Influence of chronic cadmium exposure on the tissue distribution of copper and zinc and oxidative stress parameters in rats.

The aim of this study was to investigate the effect of oral cadmium (Cd) intoxication on the antioxidant response and its relationship with essential bioelements like copper (Cu) and zinc (Zn). The experimental group was chronically exposed to Cd daily for 8 weeks via consumption of water containing 15 ppm cadmium chloride. Cu, Zn, and Cd concentrations and oxidative stress parameters were analyzed in liver, kidney, and heart tissues. Exposure to Cd led to a significant decrease in the activities of superoxide dismutase in all considered samples while a significant increase in the activity of glutathione peroxidase except for the kidney. We found a significant increase in malondialdehyde concentration in the tissues except for heart. Also oral administration of Cd caused a significant reduction of Zn and Cu in the tissues. Our results allow us to hypothesize that higher Cd concentration in the tissues causes oxidative stress by increasing malondialdehyde as a means of altering antioxidant defense system and deterioration of bioelements in rat liver, kidney, and heart. In addition, further studies are needed to explain the effect of long-term, low-dose exposure to Cd on distribution of bioelements and its relationship with oxidative stress.

Evaluation of DNA damage using 3 comet assay parameters in workers occupationally exposed to lead.

The aim of this study was to investigate the association between DNA damage and blood lead levels in individuals occupationally exposed to lead. To evaluate this association, 61 workers exposed to lead were monitored in terms of DNA damage in blood lymphocytes. The levels of DNA damage were measured according to 3 comet assay parameters, including tail intensity (TI), tail moment (TM), and DNA tail (DNAt). A statistically significant positive correlation was found between the lead levels and TI, TM, and DNAt (p < .01). Smoking had independent effects on DNA damage. A statistically significant difference was observed between smokers and nonsmokers in regards to DNA damage parameters (p < .05). In addition, the lead and DNA damage levels in smokers were found to be significantly higher than the levels observed in nonsmoking workers (p < . 05). Our results show that exposure to lead induces genotoxic effects in peripheral lymphocytes, as measured by comet assays.

The effect of relaparotomy timing on wound healing in an animal model.

BACKGROUND: The effect of the timing of the second laparotomy on wound healing is not clear. In an experimental study in rats, we aimed to investigate the effect of timing on wound healing after reoperations on the same surgical site. MATERIAL AND METHODS: Forty-eight rats were divided into four groups. The control group (GC) didn't have another laparotomy whereas the relaparotomies on the same surgical site were performed either on the 3rd, 15th or the 30th postoperative days in the three study groups (G3, G15, G30 respectively). The midline tension pressure, collagen types I, III and, histological analysis were performed from the specimens in order to assess the wound healing and strength. RESULTS: The tensile strength was the highest in GC and decreased gradually in G3, G15 and G30, the difference between the groups did not reach statistical significance. Higher collagen levels, increased fibrosis, and large defects were observed in relaparotomy groups than CG. The musculoaponeurotic gap was shortest in GC when compared to other three relaparotomy groups (P < 0.001) and, it was the longest in G30 (P = 0.004 between G3 and G30). CONCLUSIONS: Although non-statistically significant the gradual decrease in the tensile strength and the statistically significant increase in the musculoaponeurotic gap with time point out the importance of the timing of relaparotomy in the healing process. Early relaparotomies do not disrupt the healing process as much as relaparotomy performed later.

Effects of smoking during pregnancy on DNA damage and ROS level consequences in maternal and newborns' blood.

