Milk lipids and sardine oil intake modulate differently enzymatic antioxidant defense in rats fed an atherogenic diet

Abstract

Objective: The effect of milk lipids compared to sardine oil on antioxidant enzymes activities was evaluated in rats fed an atherogenic diet. Methods: Male Wistar rats were divided into three groups (n = 8 for each). Two experimental groups received a 20% casein diet combined with 5% milk lipids or sardine oil and 1% cholesterol for 4 weeks. The control group was fed a standard diet without cholesterol. Results: In red blood cells, superoxide dismutase (SOD) activity was 1.4- and 1.3-fold higher in the milk lipids group compared to the sardine oil and control groups, respectively. In tissues, SOD activity was respectively 2.5- and 1.8-fold lower in heart and aorta, but 1.2- fold higher in liver of rats fed milk lipids compared to those fed sardine oil. In milk lipids group, liver glutathione reductase (GR) and catalase (CAT) activities were respectively 2.5- and 1.2- fold lower compared to sardine oil group. In contrast, liver and heart glutathione peroxidase (GSH-Px) activities were respectively 1.2- and 2.3-fold higher. In aorta, milk lipids decreased SOD, GR, GSH-Px, and CAT activities and the values were respectively 1.8-, 1.7-, 1.2- and 1.5-fold lower than those found in the sardine oil group. Brain GSH-Px and CAT activities were respectively increased by 1.2- and 1.9-fold in the milk lipids group compared with the sardine oil. Milk lipids improved lecithin:cholesterol acyltransferase (LCAT) activity (2.5-fold) when compared with sardine oil. However, serum paraoxonase (PON)1 activity was 2-fold lower in milk lipids group vs control whereas, compared with the sardine oil group, PON1 activity had a tendency to decrease, but not significantly. Conclusion: This study shows that milk lipids and sardine oil intake modulate differently enzymatic antioxidant defense in hypercholesterolemic rats. Milk lipids improve reverse cholesterol transport from peripheral tissues to the liver by enhancing LCAT activity, leading to anti-atherogenic effects.