Reactive oxygen and carbonyl species (ROS/RCS)

This target group encompasses a broad range of highly reactive chemical entities, including reactive oxygen species (ROS), free radicals, and toxic reactive carbonyl species (RCS) such as methylglyoxal and malondialdehyde (Sies et al., 2017, Nature Reviews Molecular Cell Biology). These molecules are generated as byproducts of aerobic metabolism, lipid peroxidation, and glucose oxidation, particularly under conditions of oxidative stress and hyperglycemia. They undergo non-enzymatic reactions with cellular macromolecules, leading to the formation of Advanced Glycation End-products (AGEs) and Advanced Lipoxidation End-products (ALEs) (Baynes & Thorpe, 2000, Free Radical Biology and Medicine). The accumulation of AGEs and ALEs causes structural damage to proteins, promotes inflammation through receptors like RAGE, and contributes to the progression of chronic diseases such as diabetes, atherosclerosis, and Alzheimer's disease. Therapeutic interventions aim to neutralize these reactive intermediates through scavenging or by inhibiting the chemical pathways that lead to permanent tissue damage (Thornalley, 2003, Archives of Biochemistry and Biophysics). Because these species are heterogeneous and often involved in normal signaling, targeting them requires a balance between neutralizing pathological levels and maintaining physiological homeostasis.

Other names

Reactive oxygen speciesToxic carbonylsFree radicalsReactive intermediates leading to AGEs/ALEsReactive carbonyl speciesDicarbonylsAGE precursorsALE precursorsOxidants

Mechanism of action involves the direct chemical neutralization (scavenging) of free radicals and reactive oxygen species, the nucleophilic trapping of reactive carbonyl intermediates (e.g., methylglyoxal, glyoxal, and 4-hydroxynonenal), and the inhibition of the non-enzymatic post-translational modification of proteins and lipids that leads to the formation of Advanced Glycation End-products (AGEs) and Advanced Lipoxidation End-products (ALEs) (Thornalley, 2003; Baynes & Thorpe, 2000).