Mônica S. S. Meirelles

DNA oxidative damage in patients with dialysis treatment

Background/Aims. Chronic renal patients on hemodialysis (HD) and peritoneal dialysis (PD) treatment are exposed to oxidative stress and DNA damage. The objective of this study was to assess the oxidative damage to DNA in end-stage chronic renal failure, before and after vitamin E supplementation. Methods. Patients on HD (n = 29) and PD (n = 22) received oral supplementation with 300 mg vitamin E three times a week for 4 weeks. A blood sample was collected at the beginning and at the end of the supplementation cycle for the determination of vitamin E levels (high-performance liquid chromatography), carbonyl groups, and DNA damage (8-hydroxy 2′-deoxyguanosine [8-OHdG] and comet assay). Results. After supplementation, vitamin E concentration was increased by about 50%. Protein oxidation was initially observed in both groups, with a reduction after supplementation. DNA damage detected by the comet assay and by 8-OHdG analysis was significantly reduced (p< 0.05) after supplementation in both groups. Conclusions. Vitamin E supplementation reduced oxidative DNA damage in both HD and PD patients. Treatments such as HD and PD induce oxidative stress and consequent DNA damage, and increased plasma vitamin E levels significantly contribute to the normalization of these events.

Lipid peroxidation in nicotinamide-deficient and nicotinamide-supplemented rats with streptozotocin-induced diabetes.

Abstract Reactive oxygen species have been related to the pathogenesis of various diseases, including diabetes mellitus. Nicotinamide has been used for the prevention of the diabetogenic effects of streptozotocin (STZ) in animals. In the present study we assessed the effect of diets with deficient, normal or 17-fold supplemented nicotinamide concentrations on the rate of lipopoeroxidation in animals with STZ-induced diabetes. Male Wistar rats were divided into three groups kept on one of the diets for six weeks: DD, diabetic rats on a nicotinamide-deficient diet; DN, diabetic rats on a normal nicotinamide diet; and DS, diabetic rats on a nicotinamide-supplemented diet. During the fourth week of the experiment all animals were fasted for 24 hours and injected into the tail vein with a single STZ dose (40 mg/kg weight). Eight animals from each of the six groups were then sacrificed 24 hours, 1 week and 2 weeks after STZ injection. Mean pancreatic thiobarbituric acid reactive substances (TBARS) (nmol/mg tissue) were significantly lower in the DS group (p < 0.05) compared to the DN and DD groups at 24 hours and during the first week. Hepatic TBARS concentrations (nmol/mg protein) did not differ between groups. Mean hepatic reduced glutathione (GSH) levels were significantly higher (46.76 ± 12.33 nmol/mg protein) in the DS group compared to the DD (32.90 ± 6.70) and DN (24.55 ± 6.41) groups, but only after the 24-hour period. Hepatic vitamin E consumption (Μg/g tissue) was considerable in the groups not supplemented with nicotinamide, whereas vitamin E levels were unchanged in the supplemented group. In contrast, plasma vitamin E levels were decreased in the normal and supplemented groups after 1 and 2 weeks. A higher N-methylnicotinamide excretion (μg/ 24 hours) occurred in the supplemented group. We conclude that, after induction of diabetes with STZ, nicotinamide supplementation protected from the damage caused by the toxic action of STZ, promoting lower lipid peroxidation.

Vitamin A deficiency among Brazilian school-aged children in a healthy child service

Background/Objectives:Vitamin A deficiency (VAD) is a world public health problem contributing to the increase in childhood morbidity and mortality in developing countries and severe deficiency of vitamin A may lead to xerophthalmia and blindness. The objective of this study was to determine the prevalence of VAD among Brazilian school-aged children attended at a primary health unit and to verify if some considered risk factor was associated with VAD in this group.Subjects/Methods:A descriptive prospective transverse study was conducted on 103 randomly selected children. A total of 54 boys and 49 girls aged 5.5–11 years had the relative dose–response (RDR) test performed on. Possible ocular alterations related to vitamin A and the status of anemia, serum zinc, some acute-phase proteins, and anthropometric situation were determinate by an analytic design.Results:No child presented xerophthalmia. Serum retinol values lower than 1.05 and 0.7 μmol l−1, respectively were found in 26.2 and 5.8% of the children. The prevalence of hypovitaminosis detected by RDR test was 20.4%. The following variables and their relationship with VAD were evaluated: sex (P=0.33; 95% confidence interval 0.61–4.34), weight and height (P⩾0.5), hemoglobin (P=0.15), C-reactive protein (P=0.56; 95% confidence interval 0.75–18.26), α-1-acid-glycoprotein (P=0.56; 95% confidence interval 0.15–15.42) and serum zinc (P=0.31). None of these variables was related to VAD.Conclusions:In this population, the prevalence of VAD detected could be considered a public health problem. School-aged children can be considered at risk for VAD mainly of a subclinical level, even without some associated risk factors.

