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1.
Int. arch. otorhinolaryngol. (Impr.) ; 24(1): 47-52, Jan.-Mar. 2020. graf
Article in English | LILACS | ID: biblio-1090559

ABSTRACT

Abstract Introduction Cisplatin damages the auditory system and is related to the generation of free radicals. Glutathione peroxidase is an endogenous free radicals remover. Objective To investigate the mechanisms involved in otoprotection by N-acetylcys- teine through the expression of glutathione peroxidase in outer hair cells from rats treated with cisplatin. Methods Male Wistar rats were intraperitoneally injected with cisplatin (8 mg/Kg) and/or received oral administration by gavage of N-acetylcysteine (300 mg/Kg) for 3 consecutive days. On the 4th day, the animals were euthanized and beheaded. The tympanic bullae were removed and prepared for scanning electron microscopy and Results Among the groups exposed to ototoxic doses of cisplatin, there was an increase in glutathione peroxidase immunostaining in two groups, the one exposed to cisplatin alone, and the group exposed to both cisplatin and N-acetylcysteine. Conclusion The expression of glutathione peroxidase in the outer hair cells of rats exposed to cisplatin showed the synthesis of this enzyme under cellular toxicity conditions.


Subject(s)
Animals , Male , Acetylcysteine/therapeutic use , Free Radical Scavengers/therapeutic use , Cisplatin/toxicity , Oxidative Stress/drug effects , Antineoplastic Agents/toxicity , Acetylcysteine/metabolism , Acetylcysteine/pharmacology , Microscopy, Electron, Scanning , Evoked Potentials, Auditory, Brain Stem , Free Radical Scavengers/metabolism , Free Radical Scavengers/pharmacology , Fluorescent Antibody Technique , Cisplatin/therapeutic use , Rats, Wistar , Cochlea/anatomy & histology , Cochlea/drug effects , Free Radicals , Glutathione Peroxidase/metabolism , Hearing Loss, Sensorineural/prevention & control
2.
Acta cir. bras ; 34(7): e201900706, 2019. tab, graf
Article in English | LILACS | ID: biblio-1038113

ABSTRACT

Abstract Purpose: To investigate the protective roles of pyracantha fortune fruit extract (PFE) on acute renal toxicity induced by cadmium chloride (CdCl2) in rats. Methods: Rats were pretreated with PFE and consecutively injected with CdCl2 (6.5 mg/kg) for 5 days. Results: The concentration of Cd, kidney weight, malondialdehyde (MDA), and nitric oxide (NO) production were remarkably increased in CdCl2 group as well as the levels of plasma uric acid, urea, and creatinine (P < 0.001). However, the body weight and glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione peroxidase (GR) levels were markedly reduced by CdCl2 treatment (P < 0.001). Histological manifestations of renal tissue showed severely adverse changes. Moreover, CdCl2 treatment significantly decreased the B-cell lymphoma-2 (Bcl-2) expression while increased the Bcl-2-Associated X Protein (Bax), tumor necrosis factor-α (TNF-α) expression (P < 0.001). Additionally, the expression of Nrf2/Keap 1 related proteins Keap-1 gained a significant increase (P < 0.001), whereas the Nrf2, HO-1, γ-GCS, GSH-Px and NQO1 expression decreased by CdCl2 treatment (P < 0.05). These rats were pretreated with PFE to improve the changes caused by CdCl2 treatment. Conclusion: PFE could protect the kidney against acute renal toxicity induced by CdCl2.


Subject(s)
Animals , Male , Rats , Plant Extracts/pharmacology , Cadmium Chloride/toxicity , Pyracantha/chemistry , Chemical and Drug Induced Liver Injury/prevention & control , Kidney/drug effects , Antioxidants/pharmacology , Superoxide Dismutase/metabolism , Catalase/metabolism , Oxidative Stress/drug effects , Disease Models, Animal , Fruit/chemistry , Glutathione/metabolism , Glutathione Peroxidase/metabolism , Kidney/pathology
3.
Int. j. morphol ; 36(4): 1310-1315, Dec. 2018. tab, graf
Article in English | LILACS | ID: biblio-975701

ABSTRACT

Exposure to normobaric hyperoxia (NH) is known to increase the production of reactive oxygen species (ROS) by mitochondria. The present study was designed to examine mitochondrial ultrastructure morphological changes in the cortical brainin relation to glutathione peroxidase (GPX) activity and free radicals (FR) productions in brain tissue during hyperoxia exposure. The experimental groups were exposed to NH for 24 and 48 h continuously. Following the exposure periods, animals were sacrificed and cortical tissues were divided randomly into two parts; the first part was processed for the ultrastructural examination and the second was homogenized for GPX and FR determinations. Analysis of variance (ANOVA) showed that the main effects of O2 exposure periods were significant (p<0.05) for GPX and FR. Pair-wise means comparisons showed that NH elevated the average (+SE) GPX activity significantly (p<0.05) from the baseline control value of 5670.99+556.34 to13748.42+283.04 and 15134.19+1529.26 U/L with increasing length of NH exposure period from 24 to 48 h, respectively. Similarly, FR production was increased significantly (p<0.05) to 169.73+10.31 and 185.33+21.87, above baseline control of 105.27+5.25 Unit. Ultrastructure examination showed that O2 breathing for 48 h resulted in giant and swelled mitochondria associated with diluted inner membrane and damaged cristae. These mitochondria pathological alterations were associated with damages of myelin, axonal and cellular organelles. Normobaric-hyperoxia inducts mitochondria oxidative stress (MOS) and the subsequent rise of ROS causes variety of ultrastructure morphological pathological alterations in the organelles of cortical brain cells.


