Zinc deficiency-induced cell death.
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.
Clegg
Michael S
MS
Department of Nutrition, University of California at Davis, Davis, CA 95616, USA. msclegg@ucdavis.edu
Hanna
Lynn A
LA
Niles
Brad J
BJ
Momma
Tony Y
TY
Keen
Carl L
CL
D016475:3T3 Cells; D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology*; D049109:Cell Proliferation / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D006133:Growth Substances / Q000378:metabolism; D006801:Humans; D051379:Mice; D015398:Signal Transduction; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis / Q000502:physiology; D015032:Zinc / Q000172:deficiency*
D006133:Growth Substances; D016159:Tumor Suppressor Protein p53; D015032:Zinc