Effect of Citric Pectin on beta-Carotene Bioavailability in Rats

The effect of citric pectin on the bioavailability of synthetic beta-carotene was studied. Thirty Wistar rats were used, ten animals were sacrificed at the beginning of the experiment and remaining animals were divided into two groups and received the following diets for 30 days: control group (CG)--24 micrograms beta-carotene/g diet + 0% citric pectin; experimental group (EG)--24 micrograms beta-carotene/g diet + 7% citric pectin. Plasma and liver beta-carotene, vitamin A, and retinyl palmitate concentrations were determined by high-performance liquid chromatography (HPLC). Plasma retinol concentration was 1.42 +/- 0.36 mumol/L for CG and 1.10 +/- 0.24 mumol/L for EG (p = 0.1), and plasma beta-carotene concentration was 0.20 +/- 2.51 mumol/L for CG and 0.07 +/- 0.04 mumol/L for EG (p = 0.01). Only traces of retinyl palmitate were detected in CG and none in EG. Retinol did not differ significantly between groups CG and EG, while a significantly higher beta-carotene concentration was observed for CG. Liver concentrations of retinol (CG: 4.90 +/- 2.51 micrograms/g; EG: 2.68 +/- 1.12 micrograms/g), beta-carotene (CG: 0.98 +/- 0.28 microgram/g; EG: 0.11 +/- 0.06 microgram/g), and retinyl palmitate (CG: 95.47 +/- 45.13 micrograms/g, EG: 37.01 +/- 17.20 micrograms/g) differed significantly between groups (p < 0.05), with a lower concentration being observed for EG. We conclude that 7% citric pectin in the rat diet decreases the bioavailability of synthetic beta-carotene, reducing the liver reserves of vitamin A and beta-carotene.

Efeitos da quercetina na lesão pulmonar induzida por bleomicina: um estudo preliminar

OBJECTIVE: The aim of this study was to identify the best experimental model in which to observe the pulmonary alterations characterizing hepatopulmonary syndrome (HPS). METHODS: Male Wistar rats, with mean weight of 250 g, were used in four experimental models: inhaled carbon tetrachloride; intraperitoneal carbon tetrachloride; partial portal vein ligation; and bile duct ligation (BDL). The animals in all groups were divided into control and experimental subgroups. The following variables were measured: transaminase levels; blood gases; lipoperoxidation, using thiobarbituric acid reactive substances (TBARS) and chemiluminescence; and levels of superoxide dismutase (SOD) anti-oxidant activity. Anatomopathological examination of the lung was also performed. RESULTS: There were statistically significant differences between the BDL control and BDL experimental groups: aspartate aminotransferase (105.3 ± 43 vs. 500.5 ± 90.3 IU/L); alanine aminotransferase (78.75 ± 37.7 vs. 162.75 ± 35.4 IU/L); alkaline phosphatase (160 ± 20.45 vs. 373.25 ± 45.44 IU/L); arterial oxygen tension (85.25 ± 8.1 vs. 49.9 ± 22.5 mmHg); and oxygen saturation (95 ± 0.7 vs. 73.3 ± 12.07%). Lipoperoxidation and antioxidant activity also differed significantly between the two BDL groups (control vs. experimental): TBARS (0.87 ± 0.3 vs. 2.01 ± 0.9 nmol/mg protein); chemiluminescence (16008.41 ± 1171.45 vs. 20250.36 ± 827.82 cps/mg protein); and SOD (6.66 ± 1.34 vs. 16.06 ± 2.67 IU/mg protein). The anatomopathological examination confirmed pulmonary vasodilatation in the BDL model. In the other models, there were no alterations that were characteristic of HPS. CONCLUSIONS: The data obtained suggest that the BDL model can be used in future studies involving hepatic alterations related to oxidative stress and HPS.

Effect of β-Carotene Supplementation on Rats Submitted to Chronic Ethanol Ingestion

Abstract Chronic alcohol consumption is directly related to the induction of liver damage. The continuous use of ethanol induces the isoenzyme cytochrome P450CYP2E1, which promotes the formation of free radicals, resulting in lipid peroxidation. Among the main antioxidants are vitamin E, reduced glutathione (GSH), vitamin C, and β-carotene. β-Carotene has antioxidant activity per se, with a probable protective effect against different types of cancer. However, some studies have shown an increased number of cancer cells when β-carotene is administered in the presence of chronic ethanol ingestion. On this basis, the objective of the present study was to assess the effect of β-carotene supplementation on rats chronically treated with a hydroalcoholic solution by determining the levels of vitamin E, β-carotene, GSH, and thiobarbituric acid reactive species (TBARS). Both the plasma and liver concentrations of β-carotene were higher in the supplemented groups. Plasma vitamin E levels were decreased in the control group and liver vitamin E levels were significantly decreased (p<0.05) in all groups compared to basal levels. GSH levels were increased over basal values in the group supplemented with β-carotene for 14 days. TBARS values were increased as much as four-fold in the control group at 14 days, and declined again at 28 days, whereas they were increased in the supplemented group, with the increase remaining until the end of the experiment. The study indicates that β-carotene had no beneficial effect as an antioxidant on rats submitted to chronic alcohol intake, and could be act as prooxidant when administred with ethanol.

