Fig. 1
From: Zinc status is associated with inflammation, oxidative stress, lipid, and glucose metabolism
The influence of zinc on oxidative stress and inflammation. Zinc prevents the generation of reactive oxygen species through a number of mechanisms. Zn is a cofactor of Cu,Zn-SOD, which catalyzes the dismutation of superoxide. It up-regulates Nrf2, being the principal regulator of antioxidant system functioning, thus increasing GSH synthesis, GPx activity, and other mechanisms of detoxification. Zinc also affects the generation of reactive oxygen species through modulation of prooxidant pathways. Zn-induced decrease in NADPH oxidase activity results in decreased superoxide production. Through induction of metallothionein synthesis, Zn may decrease the availability of redox metals and their participation in Fenton reaction. Susceptibility of proteins to free radical oxidation is also inhibited by zinc through protection of thiol groups. Zn-induced inhibition of redox-sensitive proinflammatory transcription factors is accompanied by decreased production of proinflammatory cytokines, enzymes, and adhesion molecules, thus resulting in the prevention of inflammatory response