Some of the genotoxic/carcinogenic substances or metabolites in cigarette smoke are capable of passing through the placenta and harming a newborn's health. Smoking is also known as a factor in the formation of oxidative damage and the main mechanism involved in the carcinogenic process. Predetermining this genotoxic risk can be successfully achieved by measuring certain parameters of oxidative stress. The comet assay is considered an important biomarker for the evaluation of genotoxic substances and is effective for detecting DNA damage caused by smoking. This study examined third trimester bloods and the cord blood of 28 actively smoking and 22 non-smoking mothers in terms of DNA damage and oxidative stress parameters. Cu/Zn superoxide dismutase (CuZn-SOD), malondialdehyde (MDA), catalase (CAT), plasma nitrite/nitrates (NO2-/NO3-), selenium-dependent glutathione peroxidase (Se-GPx), Cu, and Zn levels were measured as indicators of oxidative damage. There were no significant increases in DNA damage of the actively smoking pregnant group in comparison with the non-smoking pregnant group, either in the third trimester or cord blood. Oxidative stress parameters of smoker and non-smoker groups were statistically different for MDA (p<0.05), CuZn-SOD (p<0.01), Se-GPx (p<0.05) values while the difference was not significant for NO2-/NO3-, CAT, Zn, and Cu values. The same values were also investigated in cord blood,and only NO2/NO3-(p<0.01), Se-GPx (p<0.01 and CAT (p<0.001) values were found statistically different.Smoking mothers may have been exposed to more oxidative stress than non-smoking mothers

Association between gene polymorphism of manganese superoxide dismutase and prostate cancer risk.

Manganese superoxide dismutase (MnSOD) is the most effective antioxidant enzyme in mitochondria and protects cells from reactive oxygen species-induced oxidative damage. The aim of this study was to investigate the association between MnSOD Ala-9 Val gene polymorphism and prostate cancer (PCa) risk in Turkish men with prostate cancer. 33 patients with PCa and 81 control individuals were included in the study. We observed an association between MnSOD Ala/Ala frequency and a higher PCa risk. In addition, we found that the increased risk of early-onset PCa (under age of 65) in the men homozygous for Ala allele was higher than the men homozygous for Val allele. However, we determined that MnSOD Ala-9 Val genotype was not associated with the aggressiveness of the disease. The results of our study suggest that MnSOD Ala/Ala genotype may influence on early-onset of PCa patients, but no effect on subsequent development of the disease in Turkish men. However, our study has a limitation that is small numbers of individuals for cases and controls. Therefore, the presented study limited our statistical power to fully investigate the gene polymorphism on cancer risk.

Induced antioxidant activity in hospital staff occupationally exposed to ionizing radiation.

PURPOSE: Occupational exposure to low levels of ionizing radiation (IR) in radiology department staff may affect their antioxidant status. The aim of this study was to evaluate the oxidative stress parameters in radiology staff that are occupationally exposed to IR in a hospital setting. MATERIALS AND METHODS: The study population included 40 exposed radiology staff and 30 control subjects. The radiation doses of exposed staff ranged between 0.10 and 3.8 milligray (mGy) per month. The subjects' antioxidant status was determined by measuring the activities of copper zinc-superoxide dismutase (CuZn-SOD), selenium dependent glutathione peroxidase (Se-GPx), catalase (CAT) enzymes, and the levels of malondialdehyde (MDA) in erythrocytes. RESULTS: Our results showed that the activities of erythrocyte CuZn-SOD and Se-GPx enzymes observed for the radiation exposed group were significantly higher than in the controls. The activity of CAT enzyme and MDA levels were significantly lower in the exposed group than in the controls. Moreover, we investigated the influence of confounding factors on antioxidant enzymes or lipid peroxidation (LP), but we could not find any associations between them. CONCLUSIONS: Our study indicates the presence of stimulant effect of chronic low-dose radiation in exposed individuals, resulting in enhanced resistance to oxidative stress.

Toxic metals in breast milk samples from Ankara, Turkey: assessment of lead, cadmium, nickel, and arsenic levels.

Toxic metals are one of the significant groups of chemical contaminants that humans are exposed to by oral, inhalation, and dermal routes. Exposure to these chemicals begins with intrauterine life and continues during lactation period at the first years of life. Breastfeeding has a much more special place than other nutrition options for infants. However, when possibility of contaminant transfer by breast milk is considered, its safety and quality is essential. Regarding infant and mother health and limited number of information on this field in Turkey, measuring contamination levels in breast milk is important. Therefore, in the present study, lead (Pb), cadmium (Cd), nickel (Ni), and arsenic (As) levels were measured by atomic absorption spectrometry in 64 breast milk samples obtained from mothers from Ankara, Turkey. Pb and Ni levels in breast milk samples were found to be 391.45±269.01 µg/l and 43.94±33.82 µg/l (mean ± SD), respectively. Cd was found only in one of 64 samples, and the level was 4.62 µg/l. As level was below the limit of quantification (LOQ, 7.6 µg/l) in all samples. These findings will accurately direct strategies and solutions of protection against contaminants in order to reduce their levels in biological fluids.

