These results suggest that HDF with highly permeable membranes is associated with a significant loss of vit C. Diffusive transport is responsible for two-thirds whereas convective phenomenon accounts for only one-third of this loss.

To give the levels of antioxidant nutrients in relation to age-related macular degeneration (AMD). Methods: Pathologies Oculaires Liées à l'Age is a population-based study on cataract and AMD and their risk factors, carried out on 2584 inhabitants of Sète, France. Age-related macular degeneration was defined by findings from fundus photographs according to an international classification. Biological measurements were taken from fasting blood samples. Results: After multivariate adjustment, plasma ␣-tocopherol levels showed a weak negative association with late AMD (P = .07). Lipid-standardized plasma ␣-tocopherol levels showed a significant negative association with EPIDEMIOLOGY AND BIOSTATISTICS

Abstract-The influence of the HMG-CoA reductase inhibitor simvastatin was assessed on the cardiovascular alterations and production of free radicals associated with chronic angiotensin II (Ang II) infusion. Simvastatin (60 mg/kg per day PO) or placebo were given concomitantly for 10 days in Sprague-Dawley rats infused with Ang II (200 ng/kg per minute SC, osmotic pump). In addition, simvastatin or placebo was also given in vehicle-infused rats. Tail-cuff pressure and albuminuria were measured before and at the end of the treatment period. Cardiac weight, carotid structure, production of reactive oxygen species (ROS, by chemiluminescence) by polymorphonuclear leukocytes and aortic wall as well as protein and lipid oxidation products were determined at the end of the study. Ang II increased tail-cuff pressure by 56Ϯ12 mm Hg and simvastatin blunted the development of hypertension by Ϸ70% (19Ϯ5 mm Hg). Increases in heart weight index and carotid cross-sectional area induced by Ang II were obliterated by simvastatin (3.18Ϯ0.09 versus 3.46Ϯ0.11 mg/g body wt and 0.125Ϯ0.010 versus 0.177Ϯ0.010 mm 2 , respectively). The Ang II-induced increases in leukocyte and aortic production of ROS as well as protein and lipid oxidation products were prevented by simvastatin. No effect of simvastatin was detected in non-Ang II-infused rats. These results indicate that simvastatin prevented the development of hypertension and cardiovascular hypertrophy together with inhibition of the induced angiotensin II production of ROS. Therefore, inhibition of HMG CoA reductase by statins may have a beneficial effect on cardiovascular alterations through its antioxidant action in experimental Ang II-dependent hypertension. A ngiotensin II (Ang II) exerts multiple effects on the cardiovascular system including hypertension and cardiovascular hypertrophy, and free radical production has been proposed as a mechanism participating in Ang II-induced cardiovascular alterations. 1 Through stimulation of its type 1 receptor, Ang II was shown to be associated with an overexpression of cytosolic proteins involved in the activation of the NAD(P)H oxidase of vascular endothelial cells, smooth muscle cells, and leukocytes. 2,3 In these cells, Ang II favors the production of reactive oxygen species (ROS) such as superoxide anions, hydrogen peroxide, and hydroxyl radicals. 2 Together with leukocyte adhesion and proliferation and migration of various cell types, these events may lead to phenotype transformation of the arterial wall and vascular hypertrophy.Experimental evidence and clinical studies strongly suggest that 3-hydroxy-3-methylglutaryl-CoA (HMG CoA) reductase inhibitors (statins) might have antiatherosclerotic effects independent of low-density lipoprotein (LDL) cholesterol reduction. Among the pleiotropic effects of statins are inhibition of smooth muscle cell proliferation (except for pravastatin), 4 reduction of matrix metalloproteinase expression, 5 and stimulation of the antithrombotic system. 6,7 In addition, it has been shown that an inhibitor...

Oxidative stress can produce profound alterations to cellular membrane lipids, impairing cell metabolism and viability. This phenomenon, previously observed in haemodialysis patients, has been proposed as a significant factor in regard to haemodialysis-related shortened red blood cells (RBC) survival. In the present study, several parameters associated with oxidative stress were evaluated in a group of haemodialysis patients either receiving erythropoietin therapy (n = 12, mean erythropoietin dose 88 +/- 24 U/kg/week) or not receiving such therapy (n = 30), and in 38 controls. Malonyldialdehyde (MDA, nmol/ml), an end-product of lipid peroxidation, and RBC antioxidant systems were measured, including RBC alpha-tocopherol (RBC vitamin E, mg/l), RBC glutathione (GSH, nmol/mgHb), and RBC superoxide dismutase activity (SOD, U/mgHb). Plasma vitamin E concentrations were also evaluated. Finally, oral vitamin E supplementation (500 mg daily), an exogenous antioxidant, was administered for 6 months to seven patients from the dialysis group receiving erythropoietin while oxidative parameters were repeatedly evaluated and erythropoietin requirements monitored, in order to appreciate the therapeutic relevance of an antioxidant supplementation. An elevation of serum MDA was observed in all haemodialysis patients and a significant decrease in RBC vitamin E, despite normal serum vitamin E levels. Furthermore, the reduction in RBC vitamin E was more important in patients treated with erythropoietin. Vitamin E supplementation resulted in a significant increase in RBC vitamin E (from 0.3 +/- 0.1 to 1.2 +/- 0.2 mg/l of pellet) and a reduction in erythropoietin dose (from 93 +/- 24 to 74 +/- 26 U/kg/week) while maintaining stable haemoglobin concentrations. These results suggest that the oxidative stress could be one of the resistance factors to erythropoietin response in haemodialysis and that vitamin E supplementation could have a sparing effect on erythropoietin dosage requirement.