Effect Of Antioxidant Treatment Research Articles

Effect of antioxidant treatment on spinal GABA neurons in a neuropathic pain model in the mouse

One feature of neuropathic pain is a reduced spinal gamma-aminobutyric acid (GABA)-ergic inhibitory function. However, the mechanisms behind this attenuation remain to be elucidated. This study investigated the involvement of reactive oxygen species in the spinal GABA neuron loss and reduced GABA neuron excitability in spinal nerve ligation (SNL) model of neuropathic pain in mice. The importance of spinal GABAergic inhibition in neuropathic pain was tested by examining the effects of intrathecally administered GABA receptor agonists and antagonists in SNL and naïve mice, respectively. The effects of SNL and antioxidant treatment on GABA neuron loss and functional changes were examined in transgenic GAD67-enhanced green fluorescent protein positive (EGFP+) mice. GABA receptor agonists transiently reversed mechanical hypersensitivity of the hind paw in SNL mice. On the other hand, GABA receptor antagonists made naïve mice mechanically hypersensitive. Stereological analysis showed that the numbers of enhanced green fluorescent protein positive (EGFP+) GABA neurons were significantly decreased in the lateral superficial laminae (I–II) on the ipsilateral L5 spinal cord after SNL. Repeated antioxidant treatments significantly reduced the pain behaviors and prevented the reduction in EGFP+ GABA neurons. The response rate of the tonic firing GABA neurons recorded from SNL mice increased with antioxidant treatment, whereas no change was seen in those recorded from naïve mice, which suggested that oxidative stress impaired some spinal GABA neuron activity in the neuropathic pain condition. Together the data suggest that neuropathic pain, at least partially, is attributed to oxidative stress, which induces both a GABA neuron loss and dysfunction of surviving GABA neurons.

Effect of Antioxidant Treatment during Parthenogenetic Activation Procedure on the Reactive Oxygen Species Levels and Development of the Porcine Parthenogenetic Embryos

Effect of Antioxidant Treatment during Parthenogenetic Activation Procedure on the Reactive Oxygen Species Levels and Development of the Porcine Parthenogenetic Embryos

Abstract WMP33: Synergistic Effect Of Dehydroascorbic Acid, Glutathione And Melatonin On Brain Endothelium Protection In Ischemic Rats

Introduction: Stroke (cerebral ischemia) is the second leading cause of death worldwide. Antioxidant strategies have been used successfully to diminish ischemic cerebral tissue damage in animals but the utility of a pharmacological agent as a clinically relevant therapeutic strategy may depend, in part, on its ability to cross the BBB. To optimally improve the therapeutic window this present study investigated whether the intravenous administration of dehydroascorbic acid (DHA), glutathione (GSH) and melatonin potentially elevates the level of cerebroprotection. Methods: Male rats were subjected to 60 min middle carotid artery occlusion (MCAO) using an intraluminal filament. Single dose of DHA (100mg/kg/ml), glutathione (500 mg/kg/ml) and melatonin (10 mg/kg/ml) was administered intravenously immediately after MCAO at a time interval of 5 min each. Western blotting was performed to delineate the effects of antioxidant treatment on the proliferation and neurogenesis in the ischemic region. We also examined the neuroprotective dosing regimen of triple antioxidants treatment and its effects on the functional outcomes following cerebral ischemia. Results: Triple antioxidant treatment significantly reduced the infarct volume and improved behavioral performance evidenced by TTC staining and neurological test score results. The significant increase in the claudin-5 and occludine expressions in the antioxidant treatment group depicts the preservation of blood-brain barrier (BBB) integrity via a reduction in the enormous amount of stroke-induced free radical production. Moreover, treatment with triple antioxidants after stroke dramatically enhanced endogenous neurogenesis (doublecortin positive) and cell proliferation (ki67 positive) in the peri-infarct regions. These outcomes were in the favor of rescuing the damaged neurons at the injury site defining the neuroprotective effects of triple antioxidants treatment following experimental stroke. Conclusion: The results from this study demonstrate that triple antioxidant treatment prevents brain edema, BBB hyperpermeability, and tight junction proteins disruption, possibly through its antioxidant effects thereby offering optimal neuroprotection in rat MCAO model.

