ABSTRACT

Iron has an essential function in living cells as it can gain and lose electrons based on two stable oxidation states, ferrous (Fe2+) and ferric (Fe3+) ions. This property makes iron a useful component of heme-bound and nonheme iron proteins. Excess ferrous ions act as a toxic catalyst to produce free radicals in the presence of H2O2 or other reactive oxygen species (ROS),1 whereas iron deciency arrests cell growth and leads to cell death. ROS induce stress conditions in cells and damage proteins, nucleotides, and lipids in cell membrane.2 Cellular iron levels are thus carefully regulated to minimize the pool of otherwise potentially toxic irons. On the other hand, iron lies at the center of a battle for nutritional resource between hosts and microbial pathogens. A host’s iron status can inuence infection in animals including humans, which affects the pathogenicity of numerous infections, such as malaria, HIV-1, and tuberculosis.3 A study on iron deciency in patients, recorded ve times the number of infections in those receiving iron supplements relative to a placebo group.4