Clinical biochemistry · 2012
Protective effect of diltiazem, a L-type calcium channel antagonist, on lysophosphatidylcholine-enhanced hydroxyl radical generation by MPP(+) in rat striatum.
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Obata Toshio, Miyashita Masahiro
Аннотация
BACKGROUND: The interaction between the PKC and oxygen free radicals.
OBJECTIVE AND METHODS: The present study examined the effects of lysophosphatidylcholine (LPC), an endogenous amphophilic lipid metabolite, on 1-methyl-4-phenylpyridinium ion (MPP(+))-induced hydroxyl radical (()OH) generation in rat striatum. LPC (50 μM) increased ()OH formation by MPP(+). Further, the effect of diltiazem, a L-type Ca(2+) channel antagonist, on MPP(+) (5mM)-induced ()OH generation was studied.
RESULTS: Diltiazem (100 μM) significantly suppressed LPC and MPP(+)-induced ()OH generation. The results indicate ()OH generation, and diltiazem may have preventive effect on MPP(+)-induced ()OH generation.
CONCLUSION: These results demonstrated that diltiazem suppressed LPC-induced generation of free radical through blockage of Ca(2+) channel in the rat striatum.
OBJECTIVE AND METHODS: The present study examined the effects of lysophosphatidylcholine (LPC), an endogenous amphophilic lipid metabolite, on 1-methyl-4-phenylpyridinium ion (MPP(+))-induced hydroxyl radical (()OH) generation in rat striatum. LPC (50 μM) increased ()OH formation by MPP(+). Further, the effect of diltiazem, a L-type Ca(2+) channel antagonist, on MPP(+) (5mM)-induced ()OH generation was studied.
RESULTS: Diltiazem (100 μM) significantly suppressed LPC and MPP(+)-induced ()OH generation. The results indicate ()OH generation, and diltiazem may have preventive effect on MPP(+)-induced ()OH generation.
CONCLUSION: These results demonstrated that diltiazem suppressed LPC-induced generation of free radical through blockage of Ca(2+) channel in the rat striatum.