Antioxidant Treatment Regulates the Humoral Immune Response during Acute Viral Infection

Generation of reactive oxygen intermediates (ROI) following antigen receptor ligation is critical to promote cellular responses. However, the effect of antioxidant treatment on humoral immunity during a viral infection was unknown. Mice were infected with lymphocytic choriomeningitis virus (LCMV) and treated with Mn(III)tetrakis(4-benzoic acid)porphyrin chloride (MnTBAP), a superoxide dismutase mimetic, from days 0 to 8 postinfection. On day 8, at the peak of the splenic response in vehicle-treated mice, virus-specific IgM and IgG antibody-secreting cells (ASC) were decreased 22- and 457-fold in MnTBAP-treated animals. By day 38, LCMV-specific IgG ASC were decreased 5-fold in the bone marrow of drug-treated mice, and virus-specific antibodies were of lower affinity. Interestingly, antioxidant treatment had no effect on the number of LCMV-specific IgG memory B cells. In addition to decreases in ASC, MnTBAP treatment decreased the number of functional virus-specific CD4(+) T cells. The decreased numbers of ASC observed on day 8 in drug-treated mice were due to a combination of Bim-mediated cell death and decreased proliferation. Together, these data demonstrate that ROI regulate antiviral ASC expansion and have important implications for understanding the effects of antioxidants on humoral immunity during infection and immunization.

Antioxidant Treatment Promotes Prostate Epithelial Proliferation in Nkx3.1 Mutant Mice

Discordant results in preclinical and clinical trials have raised questions over the effectiveness of antioxidants in prostate cancer chemoprevention. Results from the large-scale Selenium and Vitamin E Cancer Prevention Trial (SELECT) showed that antioxidants failed to prevent, and in some cases promoted, prostate cancer formation in men without a history of the disease. One possible explanation for these alarming results is the notion that the effects of antioxidant treatment on the prostate are modified by specific, intrinsic genetic risk factors, causing some men to respond negatively to antioxidant treatment. Loss of expression of the homeobox transcription factor NKX3.1 in the prostate is frequently associated with human prostate cancer. Nkx3.1 mutant mice display prostatic hyperplasia and dysplasia and are used as a model of the early stages of prostate cancer initiation. While the mechanisms by which Nkx3.1 loss promotes prostate tumorigenicity are not completely understood, published data have suggested that elevated reactive oxygen species (ROS) associated with Nkx3.1 loss may be a causative factor. Here we have tested this hypothesis by treating Nkx3.1 mutant mice with the antioxidant N-acetylcysteine (NAC) for 13 weeks post-weaning. Surprisingly, while NAC treatment decreased ROS levels in Nkx3.1 mutant mouse prostates, it failed to reduce prostatic epithelial hyperplasia/dysplasia. Rather, NAC treatment increased epithelial cell proliferation and promoted the expression of a pro-proliferative gene signature. These results show that ROS do not promote proliferation in the Nkx3.1-null prostate, but instead inhibit proliferation, suggesting that antioxidant treatment may encourage prostate epithelial cell proliferation early in prostate tumorigenesis. Our findings provide new insight that may help explain the increased prostate cancer risk observed with vitamin E treatment in the SELECT trial and emphasize the need for preclinical studies using accurate models of cancer.

Protective Effect of N-acetylcysteine on Liver Damage During Chronic Intrauterine Hypoxia in Fetal Guinea Pig

Chronic exposure to hypoxia during pregnancy generates a stressed intrauterine environment that may lead to fetal organ damage. The objectives of the study are (1) to quantify the effect of chronic hypoxia in the generation of oxidative stress in fetal guinea pig liver and (2) to test the protective effect of antioxidant treatment in hypoxic fetal liver injury. Pregnant guinea pigs were exposed to either normoxia (NMX) or 10.5% O(2) (HPX, 14 days) prior to term (65 days) and orally administered N-acetylcysteine ([NAC] 10 days). Near-term anesthetized fetuses were excised and livers examined by histology and assayed for malondialdehyde (MDA) and DNA fragmentation. Chronic HPX increased erythroid precursors, MDA (NMX vs HPX; 1.26 ± 0.07 vs 1.78 ± 0.07 nmol/mg protein; P < .001, mean ± standard error of the mean [SEM]) and DNA fragmentation levels in fetal livers (0.069 ± 0.01 vs 0.11 ± 0.005 OD/mg protein; P < .01). N-acetylcysteine inhibited erythroid aggregation and reduced (P < .05) both MDA and DNA fragmentation of fetal HPX livers. Thus, chronic intrauterine hypoxia generates cell and nuclear damage in the fetal guinea pig liver. Maternal NAC inhibited the adverse effects of fetal liver damage suggestive of oxidative stress. The suppressive effect of maternal NAC may implicate the protective role of antioxidants in the prevention of liver injury in the hypoxic fetus.

