Mechanistic studies on ketamine-induced mitochondrial toxicity in zebrafish embryos.

ABSTRACT: Ketamine, a phencyclidine derivative, is an antagonist of the Ca²⁺-permeable N-methyl-d-aspartate (NMDA)-type glutamate receptors. It is a pediatric anesthetic and has been implicated in developmental neurotoxicity. Ketamine has also been shown to deplete ATP in mammalian cells. Our previous studies showed that acetyl l-carnitine (ALCAR) prevented ketamine-induced cardiotoxicity and neurotoxicity in zebrafish embryos. Based on our finding that ALCAR's protective effect was blunted by oligomycin A, an inhibitor of ATP synthase, we further investigated the effects of ketamine and ALCAR on ATP levels, mitochondria and ATP synthase in zebrafish embryos. The results demonstrated that ketamine reduced ATP levels in the embryos but not in the presence of ALCAR. Ketamine reduced total m

SUBMITTER: Robinson BL 

PROVIDER: S-EPMC5992061 | biostudies-literature | 2018 Sep - Oct

REPOSITORIES: biostudies-literature