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ABSTRACT: The aim of this study was to evaluate the therapeutic efficacy of caffeic acid phenethyl ester (CAPE) with an experimental traumatic brain injury (TBI) model in rats. Twenty-four adult male Sprague-Dawley rats were randomly divided into three groups of 8 rats each: control, TBI, and TBI + CAPE treatment. In TBI and TBI + CAPE treatment groups, a cranial impact was delivered to the skull from a height of 7 cm at a point just in front of the coronal suture and over the right hemisphere. Rats were sacrificed at 4 h after the onset of injury. Brain tissues were removed for biochemical and histopathological investigation. To date, no biochemical and histopathological changes of neurodegeneration in the frontal cortex after TBI in rats by CAPE treatment have been reported. The TBI significantly increased tissue malondialdehyde (MDA) levels, and significantly decreased tissue superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities, but not tissue catalase (CAT) activity, when compared with controls. The administration of a single dose of CAPE (10 μmol/kg) 15 min after the trauma has shown protective effect via decreasing significantly the elevated MDA levels and also significantly increasing the reduced antioxidant enzyme (SOD and GPx) activities, except CAT activity. In the TBI group, severe degenerative changes, shrunken cytoplasma and extensively dark picnotic nuclei in neurons, as well as vacuolization indicating tissue edema formation. The morphology of neurons in the CAPE treatment group was well protected. The number of neurons in the trauma alone group was significantly less than that of both the control and TBI +CAPE treatment groups. The caspase 3 immunopositivity was increased in degenerating neurons of the traumatic brain tissue. Treatment of CAPE markedly reduced the immunoreactivity of degenerating neurons. TBI caused severe degenerative changes, shrunken cytoplasma, severely dilated cisternae of endoplasmic reticulum, markedly swollen mitochondria with degenerated cristae and nuclear membrane breakdown with chromatin disorganization in neurons of the frontal cortex. In conclusion, the CAPE treatment might be beneficial in preventing trauma-induced oxidative brain tissue damage, thus showing potential for clinical implications. We believe that further preclinical research into the utility of CAPE may indicate its usefulness as a potential treatment on neurodegeneration after TBI in rats.
Journal of molecular histology 11/2011; 43(1):49-57. · 1.75 Impact Factor
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ABSTRACT: The aim of this study was to evaluate the possible protective effects of caffeic acid phenethyl ester (CAPE) against cholestatic oxidative stress and liver damage in the common bile duct ligated rats. A total of 18 male Sprague-Dawley rats were divided into three groups: control, bile duct ligation (BDL) and BDL + received CAPE; each group contain 6 animals. The rats in CAPE treated groups were given CAPE (10 μmol/kg) once a day intraperitoneally (i.p) for 2 weeks starting just after BDL operation. The changes demonstrating the bile duct proliferation and fibrosis in expanded portal tracts include the extension of proliferated bile ducts into lobules, inflammatory cell infiltration into the widened portal areas were observed in BDL group. Treatment of BDL with CAPE attenuated alterations in liver histology. The proliferating cell nuclear antigen and the activity of TUNEL in the BDL were observed to be reduced with the QE treatment. The application of BDL clearly increased the tissue hydroxyproline (HP) content, malondialdehyde (MDA) levels and decreased the antioxidant enzyme (superoxide dismutase (SOD), glutathione peroxidase (GPx)) activities. CAPE treatment significantly decreased the elevated tissue HP content, and MDA levels and raised the reduced of SOD, and GPx enzymes in the tissues. The data indicate that CAPE attenuates BDL-induced cholestatic liver injury, bile duct proliferation, and fibrosis. The hepatoprotective effect of CAPE is associated with antioxidative potential.
Journal of molecular histology 08/2011; 42(5):451-8. · 1.75 Impact Factor
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ABSTRACT: This study was designed to determine if serum cystatin C (Cys C) levels are affected by metabolic syndome and whether they correlate with lipid peroxidation and total antioxidant status (TAS) in this disorder.
Cases with metabolic syndrome diagnosed according to the ATP III criteria (18 females, 12 males) were compared with healthy control subjects (20 females, 17 males) matched by age and gender. Plasma Cys C, malondialdehyde (MDA), and TAS levels were studied.