Antioxidant treatment prevents cognitive impairment and oxidative damage in pneumococcal meningitis survivor rats

Pneumococcal meningitis is associated with the highest fatality case ratios in the world. Most of patients that survive present neurologic sequelae at later times as well as biochemicals alterations such as oxidative stress in both earlier and later times after central nervous system infection. In this context, we evaluated the effect of antioxidant treatment on memory and oxidative parameters in the hippocampus of meningitis survivor rats 10days after infection. To this aim, the animals underwent a magna cistern tap receiving either 10 μL sterile saline as a placebo or an equivalent volume of a Streptococcus pneumoniae suspension at the concentration 5x10(9) cfu/mL. The animals submitted to meningitis were divided into the following groups: 1) treated with antibiotic, 2) treated with basic support plus N-acetylcysteine, 3) treated with basic support plus deferoxamine, 4) treated with basic support plus N-acetylcysteine and deferoxamine, or 5) treated with N-acetylcysteine plus deferoxamine. Ten days after meningitis, the animals underwent inhibitory avoidance and habituation to an open field tasks and, immediately after, were assessed for oxidative damage in the hippocampus and cortex. The meningitis group showed significantly decreased performance in latency retention compared with the sham group in the inhibitory avoidance task. In the open-field task, the meningitis group presented memory impairment after meningitis. All these memory impairments were prevented by N-acetylcysteine plus deferoxamine with or without basic support and its isolate use. In addition, there was an increase of lipid phosphorylation in cortex and hippocampus and all the combined antioxidants attenuated lipid phosphorylation in both structures. On the other hand, there was an increase of protein phosphorylation in cortex and N-acetylcysteine plus deferoxamine with or without basic support prevented it. Thus, we hypothesize that oxidative stress may be related to cognitive impairment in pneumococcal meningitis.

DNA damage in an animal model of maple syrup urine disease

Maple syrup urine disease is an inborn error of metabolism caused by a severe deficiency of the branched chain alpha-ketoacid dehydrogenase complex. Neurological dysfunction is a common finding in patients with maple syrup urine disease. However, the mechanisms underlying the neuropathology of brain damage in this disorder are poorly understood. In this study, we investigated whether acute or chronic administration of a branched chain amino acid pool (leucine, isoleucine and valine) causes transient DNA damage, as determined by the alkaline comet assay, in the brain and blood of rats during development and whether antioxidant treatment prevented the alterations induced by branched chain amino acids. Our results showed that the acute administration of branched chain amino acids increased the DNA damage frequency and damage index in the hippocampus. However, the chronic administration of branched chain amino acids increased the DNA damage frequency and damage index in both the hippocampus and the striatum, and the antioxidant treatment was able to prevent DNA damage in the hippocampus and striatum. The present study demonstrated that metabolite accumulation in MSUD induces DNA damage in the hippocampus and striatum and that it may be implicated in the neuropathology observed in the affected patients. We demonstrated that the effect of antioxidant treatment (N-acetylcysteine plus deferoxamine) prevented DNA damage, suggesting the involvement of oxidative stress in DNA damage.

Effect of Antioxidant Treatment on Fibrogenesis in Rats with Carbon Tetrachloride-Induced Cirrhosis

