Roles for cell death in zinc deficiency

Abstract

Studies of zinc deficiency (ZD) have become important for demonstrating that nutritional imbalances can readily induce programmed cell death (PCD) or apoptosis in a variety of kinds of cells. In mice, ZD caused a 300% increase in the amount of apoptosis among pre T-cells, which was a major cause of thymic atrophy that alters host defense. Embryogenesis was significantly altered in ZD mice due to increased apoptosis in the neural crest, optic, and head regions. Insufficient zinc initiated PCD in hepatocytes, glioma, kidney, monocytes, fibroblasts, and testicular cells, demonstrating the scope of this phenomenon. New forms of cell death continue to emerge. For example, autophagy is initiated by starvation and various nutritional and metabolic imbalances. Autophagy is a form of PCD whereby the cell digests some of its own organelles to provide needed nutrients. Understanding the interplay between these different forms of cell death and nutritional imbalances is very important because of their profound impact on development, growth, immune function, and health. © 2004 American Society for Nutritional Sciences.