Evaluation of genotoxic and oxidative effects in workers exposed to jet propulsion fuel.

PURPOSE: Jet fuel is a common occupational exposure risk among military and civilian populations. The purpose of this study was to evaluate genotoxic and oxidative effects in workers occupational exposure to jet propulsion fuel (JP-8). METHODS: In this study, sister-chromatid exchange (SCE), high frequency of SCE cells (HFCs), and micronuclei (MN) were determined for 43 workers exposed to JP-8 and 38 control subjects. We measured the antioxidant enzyme activities including that of superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT). The levels of thiobarbituric acid-reactive substances (TBARS) were also studied. Urinary 1- and 2-naphthol excretion was used as a biomarker of occupational exposure to JP-8. RESULTS: The results obtained from cytogenetic analysis show a statistically significant increase in frequency of SCE in the exposed workers when compared to controls (P < 0.05). Interestingly, the mean value of the frequency (%o) of MN and HFCs for workers and controls did not show any statistical differences (P > 0.05). Oxidative stress parameters were not statistically different between exposed and control groups except for TBARS levels. CONCLUSION: Urinary 1-and 2-naphthol levels of exposed workers were found to be significantly higher than those of control subjects. Occupational exposure to JP-8 resulted in no significant genotoxic and oxidative effects, while smoking is the principal confounding factor for the some parameters. To understand the genotoxic and oxidative effects of JP-8 exposure, further studies should be planned to find out whether human populations may be at increased risk for cancer because of the exposures related to occupation and lifestyle.

Involvement of galectin-3 in cadmium-induced cardiac toxicity.

OBJECTIVE: Accumulation of the wide spread environmental toxin cadmium (Cd) in tissues results in toxicity. Heart is one of the most effected tissues. Cd exposure induces inflammation in effected tissues. The present study was focused to evaluate roles of tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) in Cd toxicity and their relationships with galectin-3 levels. METHODS: In this experimental study, male Wistar rats were divided randomly to control and experimental groups. Experimental group was exposed to Cd at the dose of 15 ppm for 8 weeks (n=10/group). Inflammatory status in hearts was evaluated with measurement of tissue TNF-α and IL-6 levels. Histopathological examination of heart was carried out by light microscopy. Heart tissue caspase-3 level was used to identify apoptosis. Tissue galectin-3 level was evaluated by ELISA. Statistical difference between groups was evaluated by unpaired Student t-test, correlation was analyzed by Pearson's test. RESULTS: Heart sizes were increased after Cd toxicity. A significant increase in galectin-3 tissue levels was seen after Cd toxicity, this was accompanied with a significant increase in the TNF-α (control: 402±39, Cd: 793±26 pg/g tissue, p<0.001) and IL-6 (control: 150±78, Cd: 325±65 pg/g tissue, p<0.001) levels. Histopathological examination under light microscope suggested a combination of ongoing necrosis and apoptosis. Increased caspase-3 levels were measured after Cd toxicity (control: 12±2, Cd: 18±3 pmol/µg/min, p<0.001). CONCLUSION: Chronic Cd administration induces inflammation and apoptosis in rat hearts. Cadmium causes increased galectin-3 production from heart tissue. The formation of TNF-α due to Cd exposure may likely trigger this mechanism.

Oxidative and antioxidative effects of desflurane and sevoflurane on rat tissue in vivo.

General anaesthetics are often used in patients who are under oxidative stress due to a critical illness or surgical trauma. Some anaesthetics may worsen oxidative stress and some may act as antioxidants. The aim of this study was to evaluate liver, brain, kidney, and lung tissue oxidative stress in rats exposed to desflurane and sevoflurane and in unexposed rats. The animals were divided in three groups: control (received only air); sevoflurane (8 %), and desflurane (4 %). After four hours of exposure, we evaluated the levels of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), Cu, and Zn. Exposure to either of the anaesthetics significantly increased lung MDA levels compared to control (Mann-Whitney U test; P<0.05), probably because it is the tissue directly exposed to anaesthetic gases. Oxidative stress and antioxidant activity in other tissues varied between the desflurane and sevoflurane groups. Our results suggest that anaesthesiologist should not only be aware of the oxidative or antioxidative potential of anaesthetics they use, but should also base their choices on organs which are the most affected by their oxidative action.

