replication, inflammatory responses, decreased immune cell proliferation, loss of immune function, cellular apoptosis, chronic weight loss, and increased sensitivity to drug toxicity.In this review, we provide an overview of the oxidative metabolism pathways involved in HIV infection, examine the potential impact of antirretroviral toxicity on oxidative damage and argue how the response contribute to co-morbidities. Moreover, we also discuss recent reports from observational and interventional studies which have led to an increasing interest in the possible benefits of micronutrient supplementation as a cost-effective strategy for improving oxidative and nutritional status in HIV infection. The general strategy and combination of these interventions represent an important complementary deal for HIV infection treatment in the era of high active antiretroviral therapy.

Understanding the role of oxidative injury will allow for therapy with agents that scavenge ROS (reactive oxygen species) and antioxidants in the management of several diseases related to free radical damage. The majority of free radicals are generated by mitochondria as a consequence of the mitochondrial cycle, whereas free radical accumulation is limited by the action of a variety of antioxidant processes that reside in every cell. In the present review, we provide an overview of the mitochondrial generation of ROS and discuss the role of ROS in the regulation of endothelial and adipocyte function. Moreover, we also discuss recent findings on the role of ROS in sepsis, cerebral ataxia and stroke. These results provide avenues for the therapeutic potential of antioxidants in a variety of diseases.

Spinocerebellar ataxia type 2 (SCA2) is a redox-sensitive neurodegenerative disease affecting the cerebellum, fibre connections in the cerebellum, the peripheral nervous system, and extracerebellar central pathways. Currently, Cuba has the highest reported global rate for this disease. The aim of this review article is to summarize and discuss the current knowledge about evidence of oxidative stress during SCA2. Recent reports have suggested that ataxin 2 and other related factors contribute to the redox imbalance in this disease. It is important to recognize and clarify the molecular mechanisms associated with the redox imbalance to consider ataxias innovative approaches to counteract oxidative stress-induced tissue damage, through alternative therapeutic or nutritional intervention in SCA2 and related diseases.

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