Dysfunction of cortical synapse-specific mitochondria in developing rats exposed to lead and its amelioration by ascorbate supplementation.

摘要: Background Lead (Pb) is a widespread environmental neurotoxin and its exposure even in minute quantities can lead to compromised neuronal functions. A developing brain particularly vulnerable Pb mediated toxicity early-life leads permanent alterations development signaling plasticity, culminating into cognitive behavioral dysfunctions elevated risk of neuropsychiatric disorders later life. Nevertheless, the underlying biochemical mechanisms have not been completely discerned. Methods Because their ability fulfill high energy needs act as calcium buffers events intensity activity well adaptive regulatory capability match requirements dynamicity synaptic signaling, synapse-specific or mitochondria (SM) are critical for development, function plasticity. Our aim present study hence was characterize effects on functions SM prepubertal rats. For this purpose, employing chronic model neurotoxicity, we exposed rat pups perinatally postnatally used plethora colorimetric fluorometric assays assessing redox bioenergetic properties SM. In addition, taking advantage an antioxidant metal chelator, employed ascorbic acid (vitamin C) supplementation ameliorative therapeutic strategy against Pb-induced neurotoxicity dysfunction Results results suggest that oxidative stress cortical with consequent compromises metabolism activity. Ascorbate resulted significant recovery functional compromise Conclusion Alterations status could potentially contribute observed neurotoxicity. Additionally, our provides evidence suitability ascorbate agent tacking