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- W2364301163 abstract "Anoxiainduced damage of primary cortical neurons in culture and the protective effects of ditiocarb sodium (DTC) against it were studied. Anoxia was produced by exchanging media with serumfree oxygendepleted media and placing the cultures in an anoxia chamber. Anoxia could induce damage of neuron reflected by the decrease in both the viable neuron number and the mitochondrial activity, and induce the increase in LDH release and MDA production. Superoxide dismutase (SOD) reversed the effects of anoxia. DTC, as well as SOD, protected the viability of neuron against anoxic damage and dosedependently inhibited LDH release and MDA production. The results suggested that the formation of oxygen free radicals be implicated in anoxic damage of cortical neuron. DTC could protect the cultured neuron against anoxic damage, that might be mediated by scavenging oxygen free radicals." @default.
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- W2364301163 date "1998-01-01" @default.
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- W2364301163 title "Protective effects of ditiocarb sodium against anoxic damage of primary cortical neurons in culture" @default.
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