No abstract

Oxidative stress and generation of reactive oxygen species are believed to be implicated in Parkinson’s disease (PD). Erythrocyte activity of superoxide dismutase (SOD) and catalase, the blood glutathione system, and plasma levels of thiobarbituric-acid-reactive substances (TBARS) were measured in 80 PD patients. These biochemical parameters were also measured in 29 age-matched controls. Patients with PD had significantly higher red blood corpuscle (RBC) activity of SOD. The mean RBC activity of catalase in PD patients did not differ significantly from those of controls. RBC catalase activity was significantly lower in advanced cases of PD compared to early cases. Oxidized glutathione was significantly higher in RBCs of PD patients, although there were no changes in total glutathione and reduced glutathione compared to controls. TBARS content was increased in patients with PD. Levodopa therapy, age and duration of illness did not significantly influence the measured parameters. Our study supports the previous hypothesis that oxidative stress is implicated in the pathogenesis of PD. Perspectives for treatment of PD in the future could include antioxidant therapy.

Nickel ingestion can cause exacerbation of dermatitis in patients who are already nickel-sensitive; Chromium (Cr VI) is the 2nd allergen, after nickel. However, stainless steel is widely used in home cookware. In this study, we determined nickel and chromium levels by atomic absorption spectrometry in 11 habitual menus cooked in different grades of stainless steel utensils. We noted a great difference in nickel and chromium intake depending on the menu, and a significant difference between the glass and stainless steel saucepans, but this was very low compared with the levels of nickel and chromium contained in the menus; mean intakes of these elements were under the tolerable daily intake (TDI) recommended by the World Health Organization. Hence, there is no advantage for nickel-sensitive patients in switching to materials other than stainless steel, provided that this is of good quality.

The protective role of selenium (Se), given as a Se-rich yeast, selenomethionine or selenomethionine + vitamin E supplement, toward changes in lipid, peroxide, and fatty acid distribution in tissues of streptozotocin-induced diabetic rats, was investigated, after 24 wk of disease. Diabetes increased liver thiobarbituric acid-reactive substances and conjugated dienes; Se supplement completely corrected these changes. In kidney, as in heart, the peroxide levels were not significantly changed by diabetes. In diabetic rat liver, a significant drop in triglycerides and phospholipids (P < 0.05) was observed; this was modulated by Se + vitamin E supplementation. Se + vitamin E supplementation also inhibited the decrease in 18:2n-6 and the increase in 22:6n-3 observed in liver of diabetic rats, changes which reflect altered glycemic control. In kidney, heart, and aorta, diabetes produced some changes in lipid content and fatty acid distribution, especially an increase in heart triglycerides which was also corrected by the Se supplement. Se supplementation to diabetic rats also increased 18:0 ether-linked alcohol, 20:4 n-6, and 22:5 n-3 in cardiac lipids. In aorta, Se + vitamin E significantly increased 20:5 n-3. These polyunsaturated fatty acids are precursors, in situ, of prostaglandin I2 (PGI2) and PGI3 which may protect against cardiovascular dysfunction. In kidney, conversely, Se decreased 20:4 n-6, the precursor of thromboxane A2 implicated in diabetic glomerular injury. Thus Se, and more efficiently Se + Vitamin E supplementation, in experimental diabetes could play a role in controlling oxidative status and altered lipid metabolism in liver, thereby maintaining favorable fatty acid distribution in the major tissues affected by diabetic complications.

Seventy rats were separated into five groups: one group of 12 was used as a control and received a purified diet, and four groups of streptozotocin-induced diabetic rats, totalling 58, were fed the same diet without or with selenium (Se) supplementation. Of the noncontrol rats, 14 were without supplementation (Group D), 14 were fed a Se-rich yeast diet (i.e., selenion) (Group DSel), 14 received selenomethionine (Group DSm), and 16 received selenomethionine + tocopherol acetate (Group DSmE). Supplementation with Se in all groups was 0.99 micromole/100g of diet and with tocopherol acetate was 0.145 micromole/100 g. All diabetic rats were mildly balanced by insulin. After 24 weeks of diet, plasma glucose tended to decrease in diabetic Se-supplemented groups DSmE > DSm > DSel versus Group D. In DSm and DSmE groups, plasma lipid peroxides also decreased compared with Group D, but this decrease reached significance only for DSmE (P < 0.01 for both TBARS and conjugated dienes). Plasma triglycerides also decreased in DSm and DSmE groups versus Group D (P < 0.01; P < 0.05, respectively). At the same time, Se increased significantly in kidneys of Groups DSel and DSm versus D and more weakly in Group DSmE, but in this case was associated with a large increase of vitamin E. These beneficial effects of selenium supplement and more so of selenium combined with vitamin E were associated with a protection of kidneys in diabetic rats which found expression in a significant correction of renal hyperfiltration (P < 0.05) and in a diminution of the number and severity of glomerular lesions (P < 0.0005).