Abstract
Oxidative stress (OS) has the ability to damage different molecules and cellular structures, altering the correct function of organs and systems. OS accumulates in the body by endogenous and exogenous mechanisms. Increasing evidence points to the involvement of OS in the physiopathology of various chronic diseases that require prolonged periods of pharmacological treatment. Long-term treatments may contribute to changes in systemic OS. In this review, we discuss the involvement of OS in the pathological mechanisms of some chronic diseases, the pro- or antioxidant effects of their pharmacological treatments, and possible adjuvant antioxidant alternatives. Diseases such as high blood pressure, arteriosclerosis, and diabetes mellitus contribute to the increased risk of cardiovascular disease. Antihypertensive, lipid-lowering, and hypoglycemic treatments help reduce the risk with an additional antioxidant benefit. Treatment with methotrexate in autoimmune systemic inflammatory diseases, such as rheumatoid arthritis, has a dual role in stimulating the production of OS and producing mitochondrial dysfunction. However, it can also help indirectly decrease the systemic OS induced by inflammation. Medicaments used to treat neurodegenerative diseases tend to decrease the mechanisms related to the production of reactive oxygen species (ROS) and balance OS. On the other hand, immunosuppressive treatments used in cancer or human immunodeficiency virus infection increase the production of ROS, causing significant oxidative damage in different organs and systems without widely documented exogenous antioxidant administration alternatives.
Highlights
Oxidative stress (OS) is characterized by the imbalance between the production and degradation of reactive oxygen species (ROS) or reactive nitrogen species (RNS) [1]
Naringin reverses the metabolic complications associated with NRTI by improving OS and apoptosis in a rat model
An experimental study reveals that the administration of ascorbic acid or rose oil can help to decrease the levels of oxidative damage to lipids or proteins induced by levodopa [158]
Summary
Oxidative stress (OS) is characterized by the imbalance between the production and degradation of reactive oxygen species (ROS) or reactive nitrogen species (RNS) [1]. Angiotensin II (Ang II) causes oxidative damage in the vascular system by inducing the generation of ROS by activating NADPH oxidase with the ability to oxidize cellular biomolecules, including lipids, lipoproteins, and DNA, leading to endothelial deterioration [33]. The vitamin D analog (paricalcitol) was reported to improve oxidative vascular injury by suppressing the activity of ROS-generating enzyme NADPH oxidase, inflammatory mediators, and regulating the antioxidant defense system in ApoE-deficient mice [45].
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