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This study aimed to investigate the relationship between endogenous antioxidant system, 8-hydroxydeoxyguanosine adduct (8-OHdG) repair, and apoptosis in mice treated with chromium(VI) alone and in the presence of the antigenotoxic compound (-)-epigallocatechin-3-gallate (EGCG). Groups of 5 Hsd:ICR male mice were divided and treated as follows: (1) control, vehicle only; (2) EGCG, 8.5 mg/kg by gavage alone; (3) CrO3, 20 mg/kg intraperitoneally alone; and (4) EGCG combined with CrO3, EGCG was administered 4 hr prior to CrO3. Peripheral blood parameters were analyzed before treatment administration (time 0), and 48 hr after exposure. The administration of EGCG increased 8-OHdG levels and superoxide dismutase (SOD) activity. Treatment with CrO3 increased number of micronucleus (MN) presence, elevated apoptotic/necrotic cells frequencies, decreased 8-OHdG levels, diminished total antioxidant capacity (TAC), increased glutathione (GSH) total levels, and lowered SOD activity. Administration of EGCG prior to treatment with CrO3 resulted in lower concentrations of MN, reduced apoptotic and necrotic cell number, and restored TAC and SOD activity to control levels. It is conceivable that the dose of EGCG plays an important role in the genotoxic damage protection pathways. Thus, this study confirms the action of EGCG as an antigenotoxic agent against chromium(VI)-induced oxidative insults and demonstrates potential protective pathways for EGCG actions to counteract genotoxic damage induced by this metal. [ABSTRACT FROM AUTHOR]

This study assessed oxidatively damaged DNA and antioxidant enzyme activity in workers occupational exposure to metal oxides nanomaterials. Exposure to TiO2, SiO2, and ITO resulted in significant lower antioxidant enzymes (glutathione peroxidase and superoxide dismutase) and higher oxidative biomarkers 8-hydroxydeoxyguanosine (8-oxodG) than comparison workers. Statistically significant correlations were noted between plasma and urine 8-oxodG, between white blood cells (WBC) and urine 8-oxodG, and between WBC and plasma 8-oxodG. In addition, there were significant negative correlations between WBC 8-oxodG and SOD and between urinary 8-oxodG and GPx levels. The results showed that urinary 8-oxodG may be considered to be better biomarker. [ABSTRACT FROM PUBLISHER]

The effect of a product made of dehydrated apples enriched with mandarin juice by vacuum impregnation on markers of oxidative stress (plasma antioxidant capacity, carbonyl groups (CGs), 8-hydroxydeoxyguanosine (8OHdG) and α-tocopherol) was tested in rats. Six groups of animals were studied: one group was fed a standard diet; two groups were supplemented with dehydrated apple either impregnated or not with mandarin juice throughout 28 days; and three groups (one unsupplemented and two supplemented) were additionally treated with tamoxifen (TAM) for 21 days used for induction of oxidative stress. The rats treated with TAM showed an increase in aminotransferases, CGs and 8OHdG. All of these effects were significantly decreased in the animals after apple snack consumption; the addition of mandarin juice into the apple mainly accounts for increased levels of α-tocopherol in plasma and liver. These findings suggest that the food product have a protective action against oxidative stress induced by TAM in rats. [ABSTRACT FROM AUTHOR]

The incidence of diabetes mellitus is rapidly increasing in the world. One of the complications of diabetes includes disturbance of the reproductive tract, such as infertility, erectile dysfunction, and endocrine disruption. Nitric oxide (NO) is a free radical produced by most cells including the human male and female reproductive tracts. NO has a dual role where low concentrations are essential for homeostatic cellular biology and physiology, but high levels have detrimental effects relating to cellular damage from this reactive oxygen species (ROS). 8-hydroxydeoxyguanosine (8-OHdG) is an oxidized nucleoside of DNA that is currently used as a biomarker of cellular oxidative stress, where urinary levels can correlate with diabetic nephropathy and retinopathy. Our aim was to investigate the relationship between nitrate//nitrite levels and 8-OHdG levels in the semen of diabetic and non-diabetic men. Concentrations of nitrate//nitrite and 8-OHdG were examined in seminal plasma of 32 diabetic and 35 non-diabetic men. The level of nitrate//nitrite was assayed by colorimetric reaction and 8-OHdG was measured by ELISA. Our results showed that the seminal plasma nitrate//nitrite levels were significantly higher in the diabetic group ( p < 0. 01). There were also significantly higher 8-OHdG levels in diabetic men compared to non-diabetic men ( p < 0.05). Regression analysis indicated that in diabetic men, nitrate//nitrite levels correlated well with 8-OHdG levels (r == 0.64, p < 0.001). A significant trend between nitrate//nitrite and sperm parameters was not observed. Our data suggests that high levels of nitrate//nitrite in the semen of diabetic men is suggestive of reactive oxygen species induced DNA damage that is correlated with 8-OHdG levels but not sperm parameters. These results support the further investigation of NO and 8-OHdG as biomarkers for assessing male infertility. [ABSTRACT FROM AUTHOR]

