Article Review: Physiological Role of Oxidative Stress in Abnormal Activity and Cell Death

Abstract

Oxidative stress is a fundamental concept in the field of cell biology and pathophysiology, which refers to presence an imbalance between the production of reactive oxygen species (ROS) and the ability of biological system to detoxify these reactive intermediates or to repair the resulting damage. This disturbance in the redox state of the cell can lead to generation of toxic effects through production of peroxides and free radicals, which subsequently damage essential cellular components such as nucleic acids, lipids, and proteins. Oxidative stress can arise from various sources, both endogenous and exogenous. Endogenously, ROS generated as a byproduct of normal cellular metabolism, particularly during oxidative phosphorylation in the mitochondria; whereas exogenous sources of oxidative stress include smoking, air pollution, exposure to ultraviolet or ionizing radiation, intense physical exercise, and psychological stress. When the production of ROS overwhelms the cell’s antioxidant defenses, the resulting oxidative stress can have detrimental effects on cellular function and viability. Oxidative stress has been implicated in pathogenesis of numerous disease states due to disruption of normal signaling pathways that induce DNA damage and trigger apoptotic or necrotic cell death cascades. The deleterious effects of oxidative stress are not limited to acute events, but also contribute to development of chronic diseases. Furthermore, oxidative stress-induced DNA damage can lead to genomic instability and the activation of oncogenic signaling cascades. The physiological role of oxidative stress in cellular function is complex, as it can also serve as a signaling mechanism to maintain homeostasis. Moderate levels of reactive oxygen species can act as secondary messengers, triggering adaptive responses that enhance cellular antioxidant defenses and promote cell survival. However, when oxidative stress reaches a critical threshold, it can overwhelm these protective mechanisms and lead to abnormal cellular activities and, ultimately, cell death.