- A Alcohol consumption is understood by hepatologists to have essentially little measurable toxic effect on liver cell function, even after decades of sustained, heavy daily consumption by the patient
- B Alcohol is metabolized in liver to acetaldehyde (toxic), causing oxidative stress, fatty liver (steatosis), inflammation (alcoholic hepatitis), and eventually scarring (cirrhosis)
- C Alcohol is understood to exert its primary toxic effects mainly on brain tissue, largely sparing liver cell function, with hepatocytes remaining structurally and functionally normal indefinitely
- D Liver damage caused by chronic, long-term alcohol consumption is usually largely reversible, generally by abstaining from alcohol for a short period of time
Correct answer: B. Alcohol is metabolized in liver to acetaldehyde (toxic), causing oxidative stress, fatty liver (steatosis), inflammation (alcoholic hepatitis), and eventually scarring (cirrhosis)
Explanation: Alcohol metabolism pathway: ethanol → acetaldehyde (alcohol dehydrogenase) → acetate (aldehyde dehydrogenase). Acetaldehyde is highly toxic: forms protein adducts, causes oxidative stress, mitochondrial damage, activates hepatic stellate cells. Progression: fatty liver (reversible) → alcoholic hepatitis → cirrhosis (irreversible scarring) → liver failure/hepatocellular carcinoma.
Concept context
Pathogens, infectious diseases, non-infectious diseases, drugs, cancer, and public health. High NEET importance.