24 A. Walczewska et al. plasma of rats fed lard and FO in the same quantity in the diet. The prominent PUFA component in cellular phospho- lipids is linoleic acid and its derivate arachidonic acid [40]. A high ingestion of sunflower oil causes an incorporation of linoleic acid into erythrocyte phosphatidylocholine in the highest amount [41]. Linoleic acid and arachidonic acid are well known activators of NADPH oxidase [42, 43], and may impair GSH/glutathione peroxidase and catalase-mediated catabolism of H2O2 in erythrocytes [14]. Moreover, Yuan and co-workers [44] reported fat type-dependent changes of antioxidant enzymes activity in RBC of Wistar Kyoto rats. Other tissues are also affected by a diet containing SO as a fat source. Ghosh et al. [45] demonstrated a very low level of GSH in the myocardium associated with myocardial necrosis in rats fed high-SO diet. All these findings suggest that a high ingestion of linoleic acid has profound pro- oxidative effects in different tissues and its incorporation into membrane phosphatidylocholine may be a good bio- marker of a short-term antioxidant dietary intervention [41]. Our results suggest that high-fat diet containing sunflower oil causes oxidative stress in erythrocytes. This is consistent with recent study showing enhancement of systemic lipid peroxidation in rabbits fed with high amount of sunflower oil [46]. In addition, high DNA adducts level as markers for DNA-damage derived from lipid peroxidation products were found in the liver of sunflower oil fed rats [47]. Taking these into consideration it is difficult to explain why sunflower oil rich diet increased plasma antioxidant capacity. Total anti- oxidant plasma capacity was measured by two comple- mentary methods, and evaluated various pools of anti- oxidants in plasma [48]. One of powerful plasma anti- oxidant, uric acid, did not reach the highest level in plasma of SO fed rats (data not shown). Perhaps, this diet could facilitate ingestion of some low molecular weight anti- oxidants e.g. vitamins, thus plasma antioxidant activity was raised. On the other hand, it cannot be excluded that elevated plasma antioxidant activity is an unspecific secondary effect to systemic oxidative stress phenomenon. However, the precise explanation of sunflower oil induced rise of plasma antioxidant ability requires further studies. In summary, peripheral blood phagocytes produced less ROS in rats fed high-lard and plasma of these animals had lower ability to decompose DPPH radicals than rats fed high-SO. The erythrocyte glutathione redox status was the highest in rats fed the diet containing lard, and the lowest in rats fed SO. These findings indicate that a diet high in linoleic acid-rich sunflower oil causes a greater phagocyte oxidative burst than ingestion the same energy from saturated fatty acids and marine origin n-3 PUFA, augments oxidative stress in erythrocytes, and can lead to tissue microinjury. However, total antioxidant plasma ability in rats fed sunflower oil was higher than in rats fed equal energy from other fats. Acknowledgment We thank M. Kopytek for biochemical determinations, A. Sarniak A. Kliszko, Z. Sedzinska for technical assistance, and J. Ciechowicz for statistical analysis. This work was supported by the State Committee for Scientific Research, Poland (grant No. 214/P05/2002/23). 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