Aim. This study aimed to assess the antioxidant activity of quercetin (Q) in an experimental model of cirrhosis induced by CCl4 inhalation. Materials and Methods. We used 25 male Wistar rats (250 g) that were divided into 3 groups: control (CO), CCl4, and CCl4 + Q. The rats were subjected to CCl4 inhalation (2x/week) for 16 weeks, and they received phenobarbital in their drinking water at a dose of 0.3 g/dL as a P450 enzyme inducer. Q (50 mg/Kg) was initiated intraperitoneally at 10 weeks of inhalation and lasted until the end of the experiment. Statistical analysis was by ANOVA Student Newman-Keuls (mean ± SEM), and differences were considered statistically significant when P < 0.05. Results. After treatment with quercetin, we observed an improvement in liver complications, decreased fibrosis, as analyzed by picrosirius for the quantification of collagen, and decreased levels of matrix metalloproteinase 2 (MMP-2) compared with the CCl4 group. It also reduced oxidative stress, as confirmed by the decrease of substances reacting to thiobarbituric acid (TBARS), the increased activity of antioxidant enzymes, and the reduced glutathione ratio and glutathione disulfide (GSH/GSSG). Conclusion. We suggest that the use of quercetin might be promising as an antioxidant therapy in liver fibrosis.

Efecto de la administración de un complejo de antioxidantes en pacientes afectos de astenoteratozoospermia idiopática

IntroductionThe male factor is seen in almost 50% of the couples attending a reproductive clinic, and may be a result of a decrease in sperm count (oligozoospermia) or in sperm quality due to mobility defects (asthenozoospermia) or in its morphology (teratozoospermia). There are several studies that related the these sperm quality defects with the presence of sperm DNA fragmentation and suggest the possible beneficial effect of antioxidant treatments, although there is wide disparity in the results obtained. ObjectivesWe have studied the effect of the administration of an antioxidant complex (Androferti® Laboratory Q Pharma) in patients with idiopathic asthenoteratozoospermia in order to contribute to the clarification of the possible beneficial effect of the empirical administration of antioxidants, in the present work. Patients and methodsA total of 69 males in whom the antioxidant treatment was administered at a day dose of 1.5g for 3 months were included. After completing the treatment, significant improvement was detected in sperm mobility (global mobility a+b improved from 22.04% to 28.95%; p=0.001) and sperm morphology (the normal forms increased from 9.86% to 14.78%, p<0.001). DiscussionNumerous publications have reported the beneficial effects of administering antioxidant substances on sperm DNA fragmentation. These effects could be translated into an improvement in semen and embryo quality, in case of pregnancy. Our study is in line with these finding, showing an improvement in most of the seminal parameters resulting from the administration of L-carnitine in association with other antioxidants, a treatment that appears to be particularly effective in younger patients. ConclusionsOur results confirm the beneficial effect of the administration of an antioxidant complex in patients with idiopathic asthenoteratozoospermia, this improving their sperm quality, consequently favoring the desired pregnancy.

Effects of antioxidants, plant growth regulators and wounding on phenolic compound excretion during micropropagation of Strelitzia reginae

The aim of this study was to determine the effects of antioxidant treatments, plant growth regulators (PGRs) and explants wounding in tissue culture involving Strelitzia reginae on total phenol exudation. Results showed that various 1-naphthalene acetic acid (NAA) and 6-benzylaminopurine (BAP) concentrations significantly affected phenolic exudation. The media containing the highest plant growth regulators concentration (that is, 0.5 mg L⁻¹ NAA and 6 mg L⁻¹ BAP) resulted in the highest phenol content. Whereas, the control (the treatment free of plant growth regulators), contained the lowest phenol content. Activated charcoal (AC) was found to significantly reduce the total phenol content of media by 53%, compared with ascorbic acid (AA). Furthermore, the wounding of explants significantly increased phenolic exudation. Interactions between the higher 1-naphthalene acetic acid and 6-benzylaminopurine concentrations and ascorbic acid significantly increased the total phenol content of media. A similar result was achieved in interactions between higher plant growth regulators concentrations and the wounding of explants. Interactions between antioxidants, wounding treatments and plant growth regulators concentrations resulted in activated charcoal significantly reducing the total phenol content in all plant growth regulators concentrations in both wounded and unwounded explants. Key words: Total phenol exudation, browning, wounding, activated charcoal, ascorbic acid, 6-benzylaminopurine (BAP), NAA - 1-naphthalene acetic acid (NAA).

