Mitigating alcohol-induced liver oxidative stress and dysregulated autophagy with protein hydrolysates derived from rainbow trout by-products.

Background: Chronic alcohol consumption causes irreversible liver damage. With 23 % waste from 29 million tons of annual production, rainbow trout is a valuable source of natural antioxidants. This study explores the hepatoprotective effects of rainbow trout protein hydrolysates in an alcohol-induced fatty liver disease (AFLD) rat model, focusing on autophagy, apoptosis, and oxidative stress pathways. Methods: Twenty-four male rats were divided into four groups: Control (C), alcohol (A), protein hydrolysates (P), and alcohol + protein hydrolysates (AP). At the end of the experiment, liver tissue samples were collected for analysis. Oxidative stress markers, including malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH), were assessed. Additionally, the expression of genes related to apoptosis (p53) and autophagy (Beclin1, Atg7, P62) in the liver was evaluated. To validate the gene expression results, the protein expression levels of LC3 and p53 were also measured. Results: Alcohol exposure elevated MDA levels while reducing SOD activity and GSH. Hydrolysate treatment restored antioxidant capacity by enhancing SOD and GSH and lowering MDA. Histology showed hepatic steatosis and reduced glycogen in group A, while groups P and AP exhibited significant improvement (p˂0.05). Additionally, hydrolysates inhibited alcohol-induced P53 upregulation and modulated autophagy-related genes (p˂0.05). Immunohistochemistry showed reduced P53 and increased LC3 in the AP group, indicating a shift from apoptosis to autophagy for cellular homeostasis. Conclusion: These results suggest that protein hydrolysates derived from rainbow trout may have therapeutic potential as a dietary intervention for managing alcohol-induced liver injury, pending further validation.