Mordechai Chevion

TL;DR: In biological systems, there are traces of copper and iron that are at high enough levels to catalyze free-radical reactions, and account for such deleterious processes, and the rate constants of their reduced forms with hydrogen peroxide are sufficiently high to suggest that they might be important mediators of free radical toxicity.

TL;DR: It is demonstrated that incubation of cultured bovine aortic endothelial cells with AGE albumin resulted in the impairment of reduced glutathione and ascorbic acid levels, and supplementation of cellular antioxidative defense mechanisms by extracellularly administered α-lipoic acid reduces AGEalbumin-induced endothelial dysfunction in vitro.

TL;DR: It is demonstrated that when amyloid-β is pretreated with the iron chelator deferoxamine, neuronal toxicity is significantly attenuated while conversely, incubation of holo-amyloids-β with excess free iron restores toxicity to original levels, suggesting that the toxicity of amylid- β is mediated, at least in part, via redox-active iron that precipitates lipid peroxidation and cellular oxidative stress.

TL;DR: Experiments with DNA labeled phages indicate that both phage adsorption and DNA injection are impaired as a result of the exposure to ascorbate and copper, and a 'site-specific' Fenton mechanism according to which the binding of the transition metal ions to the biological target is a prerequisite for the production of damage.

TL;DR: Analysis of the individual organs showed this increment to be statistically significant in malignancies of the large bowel, stomach, urinary bladder and female reproductive organs, while in cancer of the breast, kidney and testis, the increase in copper level was not significant.