No abstract

1. Blood antioxidants were measured in venous blood samples from 20 runners and six sedentary individuals. All subjects were male, between 20 and 40 years old, and in steady state with respect to body weight and physical activity patterns. Dietary analysis was undertaken using a 7-day weighed food intake. Correlations were sought between antioxidants in blood and (1) weekly training distance and (2) maximum oxygen uptake. In addition, 12 runners could be classified into two groups undertaking either low (range 16-43 km, n = 6) or high (80-147 km, n = 6) weekly training. 2. Body weight (range 55.3-90.0 kg) and percentage body fat (range 7-19%) both showed negative correlations with the weekly training distance (both P less than 0.001). Energy intake and maximum oxygen uptake were both correlated with the weekly training distance (both P less than 0.001). 3. Plasma creatine kinase activity, an indicator of muscle damage, was significantly correlated with the weekly training distance (P less than 0.01), whereas the plasma concentration of thiobarbituric acid-reactive substances, an indicator of free-radical-mediated lipid peroxidation, decreased with increased maximum oxygen uptake (P less than 0.01). 4. Erythrocyte alpha-tocopherol content was greater in the two running groups (P less than 0.05) compared with the sedentary group, and lymphocyte ascorbic acid concentration was significantly elevated in the high-training group (P less than 0.01) compared with the low-training group. 5. Erythrocyte activities of the antioxidant enzymes, glutathione peroxidase and catalase, were significantly and positively correlated with the weekly training distance (P less than 0.01 and P less than 0.05, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of increasing dietary intakes of polyunsaturated fatty acids (PUFAs) and vitamin E on indices of oxidative DNA damage was investigated. Twenty-one healthy male, nonsmokers aged 28.9 +/- 1.3 years participated in a free-living, split plot/change over trial in which half the volunteers consumed diets containing 5% PUFA as food energy for 4 wk and, after a 10 wk washout period, consumed a 15% PUFA diet for another 4 wk. The other volunteers followed an identical protocol, except that they consumed the 15% PUFA diet first. The diets were provided to volunteers either with or without an additional 80 mg dalpha-tocopherol acetate/day; otherwise total fat, carbohydrates, protein, and basal vitamin E contents remained unchanged. DNA damage induced by 200 microM H(2)O(2) in lymphocytes from volunteers as well as endogenous DNA damage in the form of oxidized pyrimidines, measured by alkaline single-cell gel electrophoresis (the comet assay), significantly decreased after consumption of the 5% PUFA diet (P<0.001 and P=0.01, respectively), but significantly increased after consumption of the 15% PUFA diet when alpha-tocopherol levels were in the range of 5-7 mg/day (P=0. 008 and P=0.03, respectively). These changes were abolished by an additional 80 mg dalpha-tocopherol/day. This study indicates that increasing dietary levels of PUFA to 15% may adversely affect some indices of DNA stability. However, increasing the dietary intake of vitamin E by 80 mg/day ameliorates the damaging effects of PUFA. -Jenkinson, A. McE., Collins, A. R., Duthie, S. J., Wahle, K. W. J., Duthie, G. G. The effect of increased intakes of polyunsaturated fatty acids and vitamin E on DNA damage in human lymphocytes.

Two experiments were carried out to investigate if the supplementation with vitamin E affects refined olive oil response to oxidation regarding the stability of the oil and the protection in vivo against lipid peroxidation in rats after its intake in comparison with other edible oils. In experiment 1, samples of virgin olive oil, refined olive oil, refined olive oil supplemented by us with 200 mg/kg vitamin E, and sunflower oil were collected before and after a 60 min frying process. After frying, refined olive oil supplemented with vitamin E compared with the non-supplemented refined olive oil had a higher concentration of alpha-tocopherol (240.34+/-6.07 mg/kg vs. 131.94+/-8.14 mg/kg), more resistance against oxidation (19.01+/-1.88% vs. 10.6+/-2.08%) and less polar components (4.2+/-0.06% vs. 5.45+/-0.22%). In experiment 2, 24 male Wistar rats, divided into 4 groups, were fed on diets based on the same unfried oils (8% w/w) as in experiment 1, for 4 weeks. Two days prior to the end of the experiment, the rats were intraperitoneally administered with adriamycin (10 mg/kg/ day) to provoke an oxidative stress. The rats fed on refined olive oil plus vitamin E compared to the rats fed on non-supplemented refined olive oil had lower hydroperoxides concentrations (26.8+/-2.6 nmol/mg vs. 35.6+/-2.49 nmol/mg) higher coenzyme Q levels (128.1+/-11.97 pmol/mg vs. 81.25+/-9.25 pmol/mg) and higher alpha-tocopherol values (1.23+/-0.04 mmol/mg vs. 0.93+/-0.06 mmol/mg) in microsomes of liver. In conclusion, the supplementation of refined olive oil with 200 mg/kg of vitamin E increases the stability of this oil under pro-oxidant conditions, and its intake decreases the oxidative damage generated by adriamycin in rats.

1. During all aerobic metabolism, free radicals generated by the partial reduction of oxygen are potentially injurious to cells. Highly efficient antioxidant defence systems exist to inhibit oxidative damage to cellular lipids and proteins. Specific enzymes have a crucial role in these antioxidant defences, and their activity may be induced by regulatory mechanisms that respond to oxygen metabolite concentration. 2. To assess whether smoking induces an additional adaptive response, we compared antioxidant defence systems in erythrocytes from smokers and non-smokers and assessed whether a high intake of vitamin E (280 mg/day), a major lipophilic free-radical-scavenging antioxidant, affects the activity of antioxidant enzymes. 3. A total of 100 men, 50 smokers and 50 non-smokers, were allocated to four treatment groups in a 2 x 2 factorial design (smokers versus non-smokers and placebo versus vitamin E). For 10 weeks each subject took one capsule per day of either 280 mg dl-alpha-tocopherol acetate or a visually identical placebo (hydrogenated coconut oil with negligible vitamin E content). 4. Despite increased erythrocyte cytosolic antioxidant enzyme activities in smokers compared with non-smokers, erythrocytes from smokers were more susceptible to hydrogen peroxide-induced lipid peroxidation in vitro. 5. Vitamin E supplementation further increased erythrocyte catalase (EC 1.11.1.6) activity in both smokers and non-smokers (P < 0.001) and erythrocyte glutathione peroxidase (EC 1.11.1.9) and glutathione reductase (EC 1.6.4.2) activities in non-smokers (P < 0.001). After supplementation with vitamin E there was a concomitant fall in erythrocyte superoxide dismutase (EC 1.15.1.1) activity (P < 0.001) and total glutathione concentration (P < 0.01). Furthermore, in both smokers and non-smokers there was a significant decrease in the susceptibility of erythrocytes to peroxidation (P < 0.001). 6. Various endogenous and exogenous factors exert control over cellular protection against reactive oxygen species, and our data suggest that one such factor is the supply of vitamin E.