Role of midkine in cadmium-induced liver, heart and kidney damage.

Accumulation of the widespread environmental toxin cadmium (Cd) in tissues results in toxicity. Cd, which can induce a broad spectrum of biological effects, is a toxic substance and is associated with inflammation and apoptosis. Midkine (MK) has fibrinolytic, antiapoptotic, transforming, angiogenetic and chemotactic activities. After Cd toxicity, we found increased MK expression in liver cells in an in vitro cell culture model. The aim of this study was to determine the possibility of relationship between tissue MK expression levels, tumor necrosis factor α(TNF-α) levels and apoptosis in a chronic Cd toxicity model in rats. Male Wistar rats were exposed to Cd at the dose of 15 parts per million (ppm) for 8 weeks. MK levels were measured in kidney, heart and liver tissue by enzyme-linked-immunosorbent assay (ELISA). MK messenger RNA (mRNA) expression was evaluated by RT-PCR. Tissue apoptosis level was evaluated with tissue caspase-3 activity levels. Accumulation of Cd in liver is higher than the kidney and heart. Cd-treated rats had significantly higher tissue TNF-α and caspase-3 levels when compared with the control rats (p < 0.001). MK mRNA and protein levels were also significantly upregulated in the Cd-treated group (p < 0.05, p < 0.001, respectively). When compared with apoptosis in tissues, it was more prominent in the liver than kidney and heart. MK level is found increased 3, 1.7 and 1.3× folds in liver, kidney and heart, respectively. Our results showed that chronic Cd administration induces inflammation and apoptosis in rat liver, kidney and heart. MK involved in damage mechanisms of Cd-induced tissues. Further studies will show the underlying mechanism of increased MK expression in Cd toxicity.

Cytogenetic analysis of peripheral blood lymphocytes of hospital staff occupationally exposed to low doses of ionizing radiation.

Ionizing radiation is known to induce mutations and cell transformations, predominantly by causing single-strand and double-strand DNA breakage, thereby leading to chromosome instability and carcinogenesis. The aim of this study was to evaluate genotoxic effects in hospital staff exposed to low-dose ionizing radiation in comparison with a selected control group, by using the cytokinesis-blocked micronucleus (CBMN) and sister chromatid exchange (SCE) tests in peripheral blood lymphocytes. The study included 40 exposed radiology staff and 30 control subjects. The frequency of micronuclei (MN) was significantly increased in radiation-exposed groups compared with control persons (p < 0.05). The frequency of SCE did not show any significant difference in the exposed individuals in comparison to the controls. Our results showed that low-level chronic occupational exposure to ionizing radiation causes an increase of MN frequency in chromosomes, even though the absorbed doses were below the permissible limits. Our studies indicate that the CBMN assay is considered to be sensitive test in contrast to SCE analysis to evaluate chromosomal damage induced by ionizing radiation.

[Investigation of oxidative stress and antioxidant defense in patients with hepatitis B virus infection and the effect of interferon-alpha plus lamivudine combination therapy on oxidative stress]. / Hepatit B virus enfeksiyonlu hastalarda oksidatif stres ve antioksidan kapasitenin arastirilmasi ve interferon-alpha-lamivudin kombinasyon tedavisinin oksidatif stres üzerine etkisi.

