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The interaction between metals and catecholamines plays a pivotal role in the generation of reactive oxygen species (ROS), leading to oxidative stress and DNA damage. ROS are linked to several diseases, including neurodegenerative disorders such as Parkinson's and Alzheimer's diseases. This review examines how essential metals (iron, copper, zinc, manganese) and a few non-essential metal(loid)s (mercury, chromium, arsenic, aluminum, cadmium, and nickel) contribute to oxidative stress in the presence of catecholamines. In the presence of metals, catecholamines can cause oxidative DNA modification, possibly resulting in cell apoptosis, by taking part in redox reactions and oxidizing to the corresponding aminochrome with simultaneous ROS production. Essential metals are vital for physiological functions, but imbalances in their homeostasis can be harmful. Furthermore, non-essential metals, commonly encountered through environmental or occupational exposure, can exhibit significant toxicity. Previous studies on catecholamine-induced oxidative stress focused on copper and iron, but this review emphasizes the need to investigate other neurotoxic metals and expand existing knowledge on the interactions between metals, catecholamines, and DNA damage. Results from such research could help prioritizing the development of new assessment methods associated with adverse outcome pathways, to reliably predict harmful effects on human health, aiding in the development of therapeutical strategies. The present work will help to shed light on the interplay of metals, catecholamines, and DNA damage in different diseases hopefully fostering new research in this still understudied topic. Future research should investigate the molecular mechanisms through which these metals affect neuronal health and contribute to disease pathogenesis.
Cassera et al. (Mon,) studied this question.