Currently, bronchopulmonary dysplasia (BPD) occurs almost exclusively in pre-term infants. In addition to prematurity, other factors like oxygen toxicity and inflammation can contribute to the pathogenesis. This study aimed to compare urinary inflammatory and oxidative stress markers between the no/mild BPD group and moderate/severe BPD group and between BPD cases with significant early lung disease like respiratory distress syndrome (RDS) (''classic'' BPD) and with minimal early lung disease (''atypical'' BPD). A total of 60 patients who were a gestational age < 30 weeks or a birth weight < 1250 g were included. Urine samples were obtained on the 1st, 3rd and 7th day of life and measured the levels of leukotriene E4 (LTE4) and 8-hydroxydeoxyguanosine (8-OHdG). The 8-OHdG values on the 3rd day showed significant correlation to duration of mechanical ventilation. The 8-OHdG levels on the 7th day were the independent risk factor for developing moderate/severe BPD. In ''classic'' BPD, the 8-OHdG values on the 3rd day were higher than those of ''atypical'' BPD. In ''atypical'' BPD, the LTE4 values on the 7th day were higher than the values in ''classic'' BPD. These results suggest that oxidative DNA damage could be the crucial mechanism in the pathogenesis of current BPD and the ongoing inflammatory process could be an important mechanism in ''atypical'' BPD. [ABSTRACT FROM AUTHOR]

Polycystic ovary syndrome (PCOS) has recently been linked with genomic instability and DNA damage. The aim of this study was to test genomic damage in women PCOS, using two different methods for assessing damage in both chromosome and base level. The study was performed on 36 newly diagnosed women with PCOS and 29 healthy women as controls. The micronucleus (MN) analysis used as a biomarker of chromosomal/DNA damage was performed in peripheral lymphocytes by cytokinesis-block method. 8-hydroxydeoxyguanosine (8-OHdG) levels used as a reliable marker of oxidative DNA damage were measured in plasma using an ELISA kit. We found that MN frequencies obtained from lymphocytes of the women with PCOS were significantly higher than those of controls (4.1 ± 1.0 vs. 2.1 ± 0.6, P = 0.001), whereas, no differences in 8-OHdG level were found between the patients with PCOS and controls (0.5 ± 0.3 vs. 0.5 ± 0.2, P = 0.858). These findings indicate that women with PCOS seem to have increased genomic instability, but do not appear to have oxidative DNA damage despite the increased oxidative stress associated with PCOS. [ABSTRACT FROM AUTHOR]

Dihydropyrimidine dehydrogenase (DPD) constitutes the first step of the pyrimidine degradation pathway in which the pyrimidine bases uracil and thymine are catabolised to β-alanine and β-aminoisobutyric acid (β-AIB), respectively. The mean concentration of β-AIB was approximately 5- to 8-fold lower in urine of patients with a DPD deficiency, when compared to age-matched controls. Comparable levels of 8-hydroxydeoxyguanosine (8-OHdG) were present in urine from controls and DPD patients at the age <2 year. In contrast, slightly elevated levels of 8-OHdG were detected in urine from DPD patients with an age >2 year, suggesting the presence of increased oxidative stress. [ABSTRACT FROM AUTHOR]