Compared with the controls, Cys C and MDA levels were significantly higher (p<0.001 and p<0.001, respectively), whereas TAS was lower (p<0.001) in metabolic syndrome patients. A significant positive correlation between MDA and Cys C (r=0.308, p<0.05) and a significant negative correlation between TAS and Cys C levels (r=-0.358, p<0.01) were found.
As Cys C and MDA levels increased but TAS decreased, Cys C may be an important indicator in the pathogenesis of metabolic syndrome.
Medical science monitor: international medical journal of experimental and clinical research 03/2008; 14(2):CR97-101. · 1.70 Impact Factor
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ABSTRACT: Erdosteine is a mucolytic agent having antioxidant properties through its active metabolites in acute injuries induced by pharmacological drugs. This study was designed to investigate the renoprotective potential of Erdosteine against gentamicin (GM)-induced renal dysfunction by using Technetium-99 m dimercaptosuccinic acid (Tc-99 m DMSA) uptake and scintigraphy in rats. For this purpose, male Wistar rats were randomly allotted into one of the four experimental groups: Control, Erdosteine, GM, and GM + Erdosteine groups. GM and GM + Erdosteine groups received 100 mg/kg GM intramuscularly for 6 days. In addition, Erdosteine and GM + Erdosteine groups received 50 mg/kg Erdosteine orally for 6 days. Renal function tests were assessed by serum blood urea nitrogen (BUN), creatinine levels, as well as scintigraphic and tissue radioactivity measurements with Tc-99 m DMSA. Renal oxidative damage was determined by renal malondialdehyde (MDA) levels, by antioxidant enzyme activities; superoxide dismutase (SOD) and catalase (CAT) and activities of oxidant enzymes; xanthine oxidase (XO) and myeloperoxidase (MPO). GM administration resulted in marked renal lipid peroxidation, increased XO and MPO activities and decreased antioxidant enzyme activities. GM + Erdosteine group significantly had lower MDA levels, higher SOD and CAT activities and lower XO and MPO activities, when compared to GM. Also GM + Erdosteine had lower levels of serum BUN, creatinine and higher renal tissue Tc-99 m DMSA uptake and radioactivity with respect to GM. In conclusion, our results supported a protective role of Erdosteine in nephrotoxicity associated with GM treatment.
Molecular and Cellular Biochemistry 02/2008; 308(1-2):35-42. · 2.06 Impact Factor
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ABSTRACT: The metabolic syndrome is a cluster of cardiovascular risk factors and essential components of metabolic syndrome are hyperglycemia, hypertension, visceral obesity, hypertriglyceridemia and low high-density lipoprotein cholesterol. Oxidative stress plays a critical role in the pathogenesis of metabolic syndrome components and insulin resistance. The aim of this study was to investigate the role of oxidative stress, C-reactive protein and heat shock protein 70 levels in the pathogenesis of this disease.
A total of 36 patients diagnosed with metabolic syndrome and 33 controls were included in the study. Malondialdehyde, carbonyl protein, C-reactive protein and heat shock protein 70 levels and xanthine oxidase and superoxide dismutase activities were measured in the serum of the subjects.
Mean serum malondialdehyde, carbonyl protein, C-reactive protein (p<0.01, p<0.05 and p<0.001, respectively) and xanthine oxidase activity were significantly higher (p<0.01) in serum of the patients than the control group. Superoxide dismutase activity and heat shock protein 70 levels were significantly lower (p<0.01 and p<0.05, respectively) in serum of the patients.
These results suggest that oxidative stress parameters and components of metabolic syndrome are closely related; therefore, significant alterations may occur in the antioxidant and inflammatory status. However, further studies are required to evaluate the possible molecular mechanisms of heat shock protein 70 levels in metabolic syndrome.
