Objective To investigate the effect of vitamin E on the lag time of serum low-density lipoprotein (LDL) oxidation in vitro in patients with acute cerebral infarction (ACI). Methods Twenty-two patients with ACI received vitamin E treatment at the dose of 300 mg/day, and another 22 ACI patients matched for age, gender ratio, blood pressure, blood lipid level, location and degree of the infarction served as the control group in which no vitamin E was given. Serum samples were collected from the patients within 24 h and at 2 weeks after the onset to test the lag time of LDL oxidation in vitro and measure the levels of vitamin E, total cholesterol, triglyceride and free cholesterol. Results At two weeks after the onset of the infarction, the patients receiving vitamin E treatment had significantly prolonged lag time of LDL oxidation in comparison with that of the control patients (71.84± 9.75 vs 60.95±9.33 min, P<0.05), and showed also significantly higher vitamin E level in the serum Vitamin E and stroke index. The two groups of patients showed no significant differences in total cholesterol (5.08cholesterol (1.62oxidation in vitro is prolonged in ACI patients with vitamin E treatment, suggesting that vitamin E can increase the resistance of the patients against anti-oxidative stress.

Objective To measure the changes in urinary 8-iso-prostaglandin-F2α (8-iso-PGF2α) and oxidized low-density lipoprotein (ox-LDL) lag time in patients with Parkinson's disease (PD). Methods A case-control study was performed involving 31 male patients with PD (mean age of 59.7 years) diagnosed according to the Calne criteria and 31 age-matched healthy male subjects with comparable status of smoking and life style. For each subject, urinary 8-iso-PGF2α was measured quantitatively using enzyme-linked immunosorbent assay, and LDL oxidizability was measured by determining LDL oxidation lag time in conjugated diene product at 234 nm using Cu-stimulated oxidation. Results Compared to the levels in the control subjects, the PD patients showed significantly increased urinary 8-iso-PGF2α (81.1±1.6 vs 46.9±1.1 ng/mmol creatinine, P<0.05) and significantly reduced LDL oxidation lag time (63.5±6.0 vs 84.4±8.8 min, P<0.05). Conclusion Increased 8-iso-PGF2α and decreased anti-oxidant ability are implicated in the pathogenesis of PD, suggesting the value of appropriate antioxidant therapy in controlling the progression of PD.