The aim of our study is to determine the role of oxidative stress on hepatic damage in patients with acute and chronic hepatitis B virus (HBV) infection and the efficacy of antioxidant-enzyme system against oxidative stress. Furthermore, the effect of interferon-alpha (IFN-alpha) plus lamivudine therapy on oxidative stress was also investigated. Nineteen patients with acute hepatitis B virus (AHBV) infection, 17 patients with chronic hepatitis B virus (CHBV) infection, 24 inactive HBsAg carriers and 21 healthy controls were included in the study. In control and patient groups, serum alanine-aminotransferase (ALT) and aspartate aminotransferase (AST) levels, erythrocyte malondialdehyde (MDA) levels, erythrocyte superoxide dismutase (CuZn-SOD) and glutathione peroxidase (GSH-Px) activities were measured. In CHBV group, after IFN-alpha plus lamivudine therapy for 6 months, these parameters were measured again. In all patient groups erythrocyte MDA levels were detected higher than control group (p < 0.05). Activity of CuZn-SOD was found to be the highest in AHBV (p < 0.05), and the lowest before the treatment in CHBV group (p < 0.05) compared with other groups. Activity of GSH-Px was found to be the highest in AHBV compared with inactive HBsAg carriers (p < 0.05) and CHBV group before treatment (p < 0.05). Activity of GSH-Px was found to be the lowest in CHBV group before treatment compared with other groups (p < 0.05). In CHBV group there was a significant decrease of MDA levels after treatment (p < 0.05) while there was a significant increase in activity of CuZn-SOD and GSH-Px compared with pretreatment levels (p < 0.05). A significant positive correlation was determined between MDA values and serum ALT levels, before and after the treatment (p < 0.05). Detection of the increase of MDA levels which is a product of lipid peroxidation in all patient groups, indicates that the oxidative stress is increased in HBV infection. Correlation between the levels of erythrocyte MDA levels and serum ALT levels supports the hypothesis concerning the role of oxidative stress in pathogenesis of HBV infection. Insufficiency of antioxidant capacity in CHBV and inactive HBsAg carrier groups may lead to progression of disease and results in fibrosis. Treatment with IFN-alpha plus lamivudine causes a decrease in products of lipid peroxidation and shows antioxidant activity via increasing the antioxidant enzymes. These data suggest that the addition of antioxidant agents to IFN-alpha and lamivudin combination therapy may be useful in CHBV treatment. Further in-vitro and in-vivo studies are required to enlighten the role of antioxidants on HBV disease progression and treatment.

Increased oxidative/nitrosative stress and decreased antioxidant enzyme activities in prostate cancer.

OBJECTIVES: The study was aimed to evaluate the oxidative/nitrosative stress status in prostate cancer (CaP) and benign prostatic hyperplasia (BPH). DESIGN AND METHODS: 312 men from two different populations were included: 163 men from Macedonia (73 CaP patients, 67 BPH patients and 23 control subjects) and 149 men from Turkey (34 prostate cancer patients, 100 BPH patients and 15 control subjects). We measured erythrocyte malondialdehyde (MDA) levels, erythrocyte activities of superoxide dismutase (CuZn-SOD), glutathione peroxidase (GPX) and catalase (CAT); plasma nitrite/nitrate (NO(2)(-)/NO(3)(-)), cGMP and 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels. RESULTS: A similar pattern of alteration in the oxidative/nitrosative stress-related parameters was found in both, Macedonian and Turkish studied samples: higher MDA concentrations with lower GPX and CuZn-SOD activities in CaP patients versus controls and BPH groups. The CAT activity was decreased in the CaP patients versus controls in the Turkish studied sample. Furthermore, CaP patients had increased plasma NO(2)(-)/NO(3)(-) and cGMP levels versus controls and BPH groups in both studied samples. CONCLUSIONS: This study has confirmed an imbalance in the oxidative stress/antioxidant status and revealed an altered nitrosative status in prostate cancer patients.

Glutathione peroxidase 1 (GPX1) genetic polymorphism, erythrocyte GPX activity, and prostate cancer risk.

Glutathione peroxidase 1 (GPX1) is a ubiquitously expressed selenium-dependent enzyme that protects cells against oxidative damage by reducing hydrogen peroxide and a wide range of organic peroxides. Some epidemiological studies have correlated low GPX activity or particular GPX1 polymorphisms with enhanced risk of cancer, although these correlations have not been consistently observed in all populations. Therefore, we conducted the present study to evaluate the possible association of GPX1 Pro198Leu polymorphism and erythrocyte GPX activity with the risk of developing prostate cancer and to clarify whether erythrocyte GPX activity levels were correlated with the GPX1 Pro198Leu genotype in the Macedonian population. The GPX1 Pro198Leu genotype was determined in 82 prostate cancer cases and 123 control individuals. We found an overall protective effect of the variant Leu allele of the GPX1 polymorphism on the prostate cancer risk. Heterozygous carriers of the variant Leu allele had a significantly lower risk of prostate cancer compared with homozygous wild-type individuals (OR, 0.38; 95% CI, 0.20-0.75; P = 0.004). Erythrocyte GPX activity was analyzed in 73 cases and 91 controls. The erythrocyte GPX activity in the cancer group was lower than in the healthy controls. Additionally, we compared the erythrocyte GPX activity in the control group of 90 subjects and found no significant differences by genotype. These findings suggest that individual susceptibility of prostate cancer may be modulated by GPX1 polymorphism and that the combination of genetic factors involved in oxidative response with environmental carcinogens may play an important role in prostate carcinogenesis.

