Salivary antioxidants in patients with type 1 or 2 diabetes and inflammatory periodontal disease: a case-control study.

BACKGROUND: The purpose of this study was to evaluate and compare salivary concentrations of reduced, oxidized glutathione, uric acid, ascorbic acid, and total antioxidant capacity in subjects with diabetes and systemically healthy subjects with inflammatory periodontal disease. METHODS: Sixteen patients with type 1 diabetes mellitus (DM), 25 patients with type 2 DM, and 24 systemically healthy patients, all with inflammatory periodontal disease, were recruited. Whole-saliva samples were obtained, and full-mouth clinical periodontal measurements, including plaque index, probing depth, gingival recession, clinical attachment level, and bleeding on probing, were recorded at six sites per tooth. Saliva flow rate and salivary levels of reduced and oxidized glutathione, vitamin C, uric acid, and total antioxidant capacity were determined. Data were analyzed statistically by non-parametric tests. RESULTS: The subjects with type 2 DM had fewer teeth and more sites with probing depths >4 mm than the patients with type 1 DM (both P <0.01). The mean salivary reduced-glutathione concentration was lower in patients with type 1 DM than in the other two groups (both P <0.05). No significant differences in the salivary concentrations of the other antioxidants measured were found among the groups (P >0.05). Oxidized glutathione levels in the patients with type 1 DM were significantly lower than in the systemically healthy group (P = 0.007). In both groups with diabetes, salivary reduced-glutathione levels correlated positively with probing depth, and total antioxidant capacity correlated with salivary flow rate (P <0.01). CONCLUSION: The decrease in salivary reduced-glutathione levels in patients with type 1 DM may have a role in periodontal tissue destruction by predisposing tissues to oxidative stress.

The GCR1, GPA1, PRN1, NF-Y signal chain mediates both blue light and abscisic acid responses in Arabidopsis.

Different classes of biotic (e.g. plant hormones) and abiotic (e.g. different wavelengths of light) signals act through specific signal transduction mechanisms to coordinate higher plant development. While a great deal of progress has been made, full signal transduction chains have not yet been described for most blue light- or abscisic acid-mediated events. Based on data derived from T-DNA insertion mutants and yeast (Saccharomyces cerevisiae) two-hybrid and coprecipitation assays, we report a signal transduction chain shared by blue light and abscisic acid leading to light-harvesting chlorophyll a/b-binding protein expression in etiolated Arabidopsis (Arabidopsis thaliana) seedlings. The chain consists of GCR1 (the sole Arabidopsis protein coding for a potential G-protein-coupled receptor), GPA1 (the sole Arabidopsis Galpha-subunit), Pirin1 (PRN1; one of four members of an iron-containing subgroup of the cupin superfamily), and a nuclear factor Y heterotrimer comprised of A5, B9, and possibly C9. We also demonstrate that this mechanism is present in imbibed seeds wherein it affects germination rate.

Effects of smoking and gingival inflammation on salivary antioxidant capacity.

AIM: This study evaluated possible effects of smoking and gingival inflammation on salivary antioxidants in gingivitis patients. METHODS: Twenty otherwise healthy gingivitis patients (10 self-reported smokers) and 20 periodontally and systemically healthy volunteer subjects were enrolled in the study. Whole saliva samples and full-mouth clinical periodontal recordings were obtained at baseline and one month following initial phase of treatment in gingivitis patients. Salivary cotinine, glutathione and ascorbic acid concentrations, and total antioxidant capacity were determined, and the data generated were tested by non-parametric tests. RESULTS: Salivary cotinine measurements resulted in re-classification of three self-reported non-smokers as smokers. Smoker patients revealed significantly higher probing depths but lower bleeding values than non-smoker patients (p=0.044 and 0.001, respectively). Significant reductions in clinical recordings were obtained in non-smoker (all p<0.05) and smoker (all p<0.01) patients following periodontal treatment. Salivary total glutathione concentrations were reduced following therapy in gingivitis patients who smoke (p<0.01). Otherwise, no statistically significant differences were found between the groups in biochemical parameters at baseline or following treatment (p>0.05). CONCLUSIONS: Within the limits of this study, neither smoking nor gingival inflammation compromised the antioxidant capacity of saliva in systemically healthy gingivitis patients.