Search

Although endogenous estrogen is known to offer cardiac and vascular protection, the involvement of estrogen receptors in mediating the protective effect of estrogen on hypertension-induced cardiovascular and renal injury is not fully explained. We aimed to investigate the effects of estrogen receptor (ER) agonists on oxidative injury, cardiovascular and renal functions of rats with renovascular hypertension (RVH). Female Sprague-Dawley rats were randomly divided as control and RVH groups, and RVH groups had either ovariectomy (OVX) or sham-OVX. Sham-OVX-RVH and OVX-RVH groups received either ERβ agonist diarylpropiolnitrile (1 mg/kg/day) or ERα agonist propyl pyrazole triol (1 mg/kg/day) for 6 weeks starting at the third week following the surgery. At the end of the 9(th) week, systolic blood pressures were recorded, cardiac functions were determined, and the contraction/relaxation responses of aortic rings were obtained. Serum creatinine levels, tissue malondialdehyde, glutathione, superoxide dismutase, catalase levels, and myeloperoxidase activity in heart and kidney samples were analyzed, and Na(+), K(+)-ATPase activity was measured in kidney samples. In both sham-OVX and OVX rats, both agonists reduced blood pressure and reversed the impaired contractile performance of the heart, while ERβ agonist improved renal functions in both the OVX and non-OVX rats. Both agonists reduced neutrophil infiltration, lipid peroxidation, and elevated antioxidant levels in the heart, but a more ERβ-mediated protective effect was observed in the kidney. Our data suggest that activation of ERβ might play a role in preserving the function of the stenotic kidney and delaying the progression of renal injury, while both receptors mediate similar cardioprotective effects.

Objectives: This study aimed to investigate the antioxidant and anti-inflammatory effects of caffeic acid phenethyl ester (CAPE) on the methotrexate (MTX)-induced hepatorenal oxidative damage in rats., Methods: Following a single dose of methotrexate (20 mg/kg), either vehicle (MTX group) or CAPE (10 µmol/kg, MTX + CAPE group) was administered for five days. In other rats, vehicle (control group) or CAPE was injected for five days, following a single dose of saline injection. After decapitation of the rats, trunk blood was obtained, and the liver and kidney tissues were removed for histological examination and for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels and myeloperoxidase (MPO) and sodium potassium-adenosine triphosphatase (Na(+)/K(+) -ATPase) activity. TNF-α and IL-1β levels were measured in the blood., Key Findings: Methotrexate administration increased the tissue MDA levels, MPO activity and decreased GSH levels and Na(+)/K(+) -ATPase activity, while these alterations were reversed in the CAPE-treated MTX group. Elevated TNF-α and IL-1β levels were also reduced with CAPE treatment., Conclusions: The results of this study revealed that CAPE, through its anti-inflammatory and antioxidant actions, alleviates methotrexate-induced oxidative damage, which suggests that CAPE may be of therapeutic benefit when used with methotrexate., (© 2011 The Authors. JPP © 2011 Royal Pharmaceutical Society.)

Background: There is substantial evidence to suggest that oxidative stress plays a significant role in the development of acute brain injury after subarachnoid hemorrhage (SAH)., Objective: To investigate the putative neuroprotective effect of nesfatin-1, a novel peptide with anorexigenic properties, in a rat model of SAH., Methods: Male Wistar albino rats were randomly divided into control, saline-treated SAH, and nesfatin-1 (10 μg/kg IP)-treated SAH groups. To induce SAH, rats were injected with 0.3 mL blood into their cisterna magna. Forty-eight hours after SAH induction, neurological examination scores were recorded and the rats were decapitated. Brain tissue samples were taken for the determination of blood-brain barrier (BBB) permeability, brain water content, and oxidative stress markers and for histological analysis., Results: The neurological examination scores were increased on the second day of SAH induction. SAH resulted in impaired blood-brain barrier and edema, along with increased levels of brain tumor necrosis factor-α, interleukin-1β, interleukin-6, lipid peroxidation, protein carbonylation, and myeloperoxidase activity with concomitant decreases in antioxidant enzymes. Conversely, in the nesfatin-1-treated SAH group, SAH-induced neurological impairment and oxidative brain injury were ameliorated by nesfatin treatment. Furthermore, SAH-induced morphological changes in the basilar arteries were improved by nesfatin-1 treatment, whereas caspase-3 activity and SAH-induced elevations in the plasma levels of proinflammatory cytokines were also depressed by nesfatin-1 treatment., Conclusion: These findings suggest that nesfatin-1, which appears to have antiapoptotic and anti-inflammatory properties, exerts neuroprotection in SAH-induced injury in rats by inhibiting neutrophil infiltration and subsequent release of inflammatory mediators., (Copyright © 2011 by the Congress of Neurological Surgeons)

