Background/Aims An increase of ethanol metabolism and hepatic mitochondrial respiration
occurs in vivo after a single binge of alcohol. Here, our aim was to determine how ethanol …

Ethanol increases hepatic mitophagy driven by unknown mechanisms. Type 1 mitophagy
sequesters polarized mitochondria for nutrient recovery and cytoplasmic remodeling. In …

Oxidative stress and oxygen-derived free radicals are well known to play an important role in
the pathogenesis of ethanol-associated liver injury. Active oxidants produced during ethanol …

Acute ethanol intoxication induces oxidative stress and apoptosis in primary cultured
hepatocytes. Oxidative stress can trigger mitochondrial cytochrome c release initiating the …

Ethanol-induced hepatic steatosis may induce the progression of alcoholic liver disease.
The involvement of autophagic clearance of damaged mitochondria (mitophagy) and lipid …

Objectives Binge drinking and alcohol toxicity are often associated with myocardial
dysfunction possibly due to accumulation of the ethanol metabolite acetaldehyde although …

Chronic ethanol consumption increases sensitivity of the mitochondrial permeability
transition (MPT) pore induction in liver. Ca2+ promotes MPT pore opening, and genetic …

Pancreas is known to be vulnerable to ethanol (ETOH) at high doses, but little is known
about the effect of lower doses. Therefore, in this study, the levels of glutathione (GSH) …

Acute ethanol exposure induces oxidative stress and apoptosis in primary rat hepatocytes.
Previous data indicate that the mitochondrial permeability transition (MPT) is essential for …

Mitochondrial structure and function are central to cell physiology and are mutually
interdependent. Mitochondria represent a primary target of the alcohol-induced tissue injury …