Clinical Chemistry and Laboratory Medicine 01/2008; 46(6):785-90. · 2.15 Impact Factor
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ABSTRACT: Occupational exposure to coal dust causes pneumoconiosis and other diseases. Reactive oxygen species (ROS) have been implicated in the pathogenesis of coal dust-induced lung toxicity. In this experimental study, we investigated the oxidant/antioxidant status, nitric oxide (NO) and hydroxyproline (HP) levels in lungs and blood of rats exposed to coal dust in mine ambience. In addition, we also investigated the attenuating effects of erdosteine. At the end of the experiment processes, tissue levels of HP, malondialdehyde (MDA) and NO, as well as the activities of superoxide dismutase, glutathione peroxidase, catalase, xanthine oxidase (XO), myeloperoxidase (MPO) and proinflammatory cytokines (IL-6 and TNF-α) were evaluated in the lung tissues, plasma samples or erythrocytes of rats. Exposure to coal dust resulted in a significant increase in the oxidant parameters (MDA, NO levels, and XO activity) and HP levels, as compared to the controls. A decrease in activities of antioxidant enzymes, and an increase in MPO activity were found in the study group, compared to the controls. Increased NO levels of lung were found in the study groups, that were significantly reduced by erdosteine. Our studies provide evidence that supports the hypothesis for ROS mediated coal workers' pneumoconiosis. Erdosteine may be beneficial in the coal dust-induced lung toxicity via antioxidant and free radical scavenger properties.
Environmental Toxicology and Pharmacology 09/2007; 24(2):106-13. · 1.47 Impact Factor
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ABSTRACT: There has been much evidence in recent years that free oxygen radicals and nitric oxide (NO) may play an important role in the pathophysiology of neuropsychiatric disorders. In this study, we aimed to investigate whether NO, xanthine oxidase (XO), superoxide dismutase (SOD), and adenosine deaminase (ADA) levels are associated with major depression (MD) and to evaluate the impact of antidepressant treatments on NO, SOD, ADA and XO levels in MD.
Thirty-six patients who were diagnosed as MD according to DSM-IV criteria and 20 healthy controls were included. The serum levels of NO, XO, SOD, and ADA were measured by spectrophotometric methods both in patients and controls. Patients were treated with antidepressant drugs for 8 weeks. All patients were assessed by Hamilton Depression Rating Scale (HDRS) both before and after antidepressant treatment.
ADA and XO levels of the patients were significantly higher than the controls. SOD level of the patients was significantly lower than the controls. Although NO levels of the patients were higher than the controls, the difference was not statistically significant. There was no correlation between HDRS and the parameters studied (SOD, ADA, XO, and NO) of the patients. After 8 weeks of antidepressant treatment, ADA and SOD activities were increased, whereas NO and, XO levels decreased significantly.
ADA, XO, and SOD activity may have a pathophysiological role in MD and may predict prognosis of MD. Activity of these enzymes may be used to monitor effects of the antidepressant treatment.
Archives of Medical Research 03/2007; 38(2):247-52. · 1.88 Impact Factor
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ABSTRACT: It is well known that formaldehyde (FA) and reactive oxygen species (ROS) are cytotoxic and potentially carcinogenic. Although the individual effects of these reactants on cells have been investigated, the cytotoxicity exerted by the coexistence of FA and ROS is poorly understood. The present study was carried out to evaluate oxidant/antioxidant status and biochemical changes occurring after chronic formaldehyde toxicity in liver tissue and plasma of rats and protective effect of vitamin E (vit E) against oxidative damage. Eighteen rats were divided into three groups: (1) control rats, (2) rats treated with FA (FAt), and (3) rats treated with FA plus vit E (FAt + vit E) groups. After the treatment, the animals were sacrificed and liver tissues were removed for biochemical investigations. As a result, FA treatment significantly increased the levels of tissue malondialdehyde (MDA), protein carbonyl (PC), nitric oxide (NO) and the activity of xanthine oxidase enzyme (XO). On the other hand, FA exposure led to decrease in superoxide dismutase (SOD) and catalase (CAT) activities in liver tissues compared to control. FA caused significant decreases in total protein (TP) and albumin (ALB) whereas increases in aspartate transaminase (AST), alanine aminotransferase (AST), alkaline phosphatase (ALP) and interleukine-2 (IL-2) levels in plasma. Vit E treatment abolished these changes at a level similar to the control group. It was concluded that vit E treatment might be beneficial in preventing FA-induced liver tissue damage, and therefore have potential for clinical use.
Molecular and Cellular Biochemistry 11/2006; 290(1-2):61-7. · 2.06 Impact Factor
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ABSTRACT: This study was evaluated to investigate the efficacy of Ebselen, which is an organoselenium compound and glutathione peroxidase mimic, on the prevention of stricture development after esophageal caustic injuries in the rat.
