Can the indicators of chronic ethanol consumption be minimized by a continuous flaxseed intake?

The aim of this study was to evaluate the use of flaxseed in animals subjected to ethanol-induced hepatotoxicity. Twenty-four male rats were divided into four groups (n = 6): control group (CG) which received a control diet and water ad libitum; flaxseed group (FG) which received control diet with an addition of 25% flaxseed flour and water ad libitum; ethanol control group (ECG) which received control diet and a solution of 10% ethanol (v/v) as the only liquid source; and ethanol flaxseed group (EFG) which received control diet with an addition of 25% flaxseed flour and a solution of 10% ethanol (v/v) as the only liquid source. The animals were euthanized at 60 days, when blood was collected for biochemical analysis and liver was collected for histomorphometric analysis. Rats fed with diets containing flaxseed showed lower values of alkaline phosphatase (P = 0.020) and lower concentration of total bilirubin (P = 0.006), direct bilirubin (P = 0.013) and indirect bilirubin (P = 0.018) compared to ECG and EFG. The groups receiving flaxseed diets demonstrated higher expression of superoxide dismutase (SOD) enzyme (P < 0.001) than CG and ECG but did not affect thiobarbituric acid (TBARS) expression (P = 0.055). Regarding liver analysis, the ECG and EFG showed larger hepatocyte nuclei and paler cytoplasm than the groups who had not received ethanol, and less in fluid accumulation (oedema) in the cytoplasm than was seen in the FG and EFG livers. These latter two groups showed fewer fatty cells than was seen in the groups that had not been given flaxseed, so that the diagnosis of hepatic steatosis was not justified. In conclusion, therefore, this study showed that the indicators of ethanol chronic consumption can be reduced by the introduction of continuous flaxseed dietary intake.