The role of iron in oxidative stress


Iron is a transition metal and can give and receive an electron. Hence, the additional content of iron can be cytotoxic. Iron (Fe2+) in natural and biological environments reacts with hydrogen peroxide (H2O2) and produces OH· radical, as reported by H.J.H. Fenton over one hundred years ago. At present, Fenton's reaction is one of the most effective procedures for oxidizing organic pollutants. Therefore, Fe2+ in the cytoplasm can participate in the Fenton reaction and lead to the generation of reactive oxygen species (ROS). Excess iron in the cytoplasm is arrested by ferritin. The free amount of iron can exert toxic effects on the cell.

Núñez et al., in their review, acknowledged that ascorbate and reduced glutathione (GSH) in the cell act as reluctant to regenerate Fe2+. The intracellular amount of Fe2+, in the presence of both oxygen and GSH, can also produce ROS. Hence, the production of ROS by iron accumulation is inevitable in the cell. ROS regulates the normal activities of the cell, but an abnormal increase in ROS levels may damage the cell. ROS increases the permeability of the outer mitochondrial membrane, damages the lysosomal membrane, and triggers the release of iron from these organelles. Thus, ROS may enhance iron accumulation in the cytosol. ROS produced by iron also reacts with the cell membrane and causes lipid peroxidation. ROS generates toxic aldehyde products during this reaction, including malondialdehyde and 4-hydroxylnonenal. These toxic components react with proteins to produce carbonyl functions, which damage the proteins. The ubiquitin/proteasome system cannot recognize the damaged, misfolded proteins, which aggregate within the cytoplasm, as seen in neurodegenerative diseases.

Furthermore, ROS can modify DNA by degradation of bases, breaking of DNA chain, mutations, modification of purine, pyrimidine or sugar-bound, deletions or translocations, and cross-linking with proteins. These modifications may relate to aging, cancer, and neurodegenerative diseases. ROS can initiate cellular injuries by modifying lipids, proteins, and DNA or lead to generating secondary ROS and, finally, cell death. Accordingly, excess iron can produce ROS via Fenton's reaction, causing oxidative stress and cell damage. If you are looking for high quality, high purity and cost-effective Iron oxide, or if you require the latest price of Iron oxide, please feel free to email contact mis-asia.

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