Ovine reproduction efficiency in herds at high altitude (ha) is lower than that at low altitude (la). In ewes, ha effects are due to hypoxia and oxidative stress. Our aim was to establish the effect of antioxidant vitamin supplementation on semen traits and antioxidant status of rams exposed to short or long time ha. A total of 32 rams native to la (~500 m) were used, 16 were kept at la and the other 16 were brought to ha (~3600 m), where they were placed in the same flock as the ha native rams (n=16). Half of the animals in each group were supplemented daily with vitamins C 600 mg and E 450 IU per os, during the entire experimental period, starting the 4th day after animal’s arrival at ha (day 0). At days 0, 30 and 60 of treatment, blood and semen samples were collected for evaluation of antioxidant status and semen standard characteristics. Data were compared within each experimental time by analysis of variance using a general linear model. Elevated concentrations of oxidative stress biomarkers were present in blood from animals maintained at ha. Ejaculates from ha exposed rams showed decreased sperm concentration, progressive motility and viability, in addition to decreased antioxidant status in seminal fluid. A total of 30 days of oral supplementation with vitamins C and E prevented some ha negative effects on semen characteristics, mainly in recently ha exposed rams. It is concluded that exposure of rams to ha negatively affects semen quality, where oxidative stress plays a predominant role. These effects are mainly prevented by oral supplementation of vitamins C and E, which constitutes a simple and cheap alternative to improve semen quality of rams when they are moved to ha.

Smoking during pregnancy has been shown to be detrimental for the developing fetus. The effects of active and passive maternal smoking on umbilical cord serum levels of vitamin A and vitamin E were examined. Secondary measures included anthropometric parameters in the newborn. Maternal and umbilical cord serum levels of vitamins A and E were measured at delivery. The mothers were assigned to three groups: non-smoking (n 12); passive smoking (n 13); active smoking (n 18). Based on multivariate linear regressions, active smoking during pregnancy was associated with increased umbilical cord serum levels of vitamin A and vitamin E. While enhanced circulating levels of vitamin A in cord blood were also found in non-smoking mothers exposed to tobacco smoke during pregnancy, those of vitamin E were not influenced. Further, an inverse association between smoking behaviour during pregnancy and birth length was observed, with shortest length in active smokers followed by passive smoking mothers. Active and passive maternal smoking behaviour during pregnancy increases the fetal demand for antioxidant compounds in order to counteract the oxidative burden by cigarette smoke. Against this background, the observed increase in umbilical cord serum levels of vitamins A and E may subserve antioxidative processes in response to tobacco smoke-induced oxidative stress. This would reduce the availability of vitamins A and E for fetal maturation, which is critical inasmuch as both compounds are indispensable for the developing fetus. However, due to the cross-sectional nature of our observation, this line of reasoning definitely requires validation in cause–effect experiments in the future.

The involvement of free radicals and reactive oxygen and nitrogen species in the pathology of inflammatory and degenerative disease has been widely accepted, although the centrality of these species to the outcome of these diseases is still a matter for debate. In the case of CVD, and particularly the development of the atherosclerotic plaque, the oxidation of LDL is of particular importance and appears to explain many of the events that occur during the life history of the plaque. The corollary of this situation is that antioxidants must be a benign force to protect the population from the modern scourge of heart disease. In fact, recent evidence from intervention studies with large doses of the antioxidant vitamins and other antioxidants in foods has been very disappointing. Here, the background for the belief that antioxidants ought to be beneficial is examined and an attempt made to explain why the results of these intervention studies have been unsuccessful. It is agreed that a diet rich in fruit and vegetables is protective for both CVD and cancer, but the explanation for this effect may not necessarily lie with the presence of antioxidants.

The lungs are continually exposed to relatively-high O2 tensions, and as such, in comparison with other organs, they represent a unique tissue for the damaging effects of oxidant attack. At particular times during a lifetime this every day challenge may increase exponentially. The first oxidative insult occurs at birth, when cells are exposed to a sudden 5-fold increase in O2 concentration. Thereafter, the human lung, from infancy through to old age, can be subjected to deleterious oxidative events as a consequence of inhaling environmental pollutants or irritants, succumbing to several pulmonary diseases (including infant and adult respiratory distress syndromes, asthma, chronic obstructive pulmonary disease, cystic fibrosis and cancer) and receiving treatment for these diseases. The present paper will review the concept that consumption of a healthy diet and the consequent ability to establish and then maintain adequate micronutrient antioxidant concentrations in the lung throughout life, and following various oxidative insults, could prevent or reduce the incidence of oxidant-mediated respiratory diseases. Furthermore, the rationale, practicalities and complexities of boosting the antioxidant pool of the respiratory-tract lining fluid in diseases in which oxidative stress is actively involved, by direct application to the lung v. dietary modification, in order to achieve a therapeutic effect will be discussed.