We investigated whether habitual exercise (HE) modulates levels of oxidative DNA damage and responsiveness to oxidative stress induced by renal carcinogen Fe-nitrilotriacetic acid (Fe-NTA). During a ten week protocol, two groups of rats either remained sedentary or underwent swimming for 15-60 mm per day, 5 days per week, with or without a weight equivalent to 5% of their body weight. Then we injected Fe-NTA and sacrificed the rats 1 h after the injection. We determined the activity of superoxide dismutase (SOD) in diaphragm and kidney, evaluated levels of 8-hydroxydeoxyguanosine (8OHdG), catalase, and glutathione peroxidase, and assayed OGG 1 protein levels in kidney. SOD activity in the diaphragm and kidney was increased in HE rats. By itself, HE had no effect on the level of SOHdG, but it did significantly suppress induction of 8OHdG by Fe-NTA, and the amount of suppression correlated with intensity of exercise. These results suggest that HE induces resistance to oxidative stress and, at least at the initiation stage, inhibits carcinogenesis. [ABSTRACT FROM AUTHOR]

Very low birth weight (VLBW) infants are known to have poorly developed antioxidant system and may be at increased risk for radical damage. Previous studies have reported higher levels of lipid peroxide products in lipid emulsion used for parenteral nutrition. To examine the direct effects of parenteral lipid infusion on DNA damage in VLBW infants, we measured urinary 8-hydroxydeoxyguanosine (8-OHdG) levels in VLBW infants before, during, and after the parenteral lipid infusion. In both the lipid-infused and lipid-free groups, urinary 8-OHdG excretion levels at 14 days old were significantly ( p <0.01) lower than those at 2 and 7 days old. However, there were no significant differences in urinary 8-OHdG excretion levels between the lipid-infused and lipid-free groups at 2, 7, and 14 days old. Our results suggest that parenteral lipid infusion does not cause oxidative DNA damage, but irrespective of the infusion DNA damage during the first week of life is enhanced when compared with 14 days after birth in VLBW infants. [ABSTRACT FROM AUTHOR]

We examined the effects of dietary vitamin E (VE) on oxidative damage to DNA and lipids in the liver a few days after total body irradiation (TBI). ODS rats, which lack vitamin C synthesis, were fed either a low VE diet (4.3 mg VE/kg) or a basal VE diet (75.6 mg VE/kg) for 5 weeks while vitamin C was supplied in the drinking water. The VE level in the liver of the low VE group was lower and the levels of lipid peroxides were higher compared to those of the basal VE group: the relative levels in the two groups were 1:30 for VE, 18:1 for 4-hydroxynonenal (HNE), and 10:1 for hexanal (HA). The level of 8-hydroxydeoxyguanosine (8OHdG), a marker of oxidative DNA damage, did not differ between the low VE and the basal VE groups. When the rats received TBI at the dose of 3 Gy and were killed on day 6, the levels of HNE, HA and 8OHdG increased by 2.2-, 2-, and 1.5-times, respectively, in the low VE group, but TBI did not cause such increases in the basal VE group. Changes in antioxidative enzymes (glutathione peroxidase, catalase, and Cu/Zn-SOD) in the liver could not explain the different responses of the two diet groups to TBI-induced oxidative damage. The concentrations of vitamin C and glutathione in the liver did not differ between the two groups. These results suggest that dietary VE can prevent the oxidative damage to DNA and lipids in the liver which appear a few days after TBI at dose of 3 Gy. [ABSTRACT FROM AUTHOR]

Urinary 8-hydroxydeoxyguanosine (8OHdG) has been considered as an excellent marker of individuals at high risk of developing cancer. Until now, urinary 8OHdG has largely been measured by high-performance liquid chromatography with electrochemical detection. A new method for the analysis of urinary 8OHdG by high-performance capillary electrophoresis has been developed and optimized in our laboratory. A single step solid-phase extraction procedure was optimized and used for extracting 8OHdG from human urine. Separations were performed in an uncoated silica capillary (50cm × 50 μm i.d.) using a P/ACE MDQ system with UV detection. The separation of 8OHdG from interfering urinary matrix components is optimized with regard to pH, applied voltage, pressure injection time and concentration of SDS in running buffer. The detection limit of this method is 0.4 μg/ml, the linear range is 0.8-500 &mu:g/ml, the correlation coefficients levels is better than 0.999. The developed method is simple, fast and good reproducibility, furthermore, it requires a very small injection volumes and low costs of analysis, which makes it possible to provide a new noninvasive assay for an indirect measurement of oxidative DNA damage. [ABSTRACT FROM AUTHOR]