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Glutathione (GSH) is a tripeptide that constitutes one of the main intracellular reducing compounds. The normal content of GSH in the intestine is essential to optimize the intestinal Ca2+ absorption. The use of GSH depleting drugs such as DL-buthionine-S,R-sulfoximine, menadione or vitamin K3, sodium deoxycholate or diets enriched in fructose, which induce several features of the metabolic syndrome, produce inhibition of the intestinal Ca2+ absorption. The GSH depleting drugs switch the redox state towards an oxidant condition provoking oxidative/nitrosative stress and inflammation, which lead to apoptosis and/or autophagy of the enterocytes. Either the transcellular Ca2+ transport or the paracellular Ca2+ route are altered by GSH depleting drugs. The gene and/or protein expression of transporters involved in the transcellular Ca2+ pathway are decreased. The flavonoids quercetin and naringin highly abrogate the inhibition of intestinal Ca2+ absorption, not only by restoration of the GSH levels in the intestine but also by their anti-apoptotic properties. Ursodeoxycholic acid, melatonin and glutamine also block the inhibition of Ca2+ transport caused by GSH depleting drugs. The use of any of these antioxidants to ameliorate the intestinal Ca2+ absorption under oxidant conditions associated with different pathologies in humans requires more investigation with regards to the safety, pharmacokinetics and pharmacodynamics of them.

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BACKGROUND: In any context of iron supplementation in the prenatal prophylaxis or therapeutic dosage range, a large amount will remain unabsorbed and pass through the intestinal tract into the colonic digesta possibly causing increased oxidation. AIM: To compare the generation of fecal reactive oxygen species (ROS) in situ after daily consumption of 100 mg of elemental iron in three frequently used forms of iron supplements. METHODS: Ten healthy, iron-repleted adult males were investigated before and during supplementation with three oral iron compounds: 100 mg of oral iron were given as ferrous sulfate, Na Fe-EDTA and iron polymaltose for 6 days to each subject in an individually stratified sequence. Stool samples were collected and analyzed for iron content and the in situ generation of fecal ROS. RESULTS: Significant increases in fecal ROS generation were observed during oral iron supplementation. No statistical differences were seen in either residual concentrations of non-heme iron in stool or the level of fecal ROS generation between the three Fe compounds. There was, however, a significant association between the iron concentration in the stool and ROS generation. CONCLUSION: In spite of the differences in their chemical characteristics, none of the three distinct iron complexes reduced oxidative stress in the intestinal lumen.

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This aim of the present study was to evaluate the pulp chamber penetration of 35% hydrogen peroxide activated by LED (light-emitting diode) or Nd:YAG laser in bovine teeth, after an in-office bleaching technique. Forty-eight bovine lateral incisors were divided into four groups, acetate buffer was placed into the pulp chamber and bleaching agent was applied as follows: for group A (n = 12), activation was performed by LED; for group B (n = 12), activation was performed by Nd:YAG laser (60 mJ, 20 Hz); group C (n = 12) received no light or laser activation; and the control group (n = 12) received no bleaching gel application or light or laser activation. The acetate buffer solution was transferred to a glass tube and Leuco Crystal Violet and horseradish peroxidase were added, producing a blue solution. The optical density of this solution was determined spectrophotometrically and converted into microgram equivalents of hydrogen peroxide. The results were analysed using ANOVA and Tukey's test (5%). It was verified that the effect of activation was significant, as groups activated by LED or laser presented greater hydrogen peroxide penetration into the pulp chamber (0.499 +/- 0.622 microg) compared with groups that were not (0.198 +/- 0.218 microg). There was no statistically significant difference in the penetration of hydrogen peroxide into the pulp chamber between the two types of activation (LED or laser). The results suggest that activation by laser or LED caused an increase in hydrogen peroxide penetration into the pulp chamber.

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AIM: To investigate pulp chamber penetration of bleaching agents in teeth following restorative procedures. METHODOLOGY: Bovine lateral incisors were sectioned 3 mm apical to the cemento-enamel junction and the coronal pulpal tissue was removed. Teeth were divided into six groups (n = 10): G1, G2 and G3 were not submitted to any restorative procedure, while G4, G5 and G6 were submitted to Class V preparations and restored with composite resin. Acetate buffer was placed in the pulp chamber and treatment agents were applied for 60 min at 37 degrees C as follows: G1 and G4, immersion into distilled water; G2 and G5, 10% carbamide peroxide (CP) exposure; G3 and G6, 35% CP bleaching. The buffer solution was removed and transferred to a glass tube where leuco crystal violet and horseradish peroxidase were added, producing a blue solution. The optical density of the blue solution was determined spectrophotometrically at 596 nm. A standard curve made with known amounts of hydrogen peroxide was used to convert the optical density values of the coloured samples into microgram equivalents of hydrogen peroxide. Data were submitted to anova and Tukey's test (5%). RESULTS: Amounts of hydrogen peroxide found in the pulp chamber of G2 and G5 specimens (0.1833 +/- 0.2003 micro g) were significantly lower (P = 0.001) when compared to G3 and G6 specimens (0.4604 +/- 0.3981 micro g). Restored teeth held significantly higher (P = 0.001) hydrogen peroxide concentrations in the pulp chamber than intact teeth. CONCLUSION: Higher concentrations of the bleaching agent produced higher levels of hydrogen peroxide in the pulp chamber, especially in restored teeth.

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