Fig. 2.

Hypothetical model of mechanism of ethanol toxicity and cardiac injury through different pathways, including more rapid acetaldehyde conversion and accumulation by the activity of fast ADH1B (Step 1), delayed metabolism of toxic acetaldehyde due to reduced enzyme activity due to the variant ALDH2 (Step 2), and reactive oxygen species (ROS) generation (Step 3) by higher CYP2E1 activity due to genetic polymorphisms. CYP2E1 activity can also be induced by chronic alcohol use. Thicker arrow denotes faster metabolism, and thinner arrow denotes slower metabolism; + denotes facilitation of acetaldehyde accumulation. Arrows alone indicate enzyme functions, and arrows with a + mark denote the biological modulation resulting in acetaldehyde formation or accumulation.