Abstract

From the results on antibacterial activities, the killing mechanisms have become clear that bacteriolysis for S. aureus peptidoglycan(PGN) cell wall is due to the inhibition of PGN elongation by the activities of PGN autolysins of amidases, and the other, for E. coli cell wall are due to destruction of outer membrane structure by degrading of lipoprotein at C-, N-terminals, owing to PGN formation inhibition by activities of PGN autolysins of amidase and carboxypeptidase-transpeptidase. Clioquinol, NF-kB, Zinc-mediated cancer chemoprevention can be expected to be efficacious in the prevention and treatment of several cancers. Zinc which is essential for many cellular processes plays a potential role in signal pathway linked with various physiological actions. The imbalances in Zn homeostasis cause disease states including such as diabetes, cancer, and Alzheimer’s disease. The accumulation of zinc also inhibits mitochondrial terminal oxidation and respiration. Zn2+ ions provide formation of fluorescent product after reaction with -SH groups of thiols,

In cancer cell, Zn(II)S+-complex ion may be formed and the complex is binding with S-atom. Zinc is known to have systemic effects such as regulation of the immune system as well as direct cellular effects resulting in regulation of gene expression. Zinc can inhibit apoptosis induced by both chemical and death-receptor agonists. Apoptotic effects of zinc because zinc is reported to both induce apoptosis in some cancers and to protect other cancer cells against apoptosis induced by other factors.

Autophagy as self-eating is involved in the bulk degradation, in which autophagy is highly conserved homeostatic mechanism for the degradation and recycling of bulk cytoplasm, organelles, and long-lived proteins through the lysosomal machinery. Degradation of the mutant protein by Zn2+ ion mediated and induced autophagy lead to cell death in cancer cell line. Zinc played a key role in the regulation of EMT and metastatic behaviors, that zinc-induced EMT increases the intracellular superoxide anion and induce EMT phenotypes in lung cancer cells by up-regulating of EMT markers and down-regulating of E-cadherin protein. Thus, zinc oxide, Zn-complex compound and Zn2+-chelation induced cancer and tumor cells can occur in adaptive tumor immunity, apoptosis, anti-angiogenic effect, also through reactive oxygen species (ROS). Damage by Zn-DNA reaction may be occurred by Zn substitution into hydrogen bond within DNA base pairs.

Keywords: Zinc(II) ions; Degradation of mutant protein; Autophagy; Angiogenesis; Zinc chelation; Metastatic dissemination; DNA damage