Effect of phenolic acids on functions of rat aorta, vas deferens and on metabolic changes in streptozotocin-induced diabetes

Objectives:This study aimed to investigate the effects of antioxidant treatment on streptozotocin (STZ)-induced diabetic metabolic and smooth muscle (SM) complications in rats.Materials and Methods:Threeweeks after STZ injection (i.v.), vehicle, p-OH benzoic (p-OHBA), protocatechic (PA) and gallic acids (GA) were separately administered (10 mg/kg each, i.p.) to the rats everyday for 3 weeks. Metabolic functions were observedregularly. The rats in all groups were sacrificed andaorta and Vas deferens were dissected. Theresponses of isolated organs to agonists (acetylcholine and phenylephrine) were recorded.Results:Protocatechic acid prevented increase in food consumption and feces output significantly. The responses of isolated organs to agonists increased in the STZ-diabetic rats. The test drugs either prevented, exacerbated or didnot affect the SMchanges in the STZ-diabetic rats.Conclusions:It was concluded that p-OHBA, PA and GA may cause effects independently of their antioxidant effect and/or of diabeticcomplications. They may exhibit pro-oxidant activities in the experimental conditions applied.

Selective degeneration of synapses in the dorsal cochlear nucleus of chinchilla following acoustic trauma and effects of antioxidant treatment

The purpose of this study was to reveal synaptic plasticity within the dorsal cochlear nucleus (DCN) as a result of noise trauma and to determine whether effective antioxidant protection to the cochlea can also impact plasticity changes in the DCN. Expression of synapse activity markers (synaptophysin and precerebellin) and ultrastructure of synapses were examined in the DCN of chinchilla 10 days after a 105 dB SPL octave-band noise (centered at 4 kHz, 6 h) exposure. One group of chinchilla was treated with a combination of antioxidants (4-hydroxy phenyl N-tert-butylnitrone, N-acetyl-l-cysteine and acetyl-l-carnitine) beginning 4 h after noise exposure. Down-regulated synaptophysin and precerebellin expression, as well as selective degeneration of nerve terminals surrounding cartwheel cells and their primary dendrites were found in the fusiform soma layer in the middle region of the DCN of the noise exposure group. Antioxidant treatment significantly reduced synaptic plasticity changes surrounding cartwheel cells. Results of this study provide further evidence of acoustic trauma-induced neural plasticity in the DCN and suggest that loss of input to cartwheel cells may be an important factor contributing to the emergence of hyperactivity in the DCN after noise exposure. Results further suggest that early antioxidant treatment for acoustic trauma not only rescues cochlear hair cells, but also has impact on central auditory structures.

Investigating the Effect of Antioxidant Treatment on the Protective Effect of Preconditioning in Anesthetized Rabbits

Reactive oxygen and nitrogen species are critical in preconditioning (PC). We sought to determine the effect of N-2-mercaptopropionyl glycine (MPG) on infarct size and on the oxidative status. Rabbits were exposed to 30-minute regional ischemia of the heart, which was followed by 3-hour reperfusion: (1) a control group without further intervention, (2) a PC1 group that was subjected to one cycle of PC, (3) a PC4 group that was subjected to 4 cycles of PC, (4) an MPG group that was treated with MPG for 60 minutes, starting 10 minutes before reperfusion, (5) MPG-PC1, and (6) the MPG-PC4 groups that were treated with the same dose of MPG and with 1 or 4 cycles of PC, respectively. Blood samples were drawn and collected for metabonomic analysis. In another series of experiments, 6 groups respective to the described ones were subjected to 30-minute regional ischemia of the heart and 20 minutes of reperfusion, after which pieces of heart tissue were quickly excised for malondialdehyde, nitrotyrosine, and glutathione content assessment. All PC and MPG groups developed smaller infarct size compared with control (16.5% ± 3.9%, 13.7% ± 3.1%, 18.6% ± 5.0%, 9.7% ± 2.0%, 15.0% ± 2.8% vs. 48.05% ± 7.2%; P < 0.05). MPG did not prevent lipid peroxidation and nitrotyrosine formation but enhanced the glutathione content. PC and MPG induced similar nuclear magnetic resonance changes. Long MPG infusion reduces the infarct size without abolishing the effect of PC, providing novel insights into the activity of MPG in PC.