Se sabe que la exposición a la hiperoxia normobárica (HN) aumenta la producción de especies reactivas de oxígeno (ERO) por parte de las mitocondrias. El estudio se diseñó para examinar los cambios morfológicos de la ultraestructura mitocondrial en la corteza cerebral con la actividad de la glutatión peroxidasa (GPX) y la producción de radicales libres (RL) en el tejido cerebral durante la exposición a la hiperoxia. Los grupos experimentales fueron expuestos a HN durante 24 y 48 h continuamente. Tras los períodos de exposición, los animales se sacrificaron y los tejidos corticales se dividieron aleatoriamente en dos partes; la primera parte se procesó para el examen ultraestructural y la segunda se homogeneizó para las determinaciones de GPX y RL. El análisis de varianza (ANOVA) mostró que los efectos principales de los períodos de exposición al O2 fueron significativos (p <0,05) para GPX y RL. Las comparaciones de medias por pares mostraron que la HN elevó la actividad promedio de GPX (+ SE) significativamente (p <0,05) desde el valor de control de línea base de 5670,99 + 556,34 a 13748,42 + 283,04 y 15134,19 + 1529,26 U / L con una mayor duración del período de exposición a HN de 24 a 48 h, respectivamente. De manera similar, la producción de RL se incrementó significativamente (p <0,05) a 169,73 + 10,31 y 185,33 + 21,87, por encima del control de referencia de 105,27 + 5,25 unidades. El examen de la ultraestructura mostró que la respiración de O2 durante 48 h dio lugar a mitocondrias gigantes e hinchadas asociadas con la membrana interna diluida y las crestas dañadas. Estas alteraciones patológicas de las mitocondrias se asociaron con daños de mielina, axones y organelos celulares. La hiperoxia normobárica induce el estrés oxidativo mitocondrial (MOS) y el posterior aumento de las ERO provoca una variedad de alteraciones patológicas y morfológicas en los organelos de las células cerebrales corticales.


Subject(s)
Animals , Rats , Cerebral Cortex/ultrastructure , Hyperoxia/pathology , Mitochondria/pathology , Cerebral Cortex/enzymology , Cerebral Cortex/pathology , Analysis of Variance , Reactive Oxygen Species , Rats, Wistar , Reactive Nitrogen Species , Glutathione Peroxidase/metabolism , Mitochondria/ultrastructure
4.
Acta cir. bras ; 33(7): 556-564, July 2018. tab, graf
Article in English | LILACS | ID: biblio-949368

ABSTRACT

Abstract Purpose: To investigate the effects of baicalin on inflammatory reaction, oxidative stress and protein kinase D1 (PKD1) and nuclear factor-kappa B (NF-κB) protein expressions in severe acute pancreatitis (SAP) rats. Methods: Sixty rats were divided into sham operation, model, and low-, medium- and high-dose baicalin group. SAP model was established in later 4 groups. The later 3 groups were injected with 0.1, 0.2 and 0.4 ml/100 g 5% baicalin injection, respectively. At 12 h, the serum SAP related indexes and inflammatory factors, peripheral blood CD3 and γδT cell percentages, wet/dry ratio and pancreas ascites volume, oxidative stress indexes and PKD1 and NF-κB protein expressions in pancreatic tissue were determined. Results: Compared with model group, in high-dose baicalin group the wet/dry ratio and ascites volume, serum amylase level, phospholipase A2 activity, TNF-α, IL-1 and IL-6 levels, and pancreatic malondialdehyde level and PKD1 and NF-κB protein expression were significantly decreased (P < 0.05), and peripheral blood CD3 and γδT cell percentages and pancreatic superoxide dismutase and glutathione peroxidase levels were significantly increased (P < 0.05). Conclusion: Baicalin can resist the inflammatory reaction and oxidative stress, and down-regulate protein kinase D1 and nuclear factor-kappa B protein expressions, thus exerting the protective effects on severe acute pancreatitis in rats.


Subject(s)
Animals , Pancreatitis/drug therapy , Flavonoids/pharmacology , Protein Kinase C/metabolism , Anti-Inflammatory Agents, Non-Steroidal/pharmacology , NF-kappa B/metabolism , Oxidative Stress/drug effects , Pancreatitis/metabolism , Superoxide Dismutase/drug effects , Protein Kinase C/drug effects , Random Allocation , Down-Regulation/drug effects , Reproducibility of Results , NF-kappa B/drug effects , Interleukin-6/blood , Interleukin-1/blood , Tumor Necrosis Factor-alpha/blood , Treatment Outcome , Rats, Sprague-Dawley , CD3 Complex/drug effects , CD3 Complex/blood , Glutathione Peroxidase/drug effects , Glutathione Peroxidase/metabolism , Amylases/drug effects , Amylases/blood , Malondialdehyde/metabolism
5.
Acta cir. bras ; 33(5): 462-471, May 2018. tab, graf
Article in English | LILACS | ID: biblio-949341

