Zinc Metabolism: A Review with Regard to Zn Finger Proteins, DNA Methylation and p53; In Reference to its Deficiency Syndromes and Tracing its Immunological as Well as Epigenetic Relations
Epigenetics is the branch of biology that studies the effects of environment on genetics and vice versa. It is the connecting link between genotype and phenotype of an individual, and can be widely influenced by the nutrition and availability of certain essential micronutrients, in this review, zinc. Although a trace element, zinc is essential to the body as a core component of more than 300 proteins and enzymes, which when functioning normally impart structural and mechanical capacities to the body tissues and fluids. Zinc is ubiquitous to all parts of the body and regulates various metabolic and biological processes such as cell proliferation, apoptosis, tumorigenesis, along with the regular working of fetal and adult organs. The role of zinc-finger proteins is crucial to impart stability to a protein’s folds and in turn render it functional to play its role in gene expression to serve as oncogenes or tumor suppressor genes. Zinc deficiency is a common occurrence in various parts of the world and is generally due to inadequate intake through the diet but may also manifest itself in an inheritable form. The effects of low zinc on a cellular level can be seen through a diminishing immunity, increased oxidative stress, reduced functionality of the p53 protein leading to tumor formation, incorrect DNA methylation. While phenotypically, zinc deficit can be both congenital and acquired. Some such diseases discussed here are irritable bowel syndrome, acrodermatitis enteropathica, thymic atrophy, celiac disease and preterm birth. In this review, the focus is on the aspect of zinc availability to cells as an epigenetic modulator/regulator and the subsequent consequences arising due to imbalance of zinc in the cell.