Nitric oxide (NO) contributes to the extracellular potassium-ion concentration ([K
+]
o)-induced hydroxyl radical (
•OH) generation. Cytotoxic free radicals such as peroxinitrite (ONOO
−) and
•OH may also be implicated in NO-mediated cell injury. NO is synthesized from
L-arginine by NO synthase (NOS). NOS activation was induced by K
+ depolarization. Oxidative modification of low-density lipoprotein (LDL) is thought to contribute to the production of oxygen derived-free radicals. However, LDL oxidation may be related to noradrenaline-induced
•OH generation, but LDL oxidation may be unrelated to
•OH generation via NOS activation. Abnormal levels of extracellular free dopamine (DA) and/or intraneuronal Ca
2+ triggered by 1-methyl-4-phenylpyridinium ion (MPP
+) may be detrimental to the functioning of dopaminergic nerve terminals in the striatum. Although [K
+]
o-induced depolarization enhances the formation of
•OH product due to MPP
+, the
•OH generation via NOS activation may be unrelated to the DA-induced
•OH generation. Depolarization enhances the formation of
•OH products via NOS activation.
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