ABSTRACT

Abstract Purpose: To evaluate the effect of hyperbaric oxygenation (HBO) on the expression of the genes antioxidant glutathione peroxidase 4 (Gpx4) and lactoperoxidase (Lpo) in the lung of mice subjected to intestinal ischemia and reperfusion (IIR). Methods: Control group (CG) in which were subjected to anesthesia, laparotomy and observation for 120 minutes; an ischemia and reperfusion group (IRG) subjected to anesthesia, laparotomy, small bowel ischemia for 60 minutes and reperfusion for 60 minutes; and three groups treated with HBO during ischemia (HBOG + I), during reperfusion (HBOG + R) and during ischemia and reperfusion (HBOG + IR). Studied 84 genes of oxidative stress by the method (RT-qPCR). Genes with expression levels three times below or above the threshold cycle were considered significantly hypoexpressed or hyperexpressed, respectively (Student's t-test p<0.05). Results: Gpx4 and Lpo were hiperexpressed on IRG, showing a correlation with these genes with lung oxidative stress. Treated with HBO, there was a significant reduction on genic expression on HBOG+I. Conclusion: Hyperbaric oxygenation showed to be associated with decreased expression of these antioxidant genes, suggesting a beneficial effect on the mechanism of pulmonary oxidative stress whenever applied during the ischemia.


Subject(s)
Animals , Rats , Reperfusion Injury/metabolism , Oxidative Stress/genetics , Glutathione Peroxidase/metabolism , Hyperbaric Oxygenation/methods , Lactoperoxidase/genetics , Lung/metabolism , Oxidative Stress/drug effects , Disease Models, Animal , Intestines/blood supply , Ischemia/metabolism , Antioxidants/metabolism , Antioxidants/pharmacology
6.
Braz. j. med. biol. res ; 51(6): e6555, 2018. graf
Article in English | LILACS | ID: biblio-889109

ABSTRACT

Long non-coding RNAs (lncRNAs) play an important role in the pathogenesis of cardiovascular diseases, especially in myocardial infarction and ischemia/reperfusion (I/R). However, the underlying molecular mechanism remains unclear. In this study, we determined the role and the possible underlying molecular mechanism of lncRNA-ROR in myocardial I/R injury. H9c2 cells and human cardiomyocytes (HCM) were subjected to either hypoxia/reoxygenation (H/R), I/R or normal conditions (normoxia). The expression levels of lncRNA-ROR were detected in serum of myocardial I/R injury patients, H9c2 cells, and HCM by qRT-PCR. Then, levels of lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-PX) were measured by kits. Cell viability, apoptosis, apoptosis-associated factors, and p38/MAPK pathway were examined by MTT, flow cytometry, and western blot assays. Furthermore, reactive oxygen species (ROS) production was determined by H2DCF-DA and MitoSOX Red probes with flow cytometry. NADPH oxidase activity and NOX2 protein levels were measured by lucigenin chemiluminescence and western blot. Results showed that lncRNA-ROR expression was increased in I/R patients and in H/R treatment of H9c2 cells and HCM. Moreover, lncRNA-ROR significantly promoted H/R-induced myocardial injury via stimulating release of LDH, MDA, SOD, and GSH-PX. Furthermore, lncRNA-ROR decreased cell viability, increased apoptosis, and regulated expression of apoptosis-associated factors. Additionally, lncRNA-ROR increased phosphorylation of p38 and ERK1/2 expression and inhibition of p38/MAPK, and rescued lncRNA-ROR-induced cell injury in H9c2 cells and HCM. ROS production, NADPH oxidase activity, and NOX2 protein levels were promoted by lncRNA-ROR. These data suggested that lncRNA-ROR acted as a therapeutic agent for the treatment of myocardial I/R injury.


Subject(s)
Humans , Myocardial Ischemia/metabolism , Myocardial Reperfusion Injury/metabolism , RNA, Long Noncoding/metabolism , Apoptosis , Blotting, Western , Cell Survival , Glutathione Peroxidase/metabolism , Hydro-Lyases/metabolism , Malondialdehyde/metabolism , Myocardial Ischemia/genetics , Myocardial Reperfusion Injury/genetics , Myocytes, Cardiac , Real-Time Polymerase Chain Reaction , RNA, Long Noncoding/genetics , Signal Transduction , Superoxide Dismutase/metabolism , Transfection
7.
Int. braz. j. urol ; 43(4): 644-651, July-Aug. 2017. tab
Article in English | LILACS | ID: biblio-892875

ABSTRACT

ABSTRACT Purpose To determine enzymatic antioxidant and lipid peroxidation levels in seminal plasma of patients orchiectomized for testicular tumors. Materials and Methods The study included 52 patients: 26 control men and 26 orchiectomized patients for testicular tumor, of which 12 men had seminoma tumor and 14 men non-seminoma tumor. After semen analysis performed according to the WHO guidelines, an aliquot of semen was centrifuged and the seminal plasma was collected. Lipid peroxidation was performed by thiobarbituric acid reactive substances (TBARS) assay and antioxidant profile was assessed by analyzing catalase, glutathione peroxidase (GPx) and superoxide anion (SOD) activities using colorimetric assays with a standard spectrophotometer. Data were tested for normality and compared using one-way ANOVA (p<0.05). Results Seminoma and non-seminoma groups presented lower sperm concentration and morphology when compared to control group (p=0.0001). Both study groups (seminoma and non-seminoma) presented higher TBARS levels when compared to control group (p=0.0000013). No differences were observed for SOD (p=0.646) andGPx (p=0.328). It was not possible to access the enzymatic activity of catalase in any group. Conclusion Patients with testicular tumor present increased semen oxidative stress, but no differences were observed in antioxidant levels, even after orchiectomy. This indicates that most likely an increased generation of oxidative products takes place in these patients.


