English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Hypothetically, the strength of a toxic effect of all trace metals depends principally on the absorption, concentration, and persistence of the eventual toxicant at its location of action. The final toxicant is the metal species that reacts with the endogenous target molecule such as receptors, enzymes, DNA, protein, or lipid or critically alters the biological environment, producing structural and functional changes that result in toxic damage. More often than not, the principal toxicant is the metal species to which the organism is exposed. However, in some cases the toxicant may be a metabolite of the parent compound or reactive oxygen or reactive nitrogen species (ROS or RNS) generated during the in vivo transformations of the toxicant. In few cases an endogenous molecule or compound synthesized as a response to primary toxicant exposure may be the principal toxicant. The buildup of the definitive toxicant at its target is facilitated by various biological processes that involve absorption, distribution to the site of action, reabsorption, and metabolic activation. Contrastingly, the predominant processes involved in counteracting toxic exposure contributing to tolerance are presystemic elimination, distribution away from the site of action, excretion, and detoxication which work against the accumulation of the ultimate toxicant at the target molecule. The logical steps by which toxicity results are typically as follows: delivery of toxicants > reaction of toxicants with target molecules > manifestation of dysfunction > counter reaction (repair)/failure of counter reaction (disrepair) > toxicity. Mode of action typically starts with the reaction of metals with target molecules and ends with toxic manifestations and entire these process oxidative stress and oxidant and antioxidant imbalances play a key role. This chapter will elaborate the mechanisms of free radical biology under metal stress in physiological system with a special reference to antioxidants counteractions..

Introductory Chapter: Free Radical Biology in Metal Toxicities—Role of Antioxidants