Enhanced depolarization-evoked calcium signal and reduced [ATP]/[ADP] ratio are unrelated events induced by oxidative stress in synaptosomes.

摘要: Oxidative insult elicited by hydrogen peroxide (H2O2) was previously shown to increase the basal intracellular Ca2+ concentration in synaptosomes. In present study, effect of H2O2 on depolarization-evoked [Ca2+] signal investigated. Pretreatment synaptosomes with (0.1-1 mM) augmented rise high K+ depolarization essentially two alterations, sudden sharp [Ca2+]i due is enhanced and, instead a decrease stable plateau, slow, steady follows peak [Ca2+]i. same range lowered ATP level and [ATP]/[ADP] ratio. When carbonyl cyanide p-(trifluoromethoxy) phenylhydrazone (FCCP) (1 microM) or rotenone (2 microM)/oligomycin (10 applied initially block mitochondrial production, ratio further reduced subsequent addition 0.5 mM H2O2. The decline parallel but could not explain K+-evoked signal, indicated experiments which decreased FCCP (0.1 similar value as without causing any alteration signal. These results indicate that H2O2-evoked oxidative stress, its early phase, gives complex dysfunction homeostasis it, an impaired energy status.