Aim and background: To acquire iron (Fe), Mycobacterium tuberculosis (Mtb) expresses high-affinity Fe⁺³-specific siderophores for scavenging Fe from host insoluble and protein-bound iron-like transferrin, lactoferrin, ferritin, and hemoglobin−haptoglobin. Mycobacterium tuberculosis by its specific membrane protein and Fe transporters can internalize Fe within cell cytoplasm. With infection by Mtb, activity of transferrin, the most dynamic Fe carrier gets setback with a decrease in its level due to infection and also by a decrease in its ability to leave out Fe in bone marrow cells through specific cell surface transferrin receptors. Thus, major decompartmentalization of Fe in host tissues sets in. Zinc (Zn), a redox-inert metal, acts as an antioxidant by stabilizing membrane structures, upregulating expression of metallothionein, protecting protein sulfhydryl group, and suppressing the formation of superoxides by competing with Fe and copper in the cell membrane and thiol group binding. The study interprets the effect of Zn supplementation on serum Fe and hemoglobin (Hb) percentage for tuberculosis (TB) patients. Materials and methods: Serum Fe and blood Hb percentage were measured initially for TB patients. The same parameters were also assayed with continuation of anti-TB drugs for 1 month with or without Zn supplementation. Results: Assertive and veritable increase in baseline serum Fe in TB patients had been recorded in this study. The same TB patients with anti-TB drugs for 1 month had recorded nonsignificant serum Fe and Hb percentage increase, whereas oral zinc supplementation with anti-TB drugs for 1 month had shown significant increase in serum Fe and Hb percentage. Conclusion: Zinc hastens the process of normal compartmentalized state of Fe depriving Mtb to get Fe and superoxide required for dismutation reaction to get soluble oxygen for this obligate aerobe.