Thirty healthy male Wistar albino rats were utilized in this study. The rats were randomly allotted into one of three experimental groups: group A (sham) animals were uninjured. Caustic esophageal burn was created by applying 1 ml of 37.5% NaOH to the distal esophagus. Group B rats were injured but untreated. Group C rats were injured and received Ebselen (10 mg/kg/day) via the oral route. Blood and tissue samples for the biochemical and histopathological analysis were taken all rats at the end (28th day) of the experiment. Oxidative stress is believed to play a role in the pathogenesis of corrosive esophageal burns. To assess changes in the cellular antioxidant defense system, we measured the activities of antioxidant enzymes (such as glutathione peroxidase (GSHPx), superoxide dismutase (SOD), and catalase (CAT)) in esophagus homogenates. We also measured esophageal tissue malondialdehyde (MDA) levels, a marker of lipid peroxidation, to determine whether there is an imbalance between oxidant and antioxidant status. Efficacy of the treatment was assessed by measuring the stenosis index and histopathologic damage score and biochemically by determining tissue hydroxyproline content, lipid peroxidation and antioxidant enzyme levels.
The stenosis index in group B was significantly increased compared with group A and C (P<0.05). The hydroxyproline level was significantly increased in group B compared with group A and C (P<0.05). In group B, the histopathologic damage score was significantly higher than in group C (P<0.05). Treatment with Ebselen decreased tissue hydroxyproline levels, histological damage, and the stenosis index. Caustic esophageal burn increased the lipid peroxidation and also decreased the antioxidant enzyme levels in group B. Ebselen treatments for 28 days decreased the elevated lipid peroxidation and also increased the reduced antioxidant enzyme levels. Live weights of the rats was significantly decreased in group B compared with group A and C (P<0.05).
It is concluded that Ebselen has a preventive effect in the development of fibrosis and decrease the lipid peroxidation, and increase the antioxidant defense system activity in an experimental model of corrosive esophagitis in rats.
International Journal of Pediatric Otorhinolaryngology 01/2006; 70(1):45-52. · 1.17 Impact Factor
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ABSTRACT: The protective effect of black cumin (Nigella sativa = NS) on cadmium-induced oxidative stress was studied in rats. The rats were randomly divided into three experimental groups: A (conrol), B (Cd treated), and C (Cd + NS treated), each containing 10 animals. The Cd-treated and Cd + NS-treated groups were injected subcutaneously daily with CdCl2 dissolved in isotonic NaCl in the amount of 2 mL/kg for 30 d, resulting in a dosage of 0.49 mg Cd/kg/d. The control group was injected with only isotonic NaCl (2 mL/kg/d) throughout the experiment (for 30 d). Three days prior to induction of CdCl2, the Cd + NS-treated group received a daily intraperitoneal injection of 0.2 mL/kg NS until the end of the study. Cd treatment increased significantly the malondialdehyde levels in plasma and erythrocyte (p<0.01 and p<0.05, respectively) and also increased significantly the antioxidant levels (superoxide dismutase, glutathione peroxidase, and catalase) (p<0.05) compared to the control group. Cd + NS treatment decreased significantly the elevated malondialdehyde levels in plasma and erythrocyte (p<0.01 and p<0.05, respectively) and also reduced significantly the enhanced antioxidant levels (p<0.05). Cd treatment increased significantly the activity of iron levels (p<0.05) in the plasma compared to the control group. Cd + NS treatment decreased the activity of iron levels (p<0.05) in the plasma compared to the Cd-treated group. In the control group with no treatment, histology of erythrocytes was normal. In the Cd-treated group, there were remarkable membrane destruction and hemolytic changes in erythrocytes. In the Cd + NS-treated group, these changes were less than in the Cd-treated group. Our results show that N. sativa exerts a protective effect against cadmium toxicity.
