Transition metal ions (Iron and Copper)

Transition metal ions, particularly iron and copper, are essential cofactors that also act as potent catalysts for pathological oxidative and glycation reactions. In their labile or free forms, these ions facilitate Fenton-type chemistry, generating highly reactive hydroxyl radicals that cause extensive cellular damage (Halliwell & Gutteridge, 2015). Furthermore, these metals catalyze the autoxidation of glucose and the subsequent formation of advanced glycation end-products (AGEs), which contribute significantly to the progression of diabetes and age-related vascular diseases (Baynes & Thorpe, 2000). The accumulation of redox-active metals is a hallmark of several neurodegenerative conditions, including Alzheimer's and Parkinson's diseases, where they promote protein aggregation and oxidative stress (Jomova & Valko, 2011). Therapeutic targeting of these ions involves the use of chelating agents, such as deferoxamine or penicillamine, which bind and sequester the metals to prevent their participation in catalytic cycles (Price et al., 2001). By neutralizing these pro-oxidant centers, drugs can mitigate tissue damage and slow the development of chronic inflammatory and metabolic pathologies. However, a major challenge in targeting these ions is achieving selectivity to avoid depleting essential trace elements required for normal physiological function.

Other names

Redox-active metal ionsCatalytic transition metalsPro-oxidant metal ionsLabile metal poolTransition metal catalysts

Chelation and sequestration of redox-active metal ions to inhibit Fenton-type reactions and the autoxidation of reducing sugars, thereby reducing the production of reactive oxygen species and advanced glycation end-products.