Hepatoprotective effect of flaxseed and its protein on ethanol-induced hepatotoxicity in adult Wistar rats was investigated. The rats were divided into eight groups of which two served as control (group I: Control for AIN-93M diet groups and group II: Control for cereal-pulse diet groups) and six groups received ethanol orally every day. After 10 days along with ethanol, the rats received AIN-93M diet (group III); AIN-93M diet and commercial hepatoprotective formulation (CHF) (group IV); casein replaced by flaxseed protein in AIN-93M diet (group V); cereal-pulse diet (group VI); cereal-pulse diet and CHF (group VII); cereal-pulse diet containing flaxseed (group VIII) for four weeks. The flaxseed and its protein significantly prevented the elevation of plasma markers of hepatic damage, lowered lipid peroxidation, mitigated changes in antioxidant enzymes, and suppressed histopathological signs of hepatic damage. The hepatoprotective effect of flaxseed and its protein was comparable to CHF. These findings implicate the ameliorative effect of flaxseed and its protein on ethanol-induced hepatotoxicity. Practical applicationsOwing to globalization and an increase in earning capacity, alcohol consumption is becoming a part of social life and gradually transforming to addiction. Binge drinking is highly prevalent among low socioeconomic status population, which poses severe risks to health. Alcohol abuse is a public health problem causing three million deaths annually worldwide. Alcohol consumption is known to be a major cause of liver damage worldwide and has contributed to 44% of deaths from liver disease. As abstaining from alcohol is a challenging task, there is an escalating need to formulate potential hepatoprotective agents to prevent alcohol-induced hepatic damage. This study investigates the efficacy of flaxseed and its protein in conferring protection to the liver against ethanol-induced hepatotoxicity. This study also explores the benefits of incorporating flaxseed in the staple cereal-pulse diet. Findings of this study suggest that incorporation of flaxseed or its protein in food formulations can prevent hepatotoxicity and improve the overall quality of life among alcoholics. K E Y W O R D Sbilirubin, ethanol-induced hepatotoxicity, flaxseed, malondialdehyde, protein concentrate
Alcohol abuse causes severe metabolic abnormalities inducing hepatic damage and malnutrition. Since higher Fischer ratio proteins have therapeutic value in liver disease conditions, an investigation was undertaken to study the ameliorative effect of the enhanced Fischer ratio flaxseed protein hydrolysate (EFR-FPH) alone and in combination with antioxidant micronutrients on ethanol-induced hepatotoxicity in a rat model. The EFR-FPH was prepared by dual enzymatic hydrolysis and charcoal treatment of flaxseed protein. The ratio of the branched-chain to aromatic amino acids (Fischer ratio) was found to be 7.08. The EFR-FPH characterized using LC-MS/MS, showed the abundance of free leucine and isoleucine compared to phenylalanine and tyrosine. The MALDI-TOF MS analysis revealed the larger peptides present in EFR-FPH with mass 2.3 kDa. The EFR-FPH improved the nutritional status, liver function and antioxidant enzymes activity in the ethanol hepatotoxicity induced rat model. The hepatoprotective effect of EFR-FPH was significantly enhanced when combined with selenium or vitamin E. Ethanol-induced changes in the histology of liver tissue were effectively suppressed in the group receiving EFR-FPH. Flaxseed-based hepatoprotective dietary supplement was formulated incorporating an optimum level of EFR-FPH (10%) based on sensory acceptability and was fortified with selenium and vitamin E. The hepatoprotective formulation significantly lowered AST, ALT, ALP, and bilirubin by 47, 61, 55, and 78%, respectively, and improved the antioxidant defense system in the ethanol hepatotoxicity induced rat model. The current investigation suggests that EFR-FPH in synergy with antioxidant micronutrients is potent in ameliorating ethanol-induced hepatotoxicity and has a potential to form a hepatoprotective dietary supplement.
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