Manganese superoxide dismutase (MnSOD) genetic polymorphism is associated with risk of early-onset prostate cancer.

Prostate cancer continues to be the most frequently diagnosed neoplasm, and the second leading cause of cancer-related mortality in men. Oxidative stress may enhance prostatic carcinogenesis. Manganese superoxide dismutase (MnSOD) is the only known superoxide scavenger in mitochondria. It plays a key role in antioxidant defense as mitochondria are important for oxidative metabolism coupled to the electron transport chain and oxidative phosphorylation and hence, ROS production. A T-->C single nucleotide substitution, resulting in a Val-->Ala change at position 9 (Ala-9Val), which alters the secondary structure of the protein, has been noted to affect transport of MnSOD into the mitochondria. We have determined the MnSOD genotype in 85 prostate cancer cases and 151 control subjects. Ala-9Val polymorphism was determined using real time polymerase chain reaction (PCR) amplification with fluorescently labeled primers. No significant difference was found in prostate cancer susceptibility in the subjects with Ala/Ala and Val/Ala genotype compared with Val/Val genotype (Odds ratio (OR), 1.3; 95% confidence interval (95% CI), 0.69-2.42; p = 0.416). We did not observe an association of the MnSOD genotype or allele frequency between subgroups of cases divided by disease status (aggressive vs. non-aggressive prostate cancer). However, in the analyses stratified by the age at diagnosis we have observed that men homozygous for Ala had a 5.2-fold increased risk of early-onset prostate cancer (under age of 65) compared to men homozygous for Val allele (p = 0.05). These data suggest that Ala/Ala MnSOD genotype in the Macedonian population could have an influence on early onset of prostate cancer, but no impact on the subsequent development of the disease.

Serum aluminium levels in glue-sniffer adolescent and in glue containers.

Glue sniffing is a serious medical problem among teenagers. Various chemical substances such as toluene and benzene containing glues have been reported to be toxic. It has been demonstrated that some toxic metals such as lead are elevated in the blood of solvent-addicted patients. Whereas aluminium is an element that has toxic effects on neurological, hematopoetic system and bone metabolism. We want to determine the serum levels of aluminium in glue-sniffer adolescents in comparison with healthy subjects. In addition, we compared aluminium levels of different commercial glue preparations (i.e. metal and plastic containers), to determine which type of container is better for less aluminium toxicity. We measured serum levels of aluminium in 37 glue-sniffer and 37 healthy subjects using atomic absorption spectrophotometry. The average duration of glue-sniffer was 3.8 +/- 0.8 years. We also measured aluminium levels of 10 commercial glue preparations that seven of them with metal and three with plastic containers. We found that serum levels of aluminium were 63.29 +/- 13.20 ng/ml and 36.7 +/- 8.60 ng/ml in glue-sniffer and in control subjects, respectively (P < 0.001). The average aluminium level in the glues was 8.6 +/- 3.24 ng/g in the preparations with metal containers, whereas 3.03 +/- 0.76 ng/g with plastic containers (P < 0.001). Therefore, to decrease the incidence of aluminium toxicity in glue-sniffers, it may be a good step to market of glue preparations in plastic instead of metal containers.

The role of nickel accumulation and epithelial cell proliferation in orthodontic treatment-induced gingival overgrowth.

