Potential effects of L-NAME on alcohol-induced oxidative stress

Abstract

Our findings show that L-NAME may produce a restorative effect on ethanol-induced liver damage via decreasing oxidative stress and increasing antioxidant status.

Protective Role of Melatonin in L-Name Induced Hypertension in Male Albino Rats

“…Landmesser et al, (2003) linked the impairment endothelium mediated vasodilatation in hypertension to decrease NO bio-availability; this may be secondary to decrease NO synthesis or to increase NO degradation because of its interaction with O -2 to form peroxynitrite (ONOO -). Furthermore, Uzun et al, (2005) found that NO levels were negatively correlated with SOD, this result is consistent with those of the present study.…”

Nitric oxide reduces organ injury and enhances regeneration of reduced-size livers by increasing hepatic arterial flow

“…This rarely described positive effect of blocking nitric oxide is still a matter for debate. Some groups have ascribed this positive effect to reduced oxidative stress 35 or additional inhibition of inducible NOS 36 . The present authors further consider that the observed decrease in hepatic inflow after blockade of NOS with L-NAME is a result of systemic vasoconstriction and thus of reduced splanchnic blood flow, which first reduces the portal venous inflow and then the accompanying intrahepatic shear stress.…”

Alcohol Use, Vascular Disease, and Lipid-Lowering Drugs

“…Acetaldehyde is further oxidized by aldehyde dehydrogenase to acetate (Lieber, 2003). During both the above oxidizing processes, nitric oxide radicals are also formed (Uzun et al, 2005). In the case of chronic heavy consumption, the microsomal ethanol-oxidizing system is activated.…”

“…The close relationship between ethanol consumption and liver function is due to the fact that more than 80% of ingested Alc is metabolized in the liver (Uzun et al, 2005). Alcohol is catabolized through two different pathways according to the mode of consumption (Fig.…”

“…Nitric oxide radicals and reactive oxygen species, also produced by ethanol breakdown, contribute to this latter condition (Lieber, 2003;Uzun et al, 2005). Oxidative stress leads to protein deactivation, inactivation of essential enzymes, damage of antioxidants, such as glutathione and vitamin E, triggering of inflammatory response, and alteration of fat breakdown (McCuskey et al, 1995;Lieber, 2003).…”