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. Author manuscript; available in PMC: 2020 Sep 25.
Published before final editing as: Curr Hypertens Rev. 2019 Mar 25:10.2174/1573402115666190325124622. doi: 10.2174/1573402115666190325124622

Table 1.

Potential ethanol-induced sources of reactive oxygen species.

 Ethanol Metabolism

  • An ↑ in the flux of reducing equivalents into the electron transport chain due to an ↑ in nicotinamide adenine dinucleotide production related to ethanol metabolism (↑ NADH/NAD+ ratio).

  • An ↑ in cytochrome P450 2E1 metabolism of ethanol.

  • An ↑ in alcohol dehydrogenase metabolism of ethanol and accumulation of acetaldehyde (leading to ROS formation and acetaldehyde adduct formation).

  • Nonoxidative metabolism by fatty acid ethyl ester synthase and/or phospholipase D.

Ethanol Effects on Antioxidant Proteins and Antioxidant Enzymes

  • Alcohol-induced inhibition of transport proteins responsible for transporting glutathione from cytosol into the mitochondria (e.g., glutathione transport from cytosol into the mitochondria) and ↓ antioxidant enzyme levels and activity (e.g., superoxide dismutase).

Activation/Alteration in Neurohormonal Systems

  • Increased autoxidation of catecholamines.

  • An ↑ in angiotensin II and norepinephrine levels.

Abbreviations NADH/NAD+ - Nicotinamide adenine dinucleotide reduced/ nicotinamide adenine dinucleotide, ROS- reactive oxygen species.