The aim of this study was to investigate the role of nickel in orthodontic treatment-induced gingival hyperplasia. The nickel concentration in gingival tissues with and without overgrowth, histopathology of gingival overgrowth, and epithelial cell proliferation response to different nickel concentrations were analysed. Ten patients receiving orthodontic therapy (eight females and two males, mean age 15.4 years) were included in the study. Hyperplastic and healthy gingiva samples were collected from the same patients. The amount of nickel in the gingival tissue samples was analysed using the atomic absorption spectrometry technique. The tissues removed from hyperplastic areas during gingivectomy were also used for histological analysis. To analyse the effect of nickel on epithelial cell proliferation, four different nickel concentrations (0.5, 2, 5, and 10 microg) were incubated with keratinocyte cells for 11 days. Mann-Whitney U-test, analysis of variance, and Tukey's test were used in the statistical analyses. The results did not show any difference in nickel concentration between the study and control gingiva tissue samples, but histological analysis demonstrated an increase in epithelial thickness and a significant increase (P = 0.031, 0.02, 0.02) in epithelial cell proliferation in response to low-dose nickel concentrations, with a toxic response to a higher dose. In the limitations of this study, it is plausible that the effect of a continuing low-dose nickel release to epithelium is the initiating factor of gingival overgrowth induced by orthodontic treatment.

Do N-acetylcystein, beta-glucan, and coenzyme Q10 mollify myocardial ischemia-reperfusion injury?

BACKGROUND: N-acetylcysteine, beta-glucan, and coenzyme Q10 have been shown to have antioxidant and anti-inflammatory effects on reperfusion injury. The aim of our study was to determine and evaluate the effects of these agents on myocardial ischemia-reperfusion injury. METHODS: Forty-four New Zealand white rabbits, all female, weighing 2.4 to 4.1 kg (mean, 3.6 kg) were used in the study. Four study groups of 11 animals were arranged by randomization. The groups were the control group (group C), a group premedicated with coenzyme Q10 (group Q), a group premedicated with beta-glucan (group betaT), and a group premedicated with N-acetylcysteine (group N). After exploration of the heart, a basal myocardial biopsy was taken from the anteroapical left ventricle, and the first blood sampling was done before ischemia. For the ischemia-reperfusion experiments, the major left anterior descending artery was occluded after baseline measurements. After a 45-minute transient ischemic period, the heart was perfused for 120 minutes. After perfusion, the second myocardial biopsy was taken from the anteroapical left ventricle, and the second blood sampling was done. Blood and tissue analysis were performed and evaluated statistically. RESULTS: Baseline and reperfusion levels of glutathione peroxidase, superoxide dismutase, malonyldialdehyde, and nitric oxide changed significantly. While malonyldialdehyde levels increased in group C, they decreased in the other study groups (P =.001). The increases in glutathione peroxidase and superoxide dismutase levels were significant in all groups except group C (P =.0001 and P <.05, respectively). Levels of nitric oxide were found to be decreased in group C, whereas they increased in the other groups (P =.001). CONCLUSION: Antioxidant medication may help in lowering the risk of myocardial ischemia-reperfusion injury. All the medications in our study are shown to have effective roles in preventing ischemia-reperfusion injury to some extent through their antioxidant properties.

Effects of methylprednisolone and hyperbaric oxygen on oxidative status after experimental spinal cord injury: a comparative study in rats.

The effects of hyperbaric oxygen (HBO) therapy or methylprednisolone on the oxidative status were evaluated in experimental spinal cord injury. Clip compression method was used to produce acute spinal cord injury rats. Hyperbaric oxygen was administered twice daily for a total of eight 90 min-sessions at 2.8 atmospheres. Methylprednisolone was first injected with a bolus of 30 mg/kg followed with an infusion rate of 5.4 mg/kg/h for 24 h. Five days after clip application animals were sacrificed and their traumatized spinal cord segment were excised. Tissue levels of thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were evaluated to reflect oxidant/antioxidant status. Non-treated clip-operated animals reflected significantly higher SOD, GSH-Px and TBARS levels that were found to be significantly higher than the sham-operated. Methylprednisolone was not able to lower these levels. HBO administration diminished all measured parameters significantly; however, their levels appeared already to be high when compared with sham animals. According to these results obtained on the 5th day after induction, HBO, but not methylprednisolone, seems to procure prevention against oxidative spinal cord injury.