Animal age, packaging and antioxidant treatment effects on sensory characteristics of beef Infraspinatus muscle

SummaryThe objective was to determine effects of animal age, packaging and antioxidant treatment on colour and sensory characteristics of infraspinatus (IF) muscle of the beef shoulder (chuck). IF steaks from older animals (USDA commercial grade; &gt;42 months age) had higher (P &lt; 0.05) muscle pigment levels and redness than young select grade steaks. Steaks in 80% oxygen‐modified atmospheric packaging (O2‐MAP) had higher (P &lt; 0.05) thiobarbituric acid values than steaks in 0.4% carbon monoxide‐modified atmospheric packaging (CO‐MAP) (1.30 and 0.41, respectively). Descriptive rancidity scores were lowest for select grade steaks in CO‐MAP (1.03). Beef flavour intensity was higher (P &lt; 0.05) for steaks in CO‐MAP, even though steaks were held longer (21 days) before cooking. Sour/grassy scores were highest (P &lt; 0.05) for steaks in polyvinyl‐chloride film (5 days storage), and lowest (P &lt; 0.05) for steaks in CO‐MAP, indicating that sour/grassy flavour dissipated at longer storage times.

α-Lipoic acid normalizes nociceptive neuronal activity at the spinal cord of diabetic rats

To evaluate the effects of antioxidant treatment of streptozotocin (STZ)-diabetic rats with α-lipoic acid (α-LA) in neuronal and microglial activation at the spinal cord, an important relay station of nociceptive transmission. Because of the role of the potassium chloride co-transporter 2 (KCC2) in neuronal activation at the spinal cord and the influence of microglia in KCC2 expression, we also evaluated the effects of α-LA in KCC2 expression at the spinal cord. Four weeks after STZ injection, the rats received daily intraperitoneal injections of α-LA (100 mg/kg), during 2 weeks. Mechanical nociception was evaluated before and after α-LA treatment. Spinal cords were immunoreacted against 8-OH-dG (marker of oxidative stress damage), Fos (marker of neuronal activation) and CD11b (marker of microglia). KCC2 expression was evaluated by immunohistochemistry and western blotting. Treatment with α-LA decreased the 8-OH-dG and Fos expressions to controls' levels, but did not affect CD11b. Treatment with α-LA alleviated mechanical hyperalgesia and partially corrected KCC2 expression. This study shows that neuronal hyperactivity at the spinal cord of STZ-diabetic rats can be corrected by α-LA, which may account for alleviation of mechanical hyperalgesia. These effects are probably partially mediated by KCC2, but are independent from microglia.

Strongyloides ratti:transplantation of adults recovered from the small intestine at different days after infection into the colon of naive and infection-primed Wistar rats, and the effect of antioxidant treatment on large intestinal parasitism

Strongyloides ratti (Nagoya strain) is unique in that a portion of adults parasitizing the small intestine withstands 'worm expulsion', which starts at around day 8 post-infection (p.i.) by host immunity, and establishes in the large intestine after day 19 p.i. To investigate the mechanism, adults obtained from the small intestine at day 7 or 19 p.i. were transplanted into the colon of infection-primed immune rats. Adults obtained at day 7 p.i. were rejected quickly, whereas those obtained at day 19 p.i. could establish infection. Moreover, the body length and the number of intrauterine eggs increased in the large intestine. In a separate experiment, large intestinal parasitism was abolished by the treatment of host rats with an anti-oxidant, butylated hydroxyanisole. These results indicate that small intestinal adults between days 7 and 19 p.i. acquired the ability to parasitize the large intestine of immune rats, and that free radicals produced by the host may have played a significant role in the process.

Effect of antioxidant treatment on the shear bond strength of composite resin to bleached enamel

Introduction. This study examined the antioxidant treatment on the shear bond strength of composite resin to enamel after bleaching with two different bleaching systems. Materials and methods. Seventy flat enamel surfaces were prepared from freshly extracted human molars using a low speed diamond saw. Then the specimens were divided into seven random groups (n = 10) to apply different procedures; namely, bleaching with White Smile and bonding with composite resin (G1), bleaching with White Smile, treatment with ascorbic acid and bonding with composite resin (G2), bleaching with White Smile, immersing in artificial saliva for 2 weeks and bonding with composite resin (G3), bleaching with Opalesence and bonding with composite resin (G4), bleaching with Opalesence, treatment with ascorbic acid and bonding with composite resin (G5) and bleaching with Opalesence, immersing in artificial saliva for 2 weeks and bonding with composite resin (G6). Another group was used as a control group. Shear bond test was performed on all specimens and data were analyzed using one way ANOVA and Bonferroni's test (p < 0.05). Results. Bond strengths of bleached specimens were significantly lower than those of non-bleached specimens. No statistical difference was found in bond strength between the bleached and non-bleached groups when the antioxidant treatment was carried out. Conclusion. Ten per cent ascorbic acid treatment was found to be an effective method to reverse the compromised bond strength.