Subject(s)
Humans , Male , Adolescent , Adult , Young Adult , Semen/enzymology , Testicular Neoplasms/metabolism , Lipid Peroxidation/physiology , Seminoma/metabolism , Antioxidants/metabolism , Oligospermia , Sperm Count , Superoxide Dismutase/metabolism , Testicular Neoplasms/surgery , Orchiectomy , Catalase/metabolism , Case-Control Studies , Cross-Sectional Studies , Oxidative Stress/physiology , Semen Analysis , Glutathione Peroxidase/metabolism , Middle Aged
8.
Acta cir. bras ; 31(7): 456-462, tab, graf
Article in English | LILACS | ID: lil-787264

ABSTRACT

ABSTRACT PURPOSE: To investigate the protective effect of β-myrcene (MYR) on oxidative and histological damage in mice heart tissue caused global cerebral ischemia/reperfusion (IR) in C57BL/J6 mice. METHODS: Animals(n=40) were randomly divided into four groups: (1)control, (2)IR, (3)MYR and (4)MYR+IR. The control group was received 0.1% carboxymethyl cellulose as a vehicle following a medial incision without carotid occlusion. In the IR group, the bilateral carotid arteries were clipped for 15min, and treated with the vehicle intraperitoneally(ip) for 10 days. MYR (200mg/kg) was received dissolved in 0.1%CMC for 10 days. In the MYR+IR group, the IR model was applied exactly as in the IR group, and then they were treated with MYR 10 days. RESULTS: The cerebral IR caused oxidative damage (increase TBARS, decrease antioxidant parameters). Treatment of MYR was increased in GSH,GPx,CAT,SOD activity while TBARS level was decreased. In addition, degenerative changes in I/R group heart tissue were ameliorated by MYR administration. CONCLUSİON: The administration of β-myrcene protects oxidative and histological damage in the heart tissue after global ischemia-reperfusion and may be useful safe alternative treatment for cardiac tissue after ischemic stroke.


Subject(s)
Animals , Male , Cardiotonic Agents/pharmacology , Reperfusion Injury/complications , Brain Ischemia/complications , Monoterpenes/pharmacology , Heart/drug effects , Antioxidants/pharmacology , Superoxide Dismutase/metabolism , Catalase/metabolism , Random Allocation , Thiobarbituric Acid Reactive Substances/metabolism , Oxidative Stress/drug effects , Models, Animal , Glutathione/metabolism , Glutathione Peroxidase/metabolism , Mice, Inbred C57BL , Myocardium/metabolism , Myocardium/pathology
9.
Biol. Res ; 47: 1-6, 2014. graf
Article in English | LILACS | ID: lil-710928

ABSTRACT

BACKGROUND: Effect of aqueous extracts of Allium sativum (garlic), Zingiber officinale (ginger), Capsicum fructensces (cayenne pepper) and their mixture on oxidative stress in rats fed high Cholesterol/high fat diet was investigated. Rats were randomly distributed into six groups (n = 6) and given different dietary/spice treatments. Group 1 standard rat chow (control), group 2, hypercholesterolemic diet plus water, and groups 3, 4, 5, 6, hypercholesterolemic diet with 0.5 ml 200 mg · kg-1 aqueous extracts of garlic, ginger, cayenne pepper or their mixture respectively daily for 4 weeks. RESULTS: Pronounced oxidative stress in the hypercholesterolemic rats evidenced by significant (p < 0.05) increase in MDA levels, and suppression of the antioxidant enzymes system in rat's liver, kidney, heart and brain tissues was observed. Extracts of spices singly or combined administered at 200 mg.kg-1 body weight significantly (p < 0.05) reduced MDA levels and restored activities of antioxidant enzymes. CONCLUSIONS: It is concluded that consumption of garlic, ginger, pepper, or their mixture may help to modulate oxidative stress caused by hypercholesterolemia in rats.