Biological Trace Element Research 12/2005; 107(3):277-87. · 1.92 Impact Factor
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ABSTRACT: Nigella sativa oil (NSO), a herbaceous plant, has been used for thousands of years for culinary and medical purposes. This study aimed to investigate the anticonvulsant and antioxidant activities of NSO on pentylenetetrazol (PTZ) kindling seizures in mice. Nigella sativa oil was tested for its ability (i) to suppress the convulsive and lethal effects of PTZ in kindled mice (anti-epileptogenic effect), (ii) to attenuate the PTZ-induced oxidative injury in the brain tissue (antioxidant effect) when given as a pretreatment prior to each PTZ injection during kindling acquisition. Valproate, a major antiepileptic drug, was also tested for comparison. Both substances studied significantly decreased oxidative injury in the mouse brain tissue in comparison with the PTZ-kindling group. Nigella sativa oil was found to be the most effective in preventing PTZ-induced seizures relative to valproate. Nigella sativa oil showed anti-epileptogenic properties as it reduced the sensitivity of kindled mice to the convulsive and lethal effects of PTZ; valproate was ineffective in preventing development of any of these effects. The data obtained support the hypothesis that neuroprotective action of NSO may correlate with its ability to inhibit not only excessive reactive oxygen species (ROS) formation but also seizure generation.
Neuropharmacology 10/2005; 49(4):456-64. · 4.81 Impact Factor
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ABSTRACT: Formaldehyde (FA) can cause severe central nervous system impairment. But, there are only a few studies about biochemical and histopathological changes of frontal cortex and hippocampal tissue caused by FA toxicity. The aim of our study was to investigate these changes occurring after chronic formaldehyde toxicity in frontal cortex and hippocampal tissues, and protective effect of Vitamin E (vit E) against oxidative damage. Eighteen rats were divided into three groups: (1) control, (2) treated with FA (FAt), and (3) treated with FA and vit E (FAt+vit E) groups. After the treatment, the animals were sacrificed and frontal cortex and hippocampal tissues were removed for biochemical and histopathological investigation. FA significantly increased tissue malondialdehyde (MDA) and protein carbonyl (PC) levels and also decreased superoxide dismutase (SOD) and catalase (CAT) enzyme activities in frontal cortex and hippocampal tissue compared to control. Vit E treatment decreased MDA and PC levels and prevented inhibition of SOD and CAT enzymes in the tissues. In the FAt group, the neurons of both tissues became extensively dark and degenerated with picnotic nuclei. The morphology of neurons in FAt+vit E group was protected well, but not as neurons of the control group. The number of neurons in frontal cortex and hippocampal tissue of FAt group was significantly less than both control and FAt+vit E groups. It was concluded that vit E treatment might be beneficial in preventing FA-induced oxidative frontal cortex and hippocampal tissue damage, therefore, shows potential for clinical use.
Journal of Chemical Neuroanatomy 06/2005; 29(3):173-8. · 2.43 Impact Factor
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ABSTRACT: The role of oxygen-derived free radicals has been suggested in genesis of epilepsy and in the post seizure neuronal death. The aim of this study was to investigate whether erdosteine has a preventive effect against epilepsy and postepileptic oxidative stress. The mice (n=27) were divided into three groups: (i) PTZ-induced-epilepsy group (n=9); (ii) PTZ-induced-epilepsy+erdosteine group (n=9); (iii) control group (n=9). The animals were observed for a period of 30 min for latency to first seizure onset, total seizure duration, the number of seizure episodes. Then they were sacrificed and the brains were quickly removed, and frozen for biochemical analysis. Malondialdehyde (MDA), nitric oxide (NO), superoxide dismutase (SOD) and xanthine oxidase (XO) activities were carried out in the brain tissue. The latent period between PTZ induction and seizure are longer in the PTZ+erdosteine group than in PTZ-induced-epilepsy group (P<0.05). Biochemical analyses of brain tissue, revealed a significant increase in the MDA, XO and NO levels in the PTZ group according to erdosteine group. SOD level did not change in this group. While MDA and XO levels are significantly lower, SOD level is significantly higher in the PTZ+erdosteine group compared to PTZ and control groups (P<0.01). The present study demonstrated that erdosteine treatment both may increase latent interval between seizures and may decrease oxidative stress, thus may ameliorate neuronal death in brain during seizures. It may be used as an adjunct therapy in epilepsy.
