Prevention of neutrophil protein oxidation with vitamins C and E diet supplementation without affecting the adaptive response to exercise.

The authors studied the effects of antioxidant diet supplementation with an almond-based beverage on neutrophil antioxidants, nitrite, and protein oxidative alterations after exercise. Fourteen trained male amateur runners were randomly assigned in a double-blind fashion to receive antioxidant supplementation (152 mg/d vitamin C and 50 mg/d vitamin E) or placebo using an almond-based beverage for 1 mo and participated in a half-marathon race. Blood samples were taken before and after the half-marathon and after 3 hr recovery. Supplementation significantly increased basal neutrophil vitamin C compared with placebo (p < .05). Exercise increased neutrophil vitamin E levels in the supplemented group and decreased vitamin C in both groups after recovery (p < .05). Neutrophil catalase and glutathione peroxidase gene expression and nitrite levels were significantly increased as result of exercise (p < .05). Nitrotyrosine and protein carbonyl derivates increased only in the placebo group after exercise (p < .05), and these values remained high at recovery. No significant differences were evidenced in caspase-3 activity and DNA damage. Antioxidant supplementation with vitamins C and E reduced the exercise-induced oxidation of proteins in neutrophils, without altering the antioxidant adaptive response, as evidenced by the increased catalase and glutathione peroxidase gene expression.

The double edge of reactive oxygen species as damaging and signaling molecules in HL60 cell culture.

AIMS: Our aim was to establish the conditions in which reactive oxygen species produce pathological or hormetic effects on HL60 cells. METHODS: HL60 cells were treated with either single bouts (1, 10 and 100 microM) or a sustained production (0.1, 1.0 and 10.0 nM/s) of H(2)O(2). RESULTS: Exposure to 10 and 100 microM H(2)O(2) activated catalase, glutathione peroxidase and glutathione reductase through post-transcriptional mechanisms and induced oxidative modification of proteins. When cells where exposed to sustained H(2)O(2) production, a clear dose-response effect was detected in the activity of the antioxidant enzymes catalase, glutathione peroxidase and Mn-SOD, with higher concentrations of H(2)O(2) inducing greater enzyme activities. Catalase, HO-1, UCP-3, iNOS and PGC-1alpha expressions were activated after sustained exposure to 1 and 10 nM H(2)O(2)/s. Although the antioxidant defenses were activated, oxidative damage appeared in DNA and proteins in cells treated with 1 and 10 nM/s. CONCLUSIONS: HL60 cells respond to exposure to sustained levels of H(2)O(2) in a dose-response manner to H(2)O(2) concentration by activating the expression and activity of the antioxidant machinery, although the activation of the antioxidant defenses is not enough to avoid the appearance of oxidative damage. Of the two designs proposed, continuous exposure seems to be more appropriate to study the antioxidant response of HL60 cells to H(2)O(2).

Radiofrequency catheter ablation of a right free-wall accessory pathway in dextrocardia with complete situs inversus.

An uncommon case of orthodromic atrioventricular reentrant tachycardia in a patient with dextrocardia and complete situs inversus is reported. There was no associated cardiac abnormality apart from the mirror image dextrocardia. An electrophysiological study and successful catheter ablation of a right free-wall concealed accessory pathway was performed. A simplified three-catheter technique from a femoral approach and monoplane fluoroscopy were used in a noncomplicated procedure of normal duration.