Protective Role of Glutathione and Nitric Oxide Production in the Pathogenesis of Pterygium.

OBJECTIVE: In the pathogenesis of pterygium, the protective role of glutathione and nitric oxide production is unclear. These are important factors for homeostasis in the redox state of cells. The aim of this study was to determine the levels of these and related parameters in pterygium tissue. Patients and Methods. The study sample consisted of 120 patients diagnosed with primary or recurrent pterygium. Five groups of tissue samples were examined: control, primary pterygium, recurrent pterygium, and two groups of primary pterygium given a one-month NAC presurgery treatment (topical or systemic). The levels of endothelial nitric oxide synthase (eNOS), nitric oxide (NO), 3-nitrotyrosine (3NT), reduced and oxidized glutathione (GSH and GSSG), and catalase (CAT) were evaluated in tissue homogenates. RESULTS: Compared with the control, decreased levels of eNOS, NO, and 3-nitrotyrosine as well as the degree of oxidation of GSH (GSSG%) were observed in primary and recurrent pterygium. 3-Nitrotyrosine and GSSG% were reduced in the other pterygium groups. GSH and CAT were enhanced in recurrent pterygium and systemic-treated primary pterygium but were unchanged for topical-treated primary pterygium. There was a strong positive correlation of eNOS with NO and 3NT, GSSG% with NO and 3NT, and GSH with GSSG and CAT. Women showed a higher level of GSH and catalase in primary pterygium, whereas a lower level of GSH and a higher level of NO in recurrent pterygium. CONCLUSION: The results are congruent with the following proposed sequence of events leading to a protective response of the organism during the pathogenesis of primary pterygium: a decreased level of eNOS provokes a decline in the level of NO in pterygium tissue, which then leads to reduced S-nitrosylation of GSH or other thiols and possibly to the modulation of the intracellular level of GSH through synthesis and/or mobilization from other tissues.

Increased antioxidant capacity in healthy volunteers taking a mixture of oral antioxidants versus vitamin C or E supplementation.

The objectives of this study were (1) to evaluate the capacity of human plasma that had been obtained from healthy adult volunteers before and after they ingested vitamin E or C to inhibit induced lipoperoxidation in vitro (antioxidant capacity of plasma [ACP]), and (2) to compare the efficiency of these vitamins with that of a commercial mixture of antioxidant vitamins, cofactors, and minerals (MAOx). Seventy-nine healthy individuals between 19 and 23 y of age were randomly assigned to 1 of 4 groups. Each received a daily dose of antioxidants for 7 d: vitamin C (n=18; 500 mg), vitamin E (n=21; 400 IU), vitamins C and E (n=19), or MAOx (n=21; 1.2 g). ACP and plasma malondialdehyde were measured at 4 and 24 h and 7 d. ACP increased significantly (P<.05) in all 4 groups within 4 h of antioxidant intake, and this effect was sustained throughout supplementation. Plasma ACP increased significantly over basal values in the group taking MAOx; relative increases were 42%, 44%, and 55% at 4 h, 24 h, and 7 d, respectively (P<.001). Smaller increases in plasma ACP were observed in the vitamin C group (25%, 32%, and 36%) and, specifically, in the vitamin E group (17%, 24%, and 28%) (P<.05). The mixture of vitamins and minerals was comparatively more efficient than vitamin C or E alone, presumably because MAOx contains various antioxidant compounds with different redox potentials, leading to the possible development of chain reactions.

Caloric restriction modifies both innate and adaptive immunity in the mouse small intestine.

Although caloric restriction (CR) apparently has beneficial effects on the immune system, its effects on the immunological function of the intestinal mucosa are little known. The present study explored the effect of CR on the innate and adaptive intestinal immunity of mice. Balb/c mice were either fed ad libitum (control) or on alternate days fed ad libitum and fasted (caloric restriction). After 4 months, an evaluation was made of IgA levels in the ileum, the gene expression for IgA and its receptor (pIgR), as well as the expression of two antimicrobial enzymes (lysozyme and phospholipase A2) and several cytokines of the intestinal mucosa. CR increased the gene expression of lysozyme and phospholipase A2. The levels of IgA were diminished in the ileum, which apparently was a consequence of the reduced transport of IgA by pIgR. In ileum, CR increased the gene expression for most cytokines, both pro- and anti-inflammatory. Hence, CR differentially modified the expression of innate and adaptive immunity mediators in the intestine.