Subject(s)
Animals , Male , Diet, High-Fat , Hypercholesterolemia/drug therapy , Oxidative Stress/physiology , Phytotherapy , Plant Extracts/therapeutic use , Spices , Brain/enzymology , Capsicum/metabolism , Drug Combinations , Garlic/metabolism , Ginger/metabolism , Glutathione Peroxidase/metabolism , Glutathione Reductase/metabolism , Hypercholesterolemia/etiology , Hypercholesterolemia/metabolism , Kidney/enzymology , Lipid Peroxidation/drug effects , Liver/enzymology , Malondialdehyde/analysis , Myocardium/enzymology , Random Allocation , Rats, Wistar , Superoxide Dismutase/metabolism
10.
Indian J Biochem Biophys ; 2013 Oct; 50(5): 402-410
Article in English | IMSEAR | ID: sea-150249

ABSTRACT

Aluminum is an omnipresent neurotoxicant and has been associated with several neuropathological disorders. Cerebrum and cerebellum have been shown to face augmented oxidative stress when animals are exposed to aluminum and high doses of ethanol. To establish the link between oxidative stress and neurobehavioral alterations, the present study was conducted to determine the extent of oxidative stress in low levels of pro-oxidant (ethanol exposure) status of the functionally discrete regions of the cerebrum. Male Wistar rats were exposed to aluminum (10 mg/kg body wt) and ethanol (0.2-0.6 g/kg body wt) for 4 weeks. Spontaneous motor activity (SMA) and Rota-Rod performances (RRP) were recorded weekly during the period of exposure. At the end of 4th week, oxidative stress parameters were determined from the homogenized cerebral tissue. GSH-independent superoxide peroxide handling capacity (GI-SPHC) and GSH-dependent superoxide peroxide handling capacity (GD-SPHC) were determined for FC and TC upon exposure to ethanol in the absence and presence of aluminum exposure. Aluminum was found to augment the oxidative stress at higher doses (0.6 g Ethanol/kg body wt) of ethanol, particularly in FC. The SPHC of FC was also found to be compromised significantly in aluminum-ethanol co-exposed animals. It was concluded that even though the manifestation of oxidative stress was not observed as revealed by assaying the widely used oxidative stress biochemical markers (indices), aluminum and ethanol (low doses) exposure induced alterations in the handling capacity of oxidant imbalance that could be recognized by studying the SPHC of FC. Comparison of GD-SPHC and GI-SPHC offered a possible mechanism of compromised SPHC in FC. This observation is likely to offer insights into the mechanism of association between aluminium exposure and behavioral changes in neurodegenerative disorders towards therapeutic strategies for these disorders.


Subject(s)
Aluminum/toxicity , Animals , Catalase/metabolism , Ethanol/toxicity , Frontal Lobe/drug effects , Frontal Lobe/enzymology , Frontal Lobe/metabolism , Glutathione/metabolism , Glutathione Peroxidase/metabolism , Male , Neurotoxins/toxicity , Peroxides/metabolism , Rats , Rats, Wistar , Superoxide Dismutase/metabolism , Superoxides/metabolism , Temporal Lobe/drug effects , Temporal Lobe/enzymology , Temporal Lobe/metabolism
11.
Indian J Exp Biol ; 2013 Aug; 51(8): 635-645
Article in English | IMSEAR | ID: sea-149366

ABSTRACT

An elevated level of serum urea and creatinine was observed in doxorubicin (DOX) treated animals indicating DOX-induced nephrotoxicity. Enhanced lipid peroxidation (LPO) in the renal tissue was accompanied by a significant decrease in the levels of reduced glutathione (GSH), glutathione peroxidase (GPx), glutathione reductase (GR) and catalase (CAT) activities. Administration of lycopene (LycT) extracted from tomato to DOX treated mice showed a significant reduction in serum creatinine and urea levels which were associated with significantly low levels of LPO and significantly enhanced level of GSH and related antioxidant enzymes activity (GPx, GR and CAT) when compared to DOX group. Histopathological analysis revealed severe damage in the renal tissue of DOX treated animals. However, animals pretreated with LycT were observed to have reduced damage. Thus, from present results it may be inferred that lycopene may be beneficial in mitigating DOX induced nephrotoxicity in mice.


Subject(s)
Animals , Antibiotics, Antineoplastic/toxicity , Antioxidants/pharmacology , Carotenoids/pharmacology , Catalase/metabolism , Doxorubicin/toxicity , Female , Glutathione/metabolism , Glutathione Peroxidase/metabolism , Glutathione Reductase/metabolism , Immunoenzyme Techniques , Kidney Diseases/chemically induced , Kidney Diseases/drug therapy , Kidney Diseases/pathology , Lipid Peroxidation/drug effects , Lycopersicon esculentum/chemistry , Male , Mice, Inbred BALB C , Oxidative Stress/drug effects , Superoxide Dismutase
12.
Indian J Exp Biol ; 2013 Jun; 51(6): 458-463
Article in English | IMSEAR | ID: sea-147614

ABSTRACT

Camellia oleifera Abel. [C. oleosa (Lour.) Rehd.], an evergreen plant, is used for healthful oil production, but the shells are always discarded and need to be utilized. The present study was undertaken to explore the effect of extracts from the shells of C. oleifera on adjusting cardiovascular system. A flavonoid was obtained by reflux extraction of the shells in 70% methanol, hydrolysis in 2 M hydrochloric acid, and crystallization in acetone. Its structure was identified as a novel biflavonoid. Mice model of hyperlipidemia was setup by high fat diet for 30 d to evaluate the hypolipidemic effect of the biflavonoid at dose of 50, 100 and 200 mg/kg/d (ig). Antioxidative activity was determined by levels of malondialdehyde (MDA), superoxidase dismutase (SOD) and glutathione peroxidase (GSH-Px) in mice serum. The biflavonoid significantly controlled mice weight and liver coefficient, decreased the content of total cholesterol and triglyceride, promoted the level of high density lipoprotein in a dose dependent manner. The significant decrease of MDA content and increase of SOD and GSH-Px activity indicated it enhanced antioxidative capacity in vivo and was ascribed to hypolipidemic effect. The biflavonoid is useful in the prevention of high fat diet induced hyperlipidemia.