Lipid Peroxidation in Nicotinamide-Deficient and Nicotinamide-Supplemented Rats

Supplementation or deficiency of nicotinamide in rats may interfere with the oxidative balance, with excess leading to greater lipid peroxidation, measured by TBARS, and deficiency causing a greater consumption of antioxidants such as vitamin E and glutathione. Urinary N-methylnicotinamide excretion was much more marked in the supplemented group, whereas the difference between deficient and control animals was nonsignificant.

Caloric value in foods consumed by children and adolescents determined through direct calorimetry

Obesidade, diabetes mellitus, insuficiência renal e dislipidemias entre inúmeras outras são condições mórbidas nas quais a modificação dietética é parte essencial do tratamento (Allison et al., 1993). Diante disso, a determinação e quantificação dos nutrientes de alimentos tornase fundamental para a real ização de um planejamento alimentar adequado. O planejamento dietético geralmente é realizado com informações contidas nas tabelas de composição de alimentos, como a do Instituto Brasileiro... (1977), a de Franco (1992) e a Tabela Brasileira de Composição de Alimentos (Lajolo et al., 2000), ou nos rótulos de produtos industrializados. As informações nutricionais, entretanto, não devem ser consideradas absolutas, pois os valores energéticos e nutricionais de um mesmo alimento variam consideravelmente entre as citadas fontes de informação. Além disso, diversos produtos freqüentemente consumidos por crianças e adolescentes como balas, doces, biscoitos e bolachas (Sawaya et al., 1995), raramente são encontrados nestas tabelas.

Lipid peroxidation and urinary excretion of vitamin E in rats submitted to an immunological inflammatory process.

Abstract Inflammation is a protective physiologic response, generally controlled by the organism at the injury site. Vitamin E is the most important antioxidant in the lipid phase present in nature and acts by interrupting the chain reaction produced by free radicals. The objective of this study was to evaluate the effect of inflammation on vitamin E levels and lipid peroxidation in rats. Forty Wistar rats (four groups of 10 rats each) were studied over a period of 15 days. Two substances inducing the inflammatory process were parenterally administered, anti-rat basement membrane serum (ABMG) and Freunds complete adjuvant (FAG). Lipid peroxidation levels in hepatic and renal tissue and in plasma and urine were analyzed and compared with the control (CG). Vitamin E was determined by HPLC and lipid peroxidation by quantification of thiobarbituric acid reactive substances (TBARS). ABMG produced more (p<0.05) TBARS in renal and hepatic tissues (0.7 ± 0.11 and 1.28 ± 0.27 nmol/g protein, respectively) compared to CG (0.65 ± 0.81 and 0.69 ± 0.13 nmol/g protein). Analysis of TBARS in urine did not show statistically significant differences between the experimental groups and the control. Vitamin E levels in the hepatic tissue of ABMG and FAG (40.7 ± 10.04 and 44.26 ± 20.24 µg/g tissue) were higher than in CG (22.37 ± 8.20 µg/g tissue) while in kidney tissue and plasma these values were lower (P<0.05). Renal excretion was increased (P<0.05) in the group that received anti-rat basement membrane serum (22.39 ± 0.11 mmol/mL) compared to CG (0.56 ± 0.056 mmol/mL). We conclude that the acute inflammatory process causes important alterations in the metabolism of vitamin E and lipid peroxidation leading to a significantly increased excretion of this vitamin in the urine.

P-85 Is there a role for vitamin A on the regulation of IGF-I in children?

IGF system and vitamin A (VA) are important regulators of human growth and a wide range of physiological processes. Growth hormone and nutritional status are the main regulators of IGF system; however the role of the micronutrients is still not clear. The objective was to verify the effect of VA supplementation on IGF-I levels in VA deficient children. Ninety-four healthy children aged 5.5–11 years with regular follow-up in a pediatric clinic and no clinic evidence of vitamin A deficiency (VAD) entered the study. In order to access VA status serum retinol were determined by HPLC at baseline (BR) and 30 days (R30) after VA supplementation (200 000 IU of trans-retinyl palmitate) by +S30DR test (serum 30-day dose-response test). +S30DR was considered positive when (R30 −BR)× 100/R30 was 20%. IGF-I was also measured in both samples, by IRMA. Children were further divided in VAD and non-VAD. They were considered VAD if BR 1.05mmol/L or +S30DR positive. The samples were paired and compared using a nonparametric paired test. According to BR and +S30DR 24.5% and 28.7% of the children were considered VAD, respectively. IGF-I levels increased significantly with VA supplementation in the VAD group, either considering BR levels criterion (P = 0.001) or +S30DR test criterion (P = 0.004) while no difference was observed between baseline IGF-I and day-30 IGF-I in the non-VAD group. Baseline IGF-I was lower in the VAD than in the non-VAD group either considering BR (median: 190 vs. 260 mg/L) or +S30DR (median: 190 vs. 260mg/L) as criterion to VAD. No difference was found regarding day-30 IGF-I levels between VAD and non-VAD children. Conclusion: IGF-I levels increase after VA supplementation in children with subclinical VAD, these results suggest a possible role for VA on IGF-I regulation and support the idea that some of VA actions can be mediated by IGF-I, including the VA-supported growth.