The effects of smoking on white matter lesions, such as lacunar infarction and leukoaraiosis, are still controversial; recently the hypothesis that the eNOS T-786C genotype was a modulating factor for the effect of smoking on cerebral circulation was examined. Smokers were showed greater oxidative stress, as estimated by urinary F(2)-isoprostane excretion. In smokers, — 786CC homozygotes showed a significant decrease of cerebral blood flow and a significant increase of cerebrovascular resistance, whereas the eNOS genotype did not affect these parameters in nonsmokers (102). Further evidence for a role of smoking in modulating the activity of eNOS was demonstrated in vitro using luciferase reporter vectors with the various haplotype combinations of the — 786T > C and intron 4 repeat polymorphisms. Transcription efficiency in the T promoter was lower than in the C promoter. Treatment of the constructs with cigarette smoking extract increased the transcription efficiency significantly in the T promoter (1.7-fold, P < 0.01), it reduced further the already lower C promoter efficiency (by 10-15%) (103).
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