Subject(s)
Animals , Antioxidants/pharmacology , Biflavonoids/chemistry , Biflavonoids/isolation & purification , Biflavonoids/pharmacology , Body Weight/drug effects , Camellia/chemistry , Glutathione Peroxidase/metabolism , Hyperlipidemias/drug therapy , Lipids/analysis , Male , Malondialdehyde/metabolism , Mice , Molecular Structure , Oxidation-Reduction , Phytotherapy , Superoxide Dismutase/metabolism
13.
Indian J Exp Biol ; 2013 Mar; 51(3): 249-255
Article in English | IMSEAR | ID: sea-147589

ABSTRACT

Exposure to fluoride and excessive ethanol consumption has been identified as a serious public health problem in many parts of the world, including India. Thus, the effect of co-exposure to fluoride and ethanol for 3-6 weeks was studied on lipid peroxidation (LPO) and oxidative stress related parameters in the rat brain. After 3 weeks, co-treated animals showed 95% increase in LPO levels compared to control. However, the levels of reduced glutathione, total and protein thiols were decreased. These changes were accompanied by a decrease in the activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase. Rats exposed to fluoride together with ethanol for 6 weeks resulted in 130% increase in LPO and decrease in the reduced glutathione levels. The activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase were reduced under these conditions. Brain histology revealed excessive lymphocytes, edema and spongeosis in the cortical region after six weeks of fluoride and ethanol treatment. These results suggest that exposure to fluoride together with ethanol enhances lipid peroxidation by affecting antioxidant defence systems in the rat brain.


Subject(s)
Animals , Antioxidants/metabolism , Brain/drug effects , Ethanol/pharmacology , Fluorides/pharmacology , Free Radicals , Glutathione Peroxidase/metabolism , Glutathione Reductase/metabolism , Glutathione Transferase/metabolism , Lipid Peroxidation/drug effects , Male , Oxidative Stress , Rats , Rats, Sprague-Dawley , Sodium Fluoride/pharmacology , Time Factors
14.
Biol. Res ; 46(2): 207-213, 2013. graf, tab
Article in English | LILACS | ID: lil-683999

ABSTRACT

Oxidant/antioxidant imbalance has been reported in some infectious diseases, including community-acquired pneumonia (CAP). The aim was to assess the antioxidant status in adults with CAP and its relationship with clinical severity at admission. Fifty-nine patients with CAP were enrolled and categorized at admission by the FINE score, from July 2010 to October 2012. In the same period 61 controls were enrolled. Plasma samples were obtained at admission for determination of the ferric reducing ability of plasma (FRAP) and lipid peroxidation (8-isoprostane). Erythrocyte reduced (GSH)/oxidized (GSSG) glutathione, malondialdehyde (MDA) and antioxidant enzyme activity were assessed. Antioxidant status in adults with CAP represented by FRAP and the GSH/GSSG ratio were 16.8% (p=0.03) and 39.7% (p=0.04) lower than control values, respectively. In addition, FRAP values showed a positive correlation with GSH/GSSG ratio (r=0.852; p<0.02; n=59). The CAP group showed greater lipid peroxidation in both plasma and erythrocytes. The FINE score correlated negatively with FRAP (r= -0.718; p<0.05; n=59) and positively with MDA and F2 isoprostane levels (r=0.673; p<0.05; n=59; r=0.892; p<0.01; n=59, respectively). Antioxidant status alterations correlated with clinical severity. The FRAP assay and lipid peroxidation biomarkers may provide a useful parameter for estimating the severity and the clinical outcome of patients with CAP.


Subject(s)
Aged , Female , Humans , Male , Middle Aged , Erythrocytes/metabolism , Glutathione/blood , Lipid Peroxidation/physiology , Oxidative Stress/physiology , Pneumonia/metabolism , Biomarkers/metabolism , Case-Control Studies , Cross-Sectional Studies , Catalase/blood , Catalase/metabolism , Community-Acquired Infections/metabolism , /blood , Glutathione Peroxidase/blood , Glutathione Peroxidase/metabolism , Malondialdehyde/blood , Severity of Illness Index , Superoxide Dismutase/blood , Superoxide Dismutase/metabolism
15.
Indian J Biochem Biophys ; 2012 Oct; 49(5): 395-398
Article in English | IMSEAR | ID: sea-143563

ABSTRACT

Oxidant imbalance is one of the causative mechanisms of aluminum-induced neurotoxicity. In this study, we investigated aluminum-induced oxidant imbalance in non-neuronal tissues (liver, kidney and testis) and temporal cortex in rats. The differences in adaptations to superoxide and peroxide handling capacities (SPHC) of studied organs due to aluminum insult were also evaluated. Male Wistar rats were exposed to aluminum (10 mg/Kg body wt/day) for 4 weeks through orogastric intubation. Liver showed significant decrease in reduced glutathione level, while significant alteration in lipid peroxidation was observed in temporal cortex in aluminium-exposed animals. Superoxide dismutase activity was significantly altered in liver and temporal cortex and catalase activity significantly reduced in the liver due to aluminum exposure, while glutathione reductase and glutathione peroxidase activities were altered in all the tested organs. Among the organs, glutathione-independent SPHC was relatively higher in liver and kidney, while glutathione-dependent SPHC was relatively higher in testis and temporal cortex. As compared to control, aluminum-exposed rats demonstrated reduction in glutathione-dependent SPHC in temporal cortex and increment of the same in testis, while increment in glutathione-independent SPHC was observed in liver. In conclusion, aluminum-induced alteration in oxidant handling capacity could be the cause of oxidative stress both in the neuronal and non-neuronal tissues.


