Evidence shows that there is a rapid increase in the production of markers of oxidative damage immediately following acute stroke and that endogenous antioxidant defences are rapidly depleted, thus permitting further tissue damage. Several studies point to an antioxidant effect of B-group vitamins and a pro-oxidant effect of elevated plasma tHcy (total homocysteine). In the present study, we assessed whether supplementary B-group vitamins during this critical period will enhance antioxidant capacity and mitigate oxidative damage. Forty-eight patients with acute ischaemic stroke within 12 h of symptom onset were assigned to receive daily oral supplements of B-group vitamins comprising 5 mg of folate, 5 mg of vitamin B 2 , 50 mg of vitamin B 6 and 0.4 mg of vitamin B 12 ( n =24) or no supplements ( n =24) for 14 days. The treatment group and controls were matched for stroke subtype and age. Blood samples were obtained before intervention and also at 7 and 14 days post-recruitment for measurement of the following biomarkers: red cell folate (whole blood folate corrected with haematocrit), erythrocyte glutathione reductase activity coefficient (EGRAC; measure of vitamin B 2 status), plasma pyridoxal phosphate (vitamin B 6 status), plasma vitamin B 12 , plasma α-tocopherol, plasma ascorbic acid, plasma TAOC (total antioxidant capacity), plasma MDA (malondialdehyde), plasma tHcy and CRP (C-reactive protein). Supplementation for 14 days with B-group vitamins significantly increased the plasma concentrations of pyridoxal phosphate and red blood cell folate and improved a measure of B 2 status compared with the control group ( P <0.05). Plasma tHcy decreased in both groups albeit less in the control group, but differences in cumulative changes were not significant. There was, however, a decrease in plasma MDA concentration in the treatment group, in contrast with the increase seen in the control group and these differences were significant ( P =0.05). CRP concentration, a marker of tissue inflammation, was significantly lower in the treatment group compared with controls ( P <0.05). In conclusion, B-group vitamin supplementation immediately post-infarct may have antioxidant and anti-inflammatory effects in stroke disease independent of a homocysteine-lowering effect.

1. In healthy humans, a balance exists between oxygen-derived free-radical production and their removal by antioxidants. In preterm infants inadequate antioxidant defences may contribute to the pathogenesis of some of the complications of prematurity. 2. Plasma total antioxidant status and malondialdehyde concentration were measured during the first 11 days of life in 25 infants to determine whether increased lipid peroxidation is associated with low extracellular antioxidant status. In a second group of infants, total antioxidant status was quantified within 12 h of birth, and subsequently on days 4 and 10 to investigate the hypothesis that adverse neonatal outcome is associated with low antioxidant status. 3. There may be a weak negative correlation between the total antioxidant status of infants and the lipid peroxidation marker malondialdehyde in plasma ( r = −0.24, P = 0.056, n = 89) during the first 11 days of life. In the second group of infants, total antioxidant status was found to be significantly related to plasma urate and bilirubin levels, but not to adverse neonatal outcomes such as chronic lung disease, intraventricular haemorrhage, retinopathy of prematurity or death. 4. If adverse neonatal outcomes are due to inadequate antioxidant defences, these are likely to be intracellular or localized rather than general extracellular deficiencies.

1. The formation of thromboxane B 2 and malondialdehyde was studied in human platelet-rich plasma, in gel-filtered platelets and in bovine platelet microsomes. 2. Exogenous sodium arachidonate was converted into thromboxane B 2 and malondialdehyde in a concentration-dependent manner. Pre-incubation of platelets with aspirin inhibited the production of both thromboxane B 2 and malondialdehyde, although malondialdehyde could apparently be detected in the absence of thromboxane B 2 . 3. The aggregating agents, thrombin, collagen and the ionophore A23187 also caused production of thromboxane B 2 and malondialdehyde. ADP and adrenaline produced a smaller rise whilst the endoperoxide analogue U 46619 had only a slight influence on thromboxane and malondialdehyde, even though they all induced aggregation. 4. Pre-incubation of platelets with imidazole or 1- N -butylimidazole, which inhibit thromboxane synthetase, resulted in an inhibition of both thromboxane B 2 and malondialdehyde formation in response to collagen. 5. The results indicate that thromboxane B 2 and malondialdehyde are formed in parallel, in comparable quantities. However, under the conditions used in these studies, the apparent amounts of malondialdehyde exceed those of thromboxane B 2 , especially in the presence of exogenous arachidonate. Thus the thiobarbiturate reaction used to assay malondialdehyde may detect other products of lipid peroxidation. 6. Platelet thromboxane B 2 concentrations did not always relate to the extent of aggregation. In particular, platelet aggregation could occur in the absence of detectable thromboxane B 2 production.