Beneficiary Effect of Zinc Supplementation in Tuberculosis as Reflected by Serum Level of Diagnostic Biomolecules

Aim and objective: This author had indoctrinated a higher Mycobacterium tuberculosis (Mtb) origin serum superoxide dismutase (SOD), detectable Mtb origin serum glutamine synthetase (GS) and inhibited host origin serum cholinesterase (ChE) as diagnostics for tuberculosis (TB). Mycobacterium tuberculosis by secreting abundant siderophores, the Fe +3 chelators, scavenges iron (Fe) from transferrin, lactoferrin, etc.; and thus, major decompartmentalized state of Fe takes place in host tissues, generation of superoxides is accentuated, which are used up by Mtb for dismutation reaction to evolve soluble oxygen for survival of this obligatory aerobe. Zinc (Zn), a redox inert metal, accelerates reversion to normal compartmentalized state of Fe by replacing Fe from thiol group binding site. Zn, by decreasing generation of reactive oxygen species renders an onslaught on Mtb. In this study, the author had mulled the effect of Zn supplementation (25 mgm of elemental Zn daily orally for 1 month) on the serum level of TB diagnostics as mentioned. Materials and methods: Serum SOD, GS, and ChE were assayed for TB patients at baseline and also after 1 month with anti-TB drugs as two groups; one without and other with Zn supplementation. Same parameters were also measured for normal control and lung disease control subjects at baseline. Result: Significant decrease in serum SOD (p = 0.01) and GS (p = 0.01) in TB patients with Zn supplementation for 1 month had been recorded in comparison to those without Zn supplementation. Also, recovery of serum ChE activity with Zn supplementation was significant (p = 0.002).