Cellular macromolecules (DNA, proteins, and lipids) (ROS-mediated damage)

Cellular macromolecules via reactive oxygen species-mediated damage refers to the collective oxidative degradation of DNA, proteins, and lipids caused by reactive oxygen species (ROS) such as superoxide, hydrogen peroxide, and hydroxyl radicals (Pizzino et al., 2017, Oxidative Medicine and Cellular Longevity). ROS are generated during normal mitochondrial respiration or by enzymes like NADPH oxidase, but excessive levels lead to oxidative stress, causing mutations in DNA, misfolding of proteins, and lipid peroxidation of membranes (Sies et al., 2017, Nature Reviews Molecular Cell Biology). This damage is a central driver in the pathogenesis of cancer, neurodegenerative disorders like Alzheimer's, and cardiovascular diseases (Schieber & Chandel, 2014, Current Biology). Pharmacological intervention typically involves antioxidants (e.g., N-acetylcysteine) or scavengers (e.g., Edaravone) that neutralize ROS before they can interact with these macromolecules (Forman & Zhang, 2021, Free Radical Biology and Medicine). However, because ROS also function as essential signaling molecules in processes like immune response and cell differentiation, non-specific targeting can lead to significant safety concerns and therapeutic failure (Harris & DeNicola, 2020, Nature Reviews Cancer).

Other names

Oxidative stress targetsReactive oxygen species targetsMacromolecular oxidative damageROS-induced damage

Neutralization of reactive oxygen species (ROS) through scavenging, donation of electrons to stabilize free radicals, or induction of endogenous antioxidant enzymes to prevent oxidative modification of cellular components.