A Glance At … ethanol consumption, GSH suppression, and oxidative liver damage

- The consumption of alcoholic beverages injures the liver through concurrent tissue oxidation and suppression of reduced glutathione synthesis, activity, and recycling.
- The acute consumption of any ethanol will increase the level of hepatic oxidative stress.
- Ethanol potentiates the hepatic oxidative stress-steatosis-hepatitis-fibrosis-cirrhosis-carcinoma transformative continuum.
- Even an acute single episode of ethanol consumption initiates metabolic pathways that achieve ultimate expression as hepatic fibrosis and cirrhosis.
- In the absence of abstinence, increasing hepatic antioxidant capacity may reduce the severity of ethanol-associated hepatic injury and its consequences.