Subject(s)
Aluminum/poisoning , Aluminum/toxicity , Neurotoxicity Syndromes , Glutathione Reductase/metabolism , Glutathione Peroxidase/metabolism , Liver , Kidney , Superoxides/metabolism , Peroxides/metabolism , Temporal Lobe , Testis
16.
Braz. j. med. biol. res ; 45(8): 716-720, Aug. 2012. tab
Article in English | LILACS | ID: lil-643659

ABSTRACT

The objective of this study was to evaluate the effect of short-term levosimendan exposure on oxidant/antioxidant status and trace element levels in the testes of rats under physiological conditions. Twenty male Wistar albino rats were randomly divided into two groups of 10 animals each. Group 1 was not exposed to levosimendan and served as control. Levosimendan (12 µg/kg) diluted in 10 mL 0.9% NaCl was administered intraperitoneally to group 2. Animals of both groups were sacrificed after 3 days and their testes were harvested for the determination of changes in tissue oxidant/antioxidant status and trace element levels. Tissue malondialdehyde (MDA) was significantly lower in the levosimendan group (P < 0.001) than in the untreated control group and superoxide dismutase and glutathione peroxidase (GSH-Px) levels were significantly higher in the levosimendan group (P < 0.001). Carbonic anhydrase, catalase and GSH levels were not significantly different from controls. Mg and Zn levels of testes were significantly higher (P < 0.001) and Co, Pb, Cd, Mn, and Cu were significantly lower (P < 0.001) in group 2 compared to group 1. Fe levels were similar for the two groups (P = 0.94). These results suggest that 3-day exposure to levosimendan induced a significant decrease in tissue MDA level, which is a lipid peroxidation product and an indicator of oxidative stress, and a significant increase in the activity of an important number of the enzymes that protect against oxidative stress in rat testes.


Subject(s)
Animals , Male , Rats , Antioxidants/pharmacology , Hydrazones/pharmacology , Malondialdehyde/metabolism , Oxidative Stress/drug effects , Pyridazines/pharmacology , Reactive Oxygen Species/metabolism , Trace Elements/analysis , Glutathione Peroxidase/metabolism , Random Allocation , Rats, Wistar , Superoxide Dismutase/metabolism
17.
Article in English | WPRIM | ID: wpr-202334

ABSTRACT

Bisphenol A (BPA) has been reported to possess hepatic toxicity. We investigated the hypothesis that BPA, below the no observed adverse effect level (NOAEL), can induce hepatic damage and mitochondrial dysfunction by increasing oxidative stress in the liver. Two doses of BPA, 0.05 and 1.2 mg/kg body weight/day, were administered intraperitoneally for 5 days to mice. Both treatments impaired the structure of the hepatic mitochondria, although oxygen consumption rate and expression of the respiratory complex decreased only at the higher dose. The hepatic levels of malondialdehyde (MDA), a naturally occurring product of lipid peroxidation, increased, while the expression of glutathione peroxidase 3 (GPx3) decreased, after BPA treatment. The expression levels of proinflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) also increased. In HepG2 cells, 10 or 100 nM of BPA also decreased the oxygen consumption rate, ATP production, and the mitochondrial membrane potential. In conclusion, doses of BPA below the NOAEL induce mitochondrial dysfunction in the liver, and this is associated with an increase in oxidative stress and inflammation.


Subject(s)
Adenosine Triphosphate/metabolism , Animals , Glutathione Peroxidase/metabolism , Hep G2 Cells , Humans , Inflammation/chemically induced , Injections, Intraperitoneal , Interleukin-6/metabolism , Lipid Peroxidation/drug effects , Liver/drug effects , Male , Malondialdehyde/metabolism , Membrane Potential, Mitochondrial/drug effects , Mice , Mice, Inbred C57BL , Mitochondria/drug effects , Oxidative Stress/drug effects , Oxygen Consumption/drug effects , Phenols/toxicity , Tumor Necrosis Factor-alpha/metabolism
18.
Article in English | WPRIM | ID: wpr-69770

ABSTRACT

Malaria is still a leading cause of morbidity and mortality. The increase in lipid peroxidation reported in malaria infection and antioxidant status may be a useful marker of oxidative stress during malaria infection. The aim of this study was to investigate the role of antioxidant enzymes against toxic reactive oxygen species in patients infected with Plasmodium vivax and healthy controls. Malondialdehyde levels, superoxide dismutase, and glutathione peroxidase activities were determined in 91 P. vivax patients and compared with 52 controls. Malondialdehyde levels, superoxide dismutase, and glutathione peroxidase activities were 8.07+/-2.29 nM/ml, 2.69+/-0.33 U/ml, and 49.6+/-3.2 U/g Hb in the patient group and 2.72+/-0.50 nM/ml, 3.71+/-0.47 U/ml, and 62.3+/-4.3 U/g Hb in the control group, respectively. Malondialdehyde levels were found statistically significant in patients with vivax malaria higher than in healthy controls (P<0.001). On the other hand, superoxide dismutase and glutathione peroxidase activities were found to be significantly lower in vivax malaria patients than in controls (P<0.05). There was an increase in oxidative stress in vivax malaria. The results suggested that antioxidant defense mechanisms may play an important role in the pathogenesis of P. vivax.


