Reactive oxygen species are involved in smoking-induced dysfunction of nitric oxide biosynthesis and upregulation of endothelial nitric oxide synthase in human coronary artery endothelial cells

Cigarette smoke inhibits endometrial epithelial cell proliferation through a nitric oxide–mediated pathway

“…Excess reactive oxygen species in the serum of smokers was proposed to be the cause of defective biosynthesis of NO, because the effects of serum from smokers on eNOS expression could be reduced by antioxidants such as superoxide dismutase and catalase (39). Antioxidants have been used to prevent the detrimental effects of CS on the cardiovascular system with mixed success.…”

Acute Consumption of Flavanol-Rich Cocoa and the Reversal of Endothelial Dysfunction in Smokers

“…Data from investigations in vitro and in vivo demonstrated previously that various factors associated with oxidative stress, including smoking (1), inflammation (39), vitamin deficiency, and others resulted in a decline of NO production and in decreased levels of tetrahydrobiopterin (BH 4 ), an essential cofactor of NOS. Concordantly, free radicals present in cigarette smoke and increased endogenous radical generation secondary to cigarette smoking (2) were suggested to uncouple NOS by causing a decrease in BH 4 , subsequently leading to lower NOS and release (40). In this context, ascorbic acid administration has been shown in vivo (41) and in vitro (42) to attenuate the oxidative stress-related abrogation of NO production by either replenishing BH 4 or by preventing its loss through mechanisms that are causally linked to the antioxidant properties of ascorbic acid.…”

The pathophysiology of cigarette smoking and cardiovascular disease

“…In an attempt to produce a more physiologic in vitro model, our group has incubated endothelial cells with sera from smokers. Utilizing this model, Barua et al (31,39) demonstrated that exposure to smokers' sera decreased NO availability from both human umbilical vein endothelial cells (HUVECs) and human coronary artery endothelial cells by altering the expression and activity of the endothelial NO synthase enzyme. A significant correlation existed between flow-mediated brachial artery EDV and NO availability from cultured HUVECs exposed to serum from the same individuals (31).…”