We conducted a cross-sectional study in 118 well-trained athletes to investigate 'high exposure' to sub-deficient antioxidant status, and consequently to oxidative damage, in relation to estimated daily energy expenditure (EE) and dietary antioxidant intake. Subjects completed 7 d food and activity records. Blood samples were obtained on day 8. Of the athletes 81, 60 and 43 % had intakes of vitamins E, C and β-carotene below two-thirds of the French RDA respectively, which is adjusted for EE (FRDAa). The deficit in vitamin E intake was positively correlated with EE (r 0·51, P>0·0001). All the athletes had normal plasma vitamins E and C and 14 % had marginal plasma β-carotene. Plasma thiobarbituric acid-reactive substances (TBARS) did not increase with increased EE. As evidenced by ANOVA, EE-induced vitamin C intakes increased and consequently led to increased plasma ascorbic acid concentrations. In male athletes, plasma total carotenoids were negatively correlated with plasma TBARS concentrations (r –0·31, P>0·006). The relationship between vitamin C intakes and plasma concentrations was logarithmic (r 0·59, P> 0·0001). To summarize, it is not clear whether vitamin E requirements are overestimated with reference to EE in the FRDAa. Daily requirements for vitamin C do not exceed 200 mg. Our present results could be interpreted as meaning that carotenoids play a protective role as exogenous antioxidants. Carotenoid intakes in athletes must be considered carefully.

The effects of 12 weeks of antioxidant supplementation on exercise-induced oxidative stress were investigated in older adults (60 (SE 1) YEARS; BMI 26 (se 1) kg/m2). Subjects were randomly divided in two groups: supplementation (n 11) with 100 mg dl-α-tocopheryl acetate, 200 mg ascorbic acid, and 2 mg β-carotene, and placebo (n 9). Before and after the 12 week supplementation period, subjects cycled for 45 min at submaximal intensity (50 % maximal workload capacity). Antipyrine was used as marker for oxidative stress. Antipyrine reacts quickly with hydroxyl radicals to form para- and ortho-hydroxyantipyrine. The latter metabolite is not formed in man through the mono-oxygenase pathway of cytochrome P450. Daily supplementation significantly increased plasma concentrations of α-tocopherol and β-carotene in the supplemented group (Δ 14·4 (se 3·2) and 0·4 (se 0·1) μmol/l; P<0·001 and P<0·01). No significant differences, within and between groups, were observed in the exercise-induced increase in the ratios para- and ortho-hydroxyantipyrine to antipyrine. In addition, supplementation did not affect the exercise-induced increase in thiobarbituric acid reactive substances in plasma. In conclusion, in 60-year-old subjects antioxidant supplementation had no effect on the exercise-induced increase in oxidative stress as measured by free radical products of antipyrine.

Information on current-, never- and ex-smokers (including duration of cessation) was obtained in a cross-sectional survey of risk factors for coronary heart disease (CHD), the Scottish Heart Health Study. Diet was also assessed by food frequency questionnaire in a total of 4265 men and 4770 women. Nutrient intakes were computed by sex and smoking group and, according to their diet, the ex-smokers were categorized as current- or never-smokers using discriminant analysis techniques.

The current- and five ex-smoking groups differed negligibly in past smoking characteristics. Energy-adjusted intake of polyunsaturated fat, fibre and the antioxidant vitamins were lowest in current-smokers, and for men, intakes increased progressively with duration of ex-smoking to reach the level of never-smokers. In a similar manner, energy, sugar and alcohol decreased with duration of ex-smoking. Fewer trends were observable for women, and the diets of ex-smokers more immediately resembled that of never-smokers.

Discriminant analysis for the combined nutrients correctly categorized 72 and 69 % of male, and 66 and 65 % of female current- and never-smokers respectively. By 4 years of smoking cessation the general dietary pattern of ex-smokers was similar to never-smokers for both sexes. Whether this represents a change in diet over time or a cohort effect is unclear, but the results do suggest that the apparent healthier diet of ex-smokers may contribute to their reduction in CHD risk compared with life-long current-smokers.