Sidney J. Stohs

TL;DR: Some mechanisms associated with the toxicities of metal ions are very similar to the effects produced by many organic xenobiotics, related to differences in solubilities, absorbability, transport, chemical reactions, and the complexes that are formed within the body.

TL;DR: It is demonstrated that GSPE is highly bioavailable and provides significantly greater protection against free radicals and free radical-induced lipid peroxidation and DNA damage than vitamins C, E and beta-carotene.

TL;DR: The results clearly indicate that although different mechanisms lead to the production of reactive oxygen species by chromium and cadmium, similar subsequent mechanisms and types of oxidative tissue damage are involved in the overall toxicities.

TL;DR: The in vivo effects of structurally dissimilar polyhalogenated cyclic hydrocarbons, such as endrin and chlordane, chlorinated acetamide herbicides, and organophosphate pesticides (OPS), such as chlorpyrifos and fenthion on the production of hepatic and brain lipid peroxidation and DNA-single strand breaks (SSB), two indices of oxidative stress and oxidative tissue damage are examined.

TL;DR: Comparative studies demonstrate that a cascade of cellular events including oxidative stress, genomic DNA damage and modulation of apoptotic regulatory gene p53 are involved in chromium(VI)-induced toxicity and carcinogenesis.