Brain Research Bulletin 05/2005; 65(6):495-9. · 2.82 Impact Factor
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ABSTRACT: Since overexcitation of excitatory amino acid is an important mechanism in seizure genesis wherein free radicals have recently been suggested to play a critical role, we explored the effects of caffeic acid phenethyl ester (CAPE) administration in pentylenetetrazole (PTZ)-induced seizure in mice. CAPE prevents the oxidative damage in brain tissue induced by PTZ, scavenging reactive oxygen species (ROS). Our results demonstrate that CAPE treatment which prevents free radical production and ameliorates seizure severity may be useful at least as an adjunctive treatment of seizure disorders.
Neurochemical Research 01/2005; 29(12):2287-92. · 2.24 Impact Factor
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ABSTRACT: We aimed to investigate the possible association between Mn-SOD polymorphism in the mitochondrial targeting sequence and asthma.
Alanine or valine polymorphism in the signal peptide of Mn-SOD gene was evaluated using a primer pair to amplify a 107-bp fragment followed by digestion with NgoM IV.
No significant difference in genotype frequencies was found between patients and controls.
These results suggest no major modifying role for the Mn-SOD gene polymorphism in patients with asthma.
Clinical Biochemistry 01/2005; 37(12):1117-20. · 2.08 Impact Factor
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ABSTRACT: The aim of this experimental study was to investigate whether nebivolol has protective effects against neuronal damage induced by spinal cord ischemia/reperfusion (I/R). Twenty-one rabbits were divided into three groups: group I (control, no I/R), group II (only I/R) and group III (I/R+nebivolol). Spinal cord ischemia was induced by clamping the aorta both below the left renal artery and above the aortic bifurcation. Seventy-two hours postoperatively, the motor function of the lower limbs was evaluated in each animal. The animals were sacrificed at 72 h, and histopathological and biochemical analyses were carried out in the lumbar spinal cords. The motor deficit scores in nebivolol group were different from I/R group at 72 h (3.25+/-0.70 vs. 1.75+/-1.28, p=0.01). I/R produced a significant increase in the superoxide dismutase (SOD), xanthine oxidase (XO), adenosine deaminase (ADA) and myeloperoxidase (MPO) activities in spinal cord tissue when compared with control group. Nebivolol treatment prevented the increase of all those enzymes activities produced by I/R. A significant decrease in spinal cord glutathione peroxidase (GSH-Px) level was seen in I/R group and nebivolol treatment prevented the decrement in the spinal cord tissue GSH-Px contents. On the other hand, I/R produced a significant increase in the spinal cord tissue malondialdehyde (MDA) and nitric oxide (NO) contents, this was prevented by nebivolol treatment. In conclusion, this study demonstrates a considerable neuroprotective effect of nebivolol on neurological, biochemical and histopathological status during periods of spinal cord I/R in rabbits.
Progress in Neuro-Psychopharmacology and Biological Psychiatry 12/2004; 28(7):1153-60. · 3.25 Impact Factor
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ABSTRACT: In miners exposed to coal dusts, coal worker's pneumoconiosis (CWP) can occur. The purpose of the present study is to better understand the relations between coal dust exposure and activities of blood plasma antioxidant enzymes, namely, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and lipid peroxidation end product malondialdehyde (MDA) concentration in coal workers with early and low grade simple CWP diagnosed by high resolution computed tomography (HRCT). Forty-three coal workers who had profusions of 0/1-2/2 according to ILO 1980 chest X-ray (CXR) classification, 43 coal workers without CWP (control group 1) and 44 healthy subjects (control group 2) who were randomly selected from the population register or recruited from the hospital staff were enrolled. Coal workers were reevaluated by HRCT (Hosoda-Shida classification) due to its higher sensitivity than standard CXR. Then, blood plasma SOD and GSH-Px activities and MDA plasma levels were measured. CWP was found positive in 46 of 89 coal workers by HRCT evaluation. Profusion 0 (P0, CWP not present), profusion 1 (P1, early CWP) and profusion 2 (P2, low grade CWP) were found in 43, 23 and 19 of patients found to have CWP by HRCT, respectively. We had no worker with profusion 3 (P3). Complicated CWP was shown in four of 46 patients and thesecases were excluded as the study was restricted to early and low-grade pneumoconiosis. In respect to the plasma levels of MDA and plasma activities of SOD and GSH-Px, statistically significant differences were found between CWP cases and control groups (p < 0.01, p < 0.01, p < 0.001 respectively). Statistical differences were also obtained for the plasma activities of SOD and GSH-Px and levels of MDA in relation to HRCT profusions (p < 0.05). In conclusion, these findings suggest an oxidative stress due to increased free radicals and reactive oxygen metabolite production in early stages and low grades of simple CWP diagnosed by HRCT.