Subject(s)
Adult , Animals , Antioxidants/metabolism , Biomarkers/metabolism , Female , Glutathione Peroxidase/metabolism , Humans , Lipid Peroxidation , Malaria, Vivax/metabolism , Male , Malondialdehyde/metabolism , Oxidative Stress , Plasmodium vivax/metabolism , Reactive Oxygen Species/metabolism , Superoxide Dismutase/metabolism , Young Adult
19.
Indian J Ophthalmol ; 2011 July; 59(4): 287-290
Article in English | IMSEAR | ID: sea-136191

ABSTRACT

Context: Glutathione depletion has been postulated to be the prime reason for galactose cataract. The current research seeks the prospect of targeting erythrocytes to pursue the lens metabolism by studying the glutathione system. Aims: To study the activity of the glutathione-linked scavenger enzyme system in the erythrocyte and lens of rats with cataract. Materials and Methods: Experiments were conducted in 36 male albino rats weighing 80 ± 20 g of 28 days of age. The rats were divided into two major groups, viz. experimental and control. Six rats in each group were sacrificed every 10 days, for 30 days. Cataract was induced in the experimental group by feeding the rats 30% galactose (w/w). The involvement of reduced glutathione (GSH) and the linked enzymes was studied in the erythrocytes and lens of cataractous as well as control rats. Statistical Analysis: Parametric tests like one-way ANOVA and Student's ‘t’ test were used for comparison. Correlation linear plot was used to compare the erythrocyte and lens metabolism. Results: Theconcentration of GSH and the activity of linked enzymes were found decreased with the progression of cataract, and also in comparison to the control. The same linear fashion was also observed in the erythrocytes. Conclusion: Depletion of GSH was the prime factor for initiating galactose cataract in the rat model. This depletion may in turn result in enzyme inactivation leading to cross-linking of protein and glycation. The correlation analysis specifies that the biochemical mechanism in the erythrocytes and lens is similar in the rat model.


Subject(s)
Animal Feed , Animals , Cataract/chemically induced , Cataract/physiopathology , Disease Progression , Erythrocytes/metabolism , Galactose/administration & dosage , Glutathione/metabolism , Glutathione Peroxidase/metabolism , Glutathione Reductase/metabolism , Glutathione Transferase/metabolism , Lens, Crystalline/metabolism , Male , Rats
20.
Indian J Biochem Biophys ; 2011 June; 48(3): 197-201
Article in English | IMSEAR | ID: sea-135320

ABSTRACT

The neuroprotective potential of ethanolic extract of roots of Pseudarthria viscida (L) Wight and Arn (EEPV) was investigated against -amyloid(25-35)-induced amnesia in mice which is a suitable animal model for Alzheimer’s disease (AD). The senile plaques of -amyloid (A) are major constituents accumulated during the progression of AD as a potent neurotoxicant. In our investigation, intracerebroventricular injection of A(25-35) in mice induced the neurodegeneration, exhibited the increased time of escape latency in behavioral pattern using water maze and decreased the levels of antioxidants namley superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and vitamin C with elevated level of acetylcholinesterase enzyme (AChE). The neuroprotective potential of EEPV was determined by behavioral pattern using water maze and biochemical parameters such as SOD, CAT and GPx and vitamin C content as well as AChE. Mice were treated with EEPV at 200 and 400 mg/kg doses for 21 days. Except control, all animals received a single injection of neurotoxicant A(25-35) on 14th day. In behavioural assessment, treatment with ethanolic extract improved the cognitive function in the water maze and attenuated the elevated levels of AChE with increase in antioxidant enzymes, indicating the neuroprotection with increased levels of vitamin C. These findings suggest that ethanolic extract of P. viscida exerts anti-amnesiac effects and enhances cognitive function.


Subject(s)
Acetylcholinesterase/drug effects , Acetylcholinesterase/metabolism , Alzheimer Disease/chemically induced , Alzheimer Disease/drug therapy , Alzheimer Disease/enzymology , Alzheimer Disease/pathology , Amnesia/chemically induced , Amnesia/drug therapy , Amnesia/enzymology , Amnesia/pathology , Amyloid beta-Peptides , Animals , Antioxidants/administration & dosage , Behavior, Animal/drug effects , Catalase/drug effects , Catalase/metabolism , Disease Models, Animal , Glutathione Peroxidase/drug effects , Glutathione Peroxidase/metabolism , Lipid Peroxidation/drug effects , Male , Maze Learning/drug effects , Mice , Neuroprotective Agents/administration & dosage , Plant Extracts/administration & dosage , Superoxide Dismutase/drug effects , Superoxide Dismutase/metabolism
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