Oxidative Stress, Prooxidants, and Antioxidants: The Interplay

Abstract

Oxidative stress is a normal phenomenon in the body. Under normal conditions, the physiologically important intracellular levels of reactive oxygen species (ROS) are maintained at low levels by various enzyme systems participating in the in vivo redox homeostasis. Therefore, oxidative stress can also be viewed as an imbalance between the prooxidants and antioxidants in the body. For the last two decades, oxidative stress has been one of the most burning topics among the biological researchers all over the world. Several reasons can be assigned to justify its importance: knowledge about reactive oxygen and nitrogen species production and metabolism; identification of biomarkers for oxidative damage; evidence relating manifestation of chronic and some acute health problems to oxidative stress; identification of various dietary antioxidants present in plant foods as bioactive molecules; and so on. This review discusses the importance of oxidative stress in the body growth and development as well as proteomic and genomic evidences of its relationship with disease development, incidence of malignancies and autoimmune disorders, increased susceptibility to bacterial, viral, and parasitic diseases, and an interplay with prooxidants and antioxidants for maintaining a sound health, which would be helpful in enhancing the knowledge of any biochemist, pathophysiologist, or medical personnel regarding this important issue.

Oxidative stress and antioxidant defence markers in muscle tissue of rainbow trout (Oncorhynchus mykiss) after vaccination against Yersinia ruckeri

“…Among different markers of oxidative stress, 2-thiobarbituric acid reactive substances (TBARS), content of oxidative protein damage, and natural antioxidants: metalloenzymes, superoxide dismutase (SOD), catalase (CAT), and selenium dependent glutathione peroxidase (GPx), are currently considered to be the most important (24). Malondialdehyde (MDA) is a three-carbon compound formed from peroxidised polyunsaturated fatty acids, mainly arachidonic acid.…”

“…It is one of the end products of membrane lipid peroxidation. Since MDA content increases in various diseases with excess of reactive oxygen species (ROS), many relationships with free radical damage were observed (24). CAT and SOD are the major defences against ROS.…”

Alterations in Carotid Body Morphology and Cellular Mechanism Under the Influence of Intermittent Hypoxia

“…SOD2 acts as an antioxidant which converts superoxide to hydrogen peroxide whose presence was also demonstrated immunohistochemically. As discussed earlier, OSA disrupts equilibrium between HIF1α and HIF2α resulting in imbalance between NOX2 and SOD2 respectively [16] that leads to ROS formation [14,15]. This leads to DNA damage, depletion of intracellular antioxidant defense system, alteration in calcium homeostasis and apoptosis [30] and further causes pathophysiology.…”

“…Moreover, studies reveal that augmented activity of the CB, induced by IH plays an important role in the pathogenesis of sleep apnea [13] in anesthetized rats and humans and emphasis is being made to understand its underlying mechanisms. Furthermore, the equilibrium between HIF1α and HIF2α, hampered by chronic IH leads to an imbalance between pro-oxidant and antioxidant enzymes respectively that causes oxidative stress resulting in pathophysiology [14][15][16] and has been implicated as a risk factor for an array of cardiovascular diseases [17] affecting humans.…”

Assessment of Hepatotoxic Effects of Quetiapıne at Repeated Doses in Rats

“…However, we emphasized that liver malondialdehyde levels, the end product of lipid peroxidation, were not determined in our study. As it is known that oxidative stress is induced with the imbalance between production of reactive metabolites and antioxidant status [56,57]. On the other hand, autoimmunity, idiosyncratic reactions (immune idiosyncrasy and metabolic idiosyncrasy), disruption of calcium homeostasis and cell membrane injury, stimulation of apoptosis and mitochondrial injury are the underlying mechanisms of drug induced liver injury [2,36,37,58].…”