International Journal of Hygiene and Environmental Health 11/2004; 207(5):455-62. · 3.81 Impact Factor
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ABSTRACT: Reactive oxygen and nitrogen species have been implicated in the pathogenesis of bleomycin-induced lung fibrosis. The effects of aminoguanidine and erdosteine on the bleomycin-induced lung fibrosis were evaluated in rats. The animals were placed into five groups: Vehicle + vehicle, vehicle + bleomycin (2.5 U/kg), bleomycin + aminoguanidine (200 mg/kg), bleomycin + erdosteine (10 mg/kg), and bleomycin + erdosteine + aminoguanidine. Bleomycin administration resulted in prominent lung fibrosis as measured by lung hydroxyproline content and lung histology, which is completely prevented by erdosteine and aminoguanidine. A strong staining for nitro tyrosine antibody in lung tissue and increased levels of lung NO were found in bleomycin group, that were significantly reduced by aminoguanidine and erdosteine. Aminoguanidine and erdosteine significantly prevented depletion of superoxide dismutase and glutathione peroxidase and elevated myeloperoxidase activities, malondialdehyde level in lung tissue produced by bleomycin. Data presented here indicate that aminoguanidine and erdosteine prevented bleomycin-induced lung fibrosis and that nitric oxide mediated tyrosine nitration of proteins plays a significant role in the pathogenesis of bleomycin-induced lung fibrosis. Also our data suggest that antifibrotic affect of antioxidants may be due to their inhibitory effect on nitric oxide generation in this model.
Nitric Oxide 10/2004; 11(2):156-65. · 3.55 Impact Factor
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ABSTRACT: Because oxidative damage has been known to be involved in inflammatory and autoimmune-mediated tissue destruction, modulation of oxygen free radical production represents a new approach to the treatment of inflammatory and autoimmune diseases. Central nervous system tissue is particularly vulnerable to oxidative damage, suggesting that oxidation plays an important role in the pathogenesis of multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). Caffeic acid phenethyl ester (CAPE), an active component of honeybee propolis, has been determined to have antioxidant, anti-inflammatory, antiviral, and anticancer activities. We have previously reported that CAPE inhibits ischemia-reperfusion injury and oxidative stress in rabbit spinal cord tissue. The present study, therefore, examined effects of CAPE on oxidative tissue damage in EAE in rats. Treatment with CAPE significantly inhibited reactive oxygen species (ROS) production induced by EAE, and ameliorated clinical symptoms in rats. These results suggest that CAPE may exert its anti-inflammatory effect by inhibiting ROS production at the transcriptional level through the suppression of nuclear factor kappaB activation, and by directly inhibiting the catalytic activity of inducible nitric oxide synthase.
Free Radical Biology and Medicine 09/2004; 37(3):386-94. · 5.42 Impact Factor
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ABSTRACT: There is great evidence in recent years that oxygen free radicals play an important role in the pathophysiology of many neuropsychiatric disorders. The present study was performed to assess the changes in red blood cells thiobarbituric acid-reactive substances (TBARS) levels, and superoxide dismutase (SOD), catalase (CAT), adenosine deaminase (ADA) and xanthine oxidase (XO) activities in patients with autism (n = 27) compared to age- and sex-matched normal controls (n = 26). In the autistic group, increased TBARS levels (p < 0.001) and XO (p < 0.001) and SOD (p < 0.001) activity, decreased CAT (p < 0.001) activity and unchanged ADA activity were detected. It is proposed that antioxidant status may be changed in autism and this new situation may induce lipid peroxidation. These findings indicated a possible role of increased oxidative stress and altered enzymatic antioxidants, both of which may be relevant to the pathophysiology of autism.
European Archives of Psychiatry and Clinical Neuroscience 06/2004; 254(3):143-7. · 3.49 Impact Factor
