Background: The current study was undertaken to assess the effects of oxidized sunflower oil ingestion (obtained by heating at 98°C with air insufflation during 48 h and incorporated at 5% in a fat-free diet) on liver and brain fatty acid composition, and some serum parameters and protective enzymes against peroxidation (glutathione peroxidase, glutathione reductase, catalase and glucose-6-phosphate dehydrogenase). Results: The main results show that the oxidized oil contains 262 mmol/kg of hydroperoxides, 5.7% of the esters are oxidized and 50.4% are polymerized. In the liver, we noticed that oxidized oil exercises a toxic effect as confirmed by the increase in the thiobarbituric acid reactive substance (TBARS) concentration. In the same way, we noticed that vitamin E exercises a favorable effect in the preservation against free radicals and lipid peroxidation; however, it cannot ensure this protection alone. In the liver, only glutathione peroxidase and glutathione reductase activities were positively correlated with the TBARS concentration. In the treated groups, we also noted changes in the fatty acid profiles of liver and brain homogenates, essentially by the appearance of trans fatty acid (18:1 trans) and an increase in arachidonic acid content.
This study highlighted the pro-oxidative functions of α-tocopherol (αT) on the heart antioxidant system and tissue histopathology of oxidized sunflower oil (OSO)-exposed rats.Four groups of male Wistar rats were fed with different diets: 1) control diet containing FSO (fresh sunflower oil); 2) diet containing 5 % OSO; 3) diet containing 5 % OSO, supplemented with 600 mg αT kg-1; and 4) diet containing 5 % OSO, supplemented with 1200 mg αT kg-1. The hearts were then isolated, and the antioxidant enzymatic activities were assessed. Body weight and catalase (CAT), glutathione peroxidase (GPx) activities significantly decreased in groups fed with OSO, while the lipid peroxidation (LPO) level significantly increased. Administration of OSO with αT (600 mg · kg-1) returned the body weight values and LPO levels to similar values as the control group. The CAT and GPx activities increased but remained significantly lower compared to the control group. In the OSO group with αT (1200 mg · kg-1), the CAT and GPx activities also decreased, while LPO significantly increased. Heart tissue sections obtained from the groups revealed the presence of large areas of necrosis. This study suggested that OSO induced oxidative stress and that administration of a moderate dose of αT restored the antioxidant balance, but that high levels of αT supplementation result in a pro-oxidant effect.
Abstract. The aim of this study is to evaluate the effect of α-tocopherol supplementation at two doses (600 and 1200 mg × kg–1) on kidney antioxidant status and the histopathological changes in Wistar rats after 12 weeks of exposure at different diets. Forty rats has been divided into 4 groups of 10 rats each, the control group received basal diet with 5 % fresh sunflower oil (FSO), the second group: 5 % oxidized sunflower oil (OSO), the third group: 5 % OSO supplemented with 600 mg × kg–1 α-tocopherol and the fourth group: 5 % OSO supplemented with 1200 mg × kg–1 α-tocopherol. In OSO groups, the results showed highly significant increases of LPO (from 31.3 ± 0.9 to 53.8 ± 1.2 nmol of MDA formed/min/mg protein, p < 0.0001) with a significant decrease (p < = 0.001) of the antioxidant enzymatic activities (CAT, SOD, GPX, GR and G6PDH), body weight (339 ± 9 to 290 ± 3 g) and α-tocopherol levels (13.6 ± 0.6 to 6.5 ± 0.4 μg/mg protein). In OSO groups with 600 mg × kg–1 α-tocopherol, an antioxidant effect was found, reflected by a return of the parameters to values similar to those of the control group. However, higher doses of α-tocopherol (1200 mg × kg–1) induced a depletion of antioxidant status, α-tocopherol levels (6.0 ± 0.3 μg/mg protein, p < 0.001) and a very highly significant rise (p < 0.0001) of LPO content (54.86 ± 0.01 nmol of MDA formed/min/mg protein). The kidney tissues also showed changes in glomerular, severe inflammatory cells infiltration, and formation of novel vessels. So, we can conclude that the oxidative stress is attenuated by a moderate administration of 600 mg × kg–1 α-tocopherol, while a pro-oxidant effect occurs at 1200 mg × kg–1 α-tocopherol.
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