UC Irvine

Acute inflammation can represent an effective immune response to the corporeal presence of organisms of exogenous origin or damaged cells of intrinsic origin, both of which are potentially injurious. Very often, such inflammation persists long after the triggering stimulus no longer poses a threat. Such a chronic condition can ultimately be more harmful than the original triggering agent. The means by which metallic compounds can provoke undesirable and extended inflammatory changes within the nervous system are diverse. This short review classifies the likely mechanisms underlying their toxicity by taking into account their known chemical properties and also by reflecting on other injurious events that commonly occur together with inflammation. The brevity of this survey does not allow focusing exhaustively on each individual metal but rather seeks to uncover some intracellular susceptible biochemical loci, based on the chemistry of each class of metals. Developmental and senescence-related characteristics are considered as these stages of life often involve especial vulnerabilities. Another feature addressed is that while research is generally conducted on purified and well-defined agents, exposures in the real world generally involve diverse mixtures in which the individual toxicity of a component can be enhanced or suppressed by the presence of other chemicals.