Abstract
Previous studies have shown that fruits have different effects on alcohol metabolism and alcohol-induced liver injury. The present work selected three fruits and aimed at studying the effects of Syzygium samarangense, Passiflora edulis and Solanum muricatum on alcohol-induced liver injury in mice. The animals were treated daily with alcohol and fruit juices for fifteen days. Chronic treatment with alcohol increased the levels of aspartate transaminase (AST), alanine transaminase (ALT), total bilirubin (TBIL), triglyceride (TG), malondialdehyde (MDA), and decreased total protein (TP). Histopathological evaluation also showed that ethanol induced extensive fat droplets in hepatocyte cytoplasm. Syzygium samarangense and Passiflora edulis normalized various biochemical parameters. Solanum muricatum increased the level of ALT and induced infiltration of inflammatory cells in the liver. These results strongly suggest that treatment with Syzygium samarangense and Passiflora edulis could protect liver from the injury of alcohol, while Solanum muricatum could aggravate the damage.
Highlights
Alcohol consumption has been commonplace since ancient times all over the world [1]
Long-term excessive alcohol consumption can result in several diseases, such as gastrointestinal injury, alcoholic hepatic disease, pancreatitis, hepatocarcinoma, esophagus cancer, breast cancer, hypertension, and strokes [2,3]
Only a small amount of alcohol may be oxidized in the stomach by alcohol dehydrogenase (ADH) isoforms, and most alcohol enters the systemic circulation by the small intestine through passive diffusion [4]
Summary
Alcohol consumption has been commonplace since ancient times all over the world [1]. Only a small amount of alcohol may be oxidized in the stomach by alcohol dehydrogenase (ADH) isoforms, and most alcohol enters the systemic circulation by the small intestine through passive diffusion [4]. About 90% of ethanol is metabolized in liver, so liver is the most adversely influenced organ [5]. Ethanol is metabolized into acetaldehyde by alcohol metabolizing enzymes, including ADH (present in cytosol), cytochrome P450 2E1 (CYP2E1) (present in microsomes), and catalase (present in peroxisomes) [6,7]. The acetaldehyde is further oxidized into acetic acid by aldehyde dehydrogenase (ALDH) in the mitochondria. The CYP2E1-mediated metabolism of ethanol requires nicotinamide adenine dinucleotide phosphate (NADPH) and the incomplete reduction of
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