Effect of 10% sodium ascorbate hydrogel and delayed bonding on shear bond strength of composite resin and resin-modified glass ionomer to bleached enamel

Objective:The aim of this study was to comparatively investigate the neutralizing effect of antioxidant treatment and delayed bonding after bleaching with hydrogen peroxide on the shear bond strength of a composite resin (CR) and resin-modified glass ionomer (RmGI) to enamel.Materials and Methods:Ninety-six freshly extracted human 3rd molars with flat enamel surfaces were divided into six experimental groups (n=12/group) and two control groups (n=12/group). After initial preparation, specimens in Groups 1 and 5 (control groups) were not bleached and the buccal enamel surface of specimens were bonded immediately with CR and RmGI. The samples of the remaining groups were all bleached six hours a day for seven days consecutively. Immediately after bleaching, groups two and six specimens were bonded with CR and RmGI. Groups 3 and 7 specimens were immersed in distilled water at 37°C for 7 days and the specimens in Groups 4 and 8 were treated with 10% sodium ascorbate as an antioxidant agent after bleaching. Specimens in Groups 3 and 4 were bonded with CR and Groups 7 and 8 specimens were bonded with RmGI immediately. After specimens were bonded, the shear bond strength (SBS) was measured. The SBS data analyses were subjected to one-way analysis of variance (ANOVA) followed by Tukey test for comparison of specific mean values.Results:The mean SBS value in Group 2 (immediately bonded with CR after bleaching) was significantly lower than other CR groups (P=0.045). RmGI did not bond to buccal enamel surface of specimens in group 6. There was no significant difference between other groups bonded with RmGI (P>0.05).Conclusions:Applying 10% sodium ascorbate hydrogel and one week delay before bonding resulted in reversal of reduced bond strength of CR and RmGI to bleached enamel.

Glycoxidative stress and cardiovascular complications in experimentally-induced diabetes: effects of antioxidant treatment.

Diabetes mellitus (DM) is a common metabolic disease, representing a serious risk factor for the development of cardiovascular complications, such as coronary heart disease, peripheral arterial disease and hypertension. Oxidative stress (OS), a feature of DM, is defined as an increase in the steady-state levels of reactive oxygen species (ROS) and may occur as a result of increased free radical generation and/or decreased anti-oxidant defense mechanisms. Increasing evidence indicates that hyperglycemia is the initiating cause of the tissue damage in DM, either through repeated acute changes in cellular glucose metabolism, or through long-term accumulation of glycated biomolecules and advanced glycation end products (AGEs). AGEs are formed by the Maillard process, a non-enzymatic reaction between ketone group of the glucose molecule or aldehydes and the amino groups of proteins that contributes to the aging of proteins and to the pathological complications of DM. In the presence of uncontrolled hyperglycemia, the increased formation of AGEs and lipid peroxidation products exacerbate intracellular OS and results in a loss of molecular integrity, disruption in cellular signaling and homeostasis, followed by inflammation and tissue injury such as endothelium dysfunction, arterial stiffening and microvascular complications. In addition to increased AGE production, there is also evidence of multiple pathways elevating ROS generation in DM, including; enhanced glucose auto-oxidation, increased mitochondrial superoxide production, protein kinase C-dependent activation of NADPH oxidase, uncoupled endothelial nitric oxide synthase (eNOS) activity, increased substrate flux through the polyol pathway and stimulation of eicosanoid metabolism. It is, therefore, not surprising that the correction of these variables can result in amelioration of diabetic cardiovascular abnormalities. A linking element between these phenomena is cellular redox imbalance due to glycoxidative stress (GOS). Thus, recent interest has focused on strategies to prevent, reverse or retard GOS in order to modify the natural history of diabetic cardiovascular abnormalities. This review will discuss the links between GOS and diabetes-induced cardiovascular disorders and the effect of antioxidant therapy on altering the development of cardiovascular complications in diabetic animal models.