Mitochondria as main targets of heavy metal-mediated neurotoxicity

VERSTRAETEN SV

Brain Mitochondria: Distribution and Function

Nova Science Publishers

Año: 2020;

Therequirement of metals for industrial purposes had an outburst at the end of theXVIIIth century, during the Industrial Revolution, and continued increasingsteadily until present days. Their removal from the Earth?s crust by mining had?and still has? noxious consequences on the environment, as mobilized metalscontaminate waters and soils, becoming available for living organisms. Humanexposure to heavy metals occurs through the inhalation of fumes or air-borneparticles, the ingestion of contaminated foods or water, or dermal contact.Upon reaching the bloodstream, heavy metals distribute among organs andtissues, the central nervous system (CSN) being particularly susceptible tothem. As CNS has high tendency to accumulate heavy metals, their localconcentration could reach relative high values, harming intracellularorganelles and affecting metabolic pathways therein. Mitochondria areparticularly vulnerable organelles to the effects of heavy metals, and theirdysfunction results in the impairment of energy supply to cells, exacerbatedproduction of oxidants, and potential activation intrinsic pathway ofapoptosis, among others. All these factors contribute to the neurotoxic effectsof heavy metals that ultimately lead to cognitive and/or motor impairment.In thepresent work, current knowledge regarding the mechanisms underlying heavymetal-mediated damage to CNS mitochondria will be discussed, with special focuson those considered worldwide as the most pollutant metals: arsenic, thallium,lead, cadmium and mercury.