TABLE 2.

Selenium and Zinc with pro-and anti-inflammatory effects as well as anti-tumor.

Nutrients	Anti-inflammatory effects	Pro-inflammatory effects	Antitumor effects
Zinc	Zinc may block the NF-κB signaling pathway through chelating with a distinctive intracellular membrane chelator such as TPEN (132). NF-κB signaling pathways may be inhibited by Zinc through a lot of suggested mechanisms (29). Through a decline of IL-1β gene expression, Zinc is responsible for the inflammatory cytokines number reduction. It is capable to inhibit TNF-α (134). It was observed that obese persons with low plasma concentrations of zinc had overexpression of, IL-1β, IL-1α and IL-6 genes (135). The cytokine production is much higher in patients with a critical state of health who were evaluated immediately after intensive therapy due to their decrease in plasma zinc concentration (137). It is able to induce the initiation of the CD8+ T cells proliferation (36, 139)	Some information has shown that the initiation of LPS-induced NF-κB is dependent on zinc (132).
Selenium	Could be implied in inflammatory mediators production (143, 144). It may acts as a cofactor in immunity that is mediated by the vaccine (148). After selenium treatment was observed a decline in IL-1 and TNF-α gene expression (149). Can enhance the immune response of Th1 cells and the stimulation of T cells (11). Antibody increase titers due to selenium supplementation cause an enhancer of vaccine effects (145, 146).		In patients with cancer, the supplementation of selenium increased antibody titers of IgA and IgG as well as the number of neutrophils (150).

IL, interleukin; IFNγ, Interferon γ; NF-κB, pro-inflammatory factor Kappa B; ROS, reactive oxygen species; Th, helper T cell; TNF-α, tumor necrosis factor; TPEN, N,N,N’,N’-tetrakis (2-pyridinylmethyl)-1,2-ethanediamine.