Intracellular Redox Status and Disease Development: An Overview of the Dynamics of Metabolic Orchestra

Abstract

Normal aerobic cellular metabolic processes promote free radical generation wherein the activation of the antioxidant defense mechanism maintains redox homeostasis. A state of imbalance generates when cells fail to detoxify the excess of free radicals formed, resulting in the development of oxidative stress. Oxidation of various cellular components stimulates structural, biological alterations, and homeostatic imbalances in cellular metabolism. The products of complex biomolecular interactions between free radicals and the molecular targets represent the oxidative markers of lipid, protein, and DNA damages and serve as the basis for the onset of various disease complications. In recent years, there has been a significant advancement in research regarding the contributory role of oxidative stress in disease pathophysiology. Oxidative stress promotes the development and progression of acute pathologies, chronic illness, cognitive deteriorations and neurodegenerative disorders. Also, the impact of oxidative stress is established for alcohol and drug abuse cases, multiple seizures, and complications in transplant recipients. The clinical manifestations highlight that oxidative stress rarely occurs in isolation but involves complex interactions with other forms of stress. Oxidative stress during pregnancy has been linked to miscarriage, pre-eclampsia, foetal morbidity, congenital disabilities with prolonged consequences for the mature organism. The contribution of oxidative stress in the patho-physiology of different disease warrants further exploration to establish a firm correlation as there are many diseases which present an apparent indirect association with oxidative stress. Prognosis and diagnosis of various disease complications depend on the successful identification of biomarkers of oxidative modifications and their realization as crucial therapeutic targets.