Zinc is required as a cofactor for many enzymes. Zinc deficiency causes impaired wound healing, acrodermatitis enteropathica, and immune dysfunction. The molecular basis of immune impairment is PRIMARILY due to:
- A Zinc is required for thymulin activity and lymphocyte proliferation; deficiency causes thymic atrophy and reduced T-cell function ✓
- B Zinc is the cofactor for lysyl oxidase, impairing collagen cross-linking and bacterial entrapment
- C Zinc deficiency reduces ferroportin expression, causing secondary iron deficiency anaemia and neutropaenia
- D Zinc is required for carbamoyl phosphate synthetase, reducing urea production and causing immune cell cytotoxicity
Explanation
Zinc is essential for the zinc-dependent hormone thymulin, produced by thymic epithelial cells, which is required for T-lymphocyte differentiation and maturation. Zinc also stabilises zinc-finger transcription factors critical for lymphocyte gene expression. Deficiency causes thymic atrophy, reduced CD4+ T-cell numbers, impaired NK cell activity, and susceptibility to opportunistic infections. Zinc also regulates metallothionein-mediated antioxidant defence. Lysyl oxidase uses copper, not zinc.
Reference: Harper's Illustrated Biochemistry, 32nd ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.