Dietary Zinc Deficiency and Testicular Apoptosis

摘要: Abstract Zinc, an essential trace element, is integral to many proteins and transcription factors that are involved in diverse biological functions such as DNA replication, damage repair, gene expression, cell division, cycle progression, membrane integrity, apoptosis. Since it has a wide spectrum of activities, there widespread consequences well complexity inadequate dietary supply zinc depletion. Apoptosis, programmed death, can be modulated by various upstream signaling pathways converging on thereby altering the activity bcl-2 family proteins, caspases, p53, death factors, NF-κB, inhibitor apoptosis (IAPs). Zinc acts at multiple sites apoptotic cascade, including regulation from bax families, cytochrome c release, apoptosome function, caspase activation; also against oxidative stress protecting SH groups increasing synthesis metallothionein. Several vitro cell-culture studies have demonstrated deficiency induces apoptosis, whereas supplementation protect death. This chapter focuses current understanding how linked with deficiency. Findings indicate protective role steps pathway. However, need for further exploration regard extensive involvement