Alcoholic liver disease-from steatosis to cirrhosis - a biochemistry approach

Abstract

Nowadays, chronic alcoholism and its health implications represent a global concern. Over three million deaths are linked to chronic alcohol intake every year. This article aims to spread awareness about the negative impact ethanol can have on almost every organ in the body, especially the liver. Understanding ethanol metabolism and the cellular pathways through which alcohol increases liver oxidative stress may prevent a broad spectrum of hepatic lesions such as steatosis, steatohepatitis, and, ultimately, cirrhosis. After a short review of ethanol metabolism and liver oxidative stress, each hepatic lesion will be individually discussed regarding the mechanism of apparition, treatment, and future targeted therapies.

Keywords: -OH – hydroxyl radical; A(2)C – 2-(2-methoxy ethoxy) ethyl 8-(cis-2-n-octylcyclopropyl); ADH – alcohol dehydrogenase; ALDH2 – aldehyde dehydrogenase 2; AMPK – adenosine monophosphate-activated protein kinase; CD14 – cluster of differentiation; CYP2E1 – cytochrome P450 2E1; DNA – deoxyribonucleic acid; ER – endoplasmic reticulum; GSH – glutathione; H2O2 – hydrogen peroxide; HER – hydroxyethyl radical; HSC – hepatic stellate cells; JNK – Janus Kinase; KC – Kupffer cells; LPS – lipopolysaccharides; MAA – malondialdehyde-acetaldehyde compounds; NAD+ – nicotinamide adenine dinucleotide; NADH – reduced nicotinamide adenine dinucleotide; NADP+ – nicotinamide adenine dinucleotide phosphate; NADPH – reduced nicotinamide adenine dinucleotide phosphate; O2-∙ – superoxide anion; PPARalpha – peroxisome proliferator-activated receptor-alpha; ROS – reactive oxygen species; SREBP-1 – sterol regulatory element-binding protein 1; TLR4 – toll-like receptor 4; TNFalpha – tumor necrosis factor-alpha; cirrhosis; ethanol; oxidative stress; steatohepatitis; steatosis.