Zinc deficiency-induced cell death
Michael S. Clegg(University of California, Davis), Lynn A. Hanna(University of California, Davis), Brad J. Niles(University of California, Davis), Tony Y. Momma(University of California, Davis), Carl L. Keen(University of California, Davis)
Cited by 137Open Access
Abstract
Zinc deficiency is characterized by an attenuation of growth factor signaling pathways and an amplification of p53 pathways. This outcome is facilitated by hypo-phosphorylation of AKT and ERK secondary to zinc deficiency, which are permissive events to the activation of the intrinsic cell death pathway. Low zinc concentrations provide an environment that is also conducive to the production of reactive oxygen/reactive nitrogen species (ROS/RNS) and caspase activation. Additionally, during zinc deficiency endogenous survival pathways such as NF-kappaB are inhibited in their transactivation potential. The above factors contribute to the irreversible commitment of the zinc deficient cell to death.