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The unexpected activity can be explained by the formation of variable amounts of disulfide-bridged PfGrx C32S/C88S homodimers and potential Diamide-modified monomers, summarized as PfGrx C32S/C88S (SX), as revealed by non-reducing SDS-PAGE (Fig

While the full picture has yet to be unmasked, in vitro approaches based on cultured cells, isolated mitochondria and tissue slices, as well as in vivo studies based mainly on the use of rodents, point to impairment in intracellular calcium homeostasis, alteration of glutamate homeostasis and oxidative stress as important events in MeHg-induced neurotoxicity