International Journal of Molecular Sciences · 5 authors, 8 centres
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This narrative review examines how vanadium salts and compounds modulate reactive oxygen species formation and lipid peroxidation in cells, tissues, and mitochondria. The central finding is that vanadium species can both exacerbate and protect against lipid peroxidation depending on their speciation, with decavanadate being 10 to 100 times more potent than monomeric vanadate at mitochondrial targets.
This narrative review synthesizes preclinical literature on how vanadium salts and complexes affect reactive oxygen species (ROS) formation and lipid peroxidation (LPO) in cells, tissues, and organisms. The review describes LPO as the autocatalyzed chain oxidation of bis-allylic bonds in fatty acids, noting that vanadium compounds can induce ROS formation both directly and indirectly. A key conclusion is that decavanadate (V10) is consistently 10 to 100 times more potent than monomeric vanadate (V1) as a mitochondrial membrane-depolarizing agent and inhibitor of oxygen consumption in hepatic and cardiac mitochondria. The review highlights that complex vanadium chemistry under physiological conditions produces diverse species with different biological effects, making speciation studies essential. Biomarkers of LPO discussed include malondialdehyde (MDA), hydroxynonenal (4-HNE), and enzymes such as superoxide dismutase and catalase. The authors suggest that understanding vanadium speciation is important for evaluating reported beneficial effects in cancer, diabetes, and neurodegenerative diseases.