Objective: The aim of this study was to reveal the effect of apocynin (APO) on the factors involved in obesity-related endothelial dysfunction (ED) and atherosclerosis (AS). Materials and Methods: Male Wistar albino rats were divided into control (CNT), high-fat diet (HFD) and HFD+APO groups. HFD and HFD+APO groups were fed HFD for sixteen weeks. APO (25 mg/kg) was administered to the HFD+APO group for the last four weeks. The effects of APO on: AS-related metabolic parameters (triglyceride, total cholesterol, high-density lipoprotein-cholesterol, insulin and leptin), oxidative stress (OS), [ malondialdehyde, glutathione, nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase-2, oxidised-low-density lipoprotein (ox-LDL) and 8-hydroxy-2-deoxyguanosine], low-density lipoprotein and ox-LDL uptake potential (activin receptor-like kinase-1 and lectin-like oxidized low-density lipoprotein receptor-1, respectively), tissue inflammation (myeloperoxidase, monocyte-chemoattractant-protein-1, tumor necrosis factor-alpha), ED (endothelial-nitric oxide synthase, inducible-nitric oxide synthase, nitric oxide), programmed cell death (terminal deoxynucleotidyl-transferase-dUTP-nick-end labeling, cleaved-poly-ADP-ribose-polymerase, gasdermin-D N-terminal fragment, caspase-1), smooth muscle cell transformation (alpha-smooth muscle actin), histology and ultrastructure of thoracic aorta were evaluated. Results: In obesity, APO had an ameliorative effect on metabolic parameters, OS, inflammation, ED, programmed cell death and ox-LDL uptake potential, but not on foam cell formation and LDL uptake potential. Conclusion: Apocynin may improve ED and AS in obesity by suppressing OS-linked factors involved in the early stage of AS. [ABSTRACT FROM AUTHOR]

Background and Aims: To analyze the potential therapeutic effects of chard against streptozotocin (STZ) -induced erectile dysfunction (ED) and oxidative damage in the corpus cavernousum in rats. Materials and Methods: In this study, Sprague-Dawley rats (250-300g) were allocated into groups as follows: control, diabetic, diabetic + chard, and diabetic + insulin. In order to induce diabetes, rats were given 65 mg/kg intraperitoneal streptozotocin. Chard extract was given orally at a dose 2 g/kg for 45 days beginning on 15th days. Sixty days after STZ injection, intracavernosal pressure (ICP) was measured and rats were decapitated. Blood samples were obtained for glucose, asymmetric dimethylarginine (ADMA)levels, and lactate dehydrogenase (LDH) activity while cavernous tissues were taken to analyze luminol and lucigenin chemiluminescence (CL), malondialdehyde and glutathione and along with histological analysis. Results: The results revealed that diabetes caused significant decreases in cavernosal tissue glutathione levels, while luminol and lucigenin CL, and malondialdehyde levels were significantly elevated. Plasma glucose, ADMA levels, and LDH activity were also found to be increased in diabetic group. On the other hand, both chard extract and insulin treatment reversed these biochemical parameters significantly. Furthermore, it was found that the ICP value examined for evaluating erectile functions were lower in the diabetic group, but increased in both treatment groups which were similar to the control values. Conclusion: According to our results, chard extract, similar to insulin, reduced diabetes-induced oxidative damage in cavernosal tissue and protected erectile functions. This effects may be attributed its hypoglycemic and antioxidant properties. [ABSTRACT FROM AUTHOR]

Methotrexate (MTX) is a cytotoxic immunosuppressant that is widely used in the treatment of tumours, rheumatoid arthritis and psoriasis. This study aims to evaluate the effects of whey proteins on MTX-induced liver and kidney damage by focusing on oxidant–antioxidant systems and eating habits. The study was conducted in four groups of thirty Sprague–Dawley rats (control, control + whey protein concentrate (WPC), MTX, MTX + WPC). A single dose of 20 mg/kg MTX was administered intraperitoneally to the MTX groups. Control and MTX groups were given 2 g/kg WPC by oral gavage every day for 10 d. At the end of day 10, blood samples were drawn and liver and kidney tissues were removed. MTX administration increased the lipid peroxidation level and decreased glutathione level, superoxide dismutase and glutathione-S-transferase activities in the liver and kidney. Administration of WPC significantly reduced the damage caused by MTX in the liver and kidney. While a decrease in serum urea level and an increase in serum creatinine level were detected in the MTX group, WPC administration reversed these results up to control group levels. Administration of WPC to the MTX group significantly reversed the histopathological damage scores of the liver and kidney. WPC administration ameliorated the MTX-induced oxidative damage in the liver and kidney tissues due to its antioxidant properties. Liver and kidney damage can be prevented by using whey proteins as a nutraceutical in MTX therapy. In conclusion, whey proteins demonstrated a protective effect against MTX-induced liver and kidney damage. [ABSTRACT FROM AUTHOR]

Radiotherapy, which is routinely used to treat a wide range of oncological disorders, primarily affects the malignant tissue in the targeted area, but also have negative effects in the surrounding tissues. Pelvic radiotherapy causes early and late effects on the colon and rectum. Resveratrol (RVT) has been revealed to have a number of pharmacological effects in a variety of experimental models and clinical circumstances, therefore it has piqued the interest of scientists in recent years. In this study, we aimed to investigate the potential protective effects of resveratrol (RVT), a strong antioxidant, anti-inflammatory and anti-mutagenic agent, against toxicity of colonic and rectal tissues seen in the early and late stages after pelvic radiation. The treatment durations of the current study were designed as one week and ten weeks interval by following radiation exposure. Sprague Dawley rats were divided into 5 groups (8 animals/group) as the control, radiation-early effects (Rd-E), radiation-late effects (Rd-L), and RVT-treated Rd-E (Rd-E+RVT) and RVT-treated Rd-L (Rd-L+RVT) groups. İonizing radiation was performed to the pelvic area that covers colon and rectum in single fraction of 20 Gy in a linear accelerator using with 6 MV photon energy. RVT was orally administered (10 mg/kg/day) immediately following the radiation exposure and continued daily for 1 and 10 weeks for early and late groups, respectively. Pelvic radiation caused a significant decrease in glutathione level, while malondialdehyde levels, myeloperoxidase activity and 8-hydroxydeoxyguanosine were increased in both Rd-E and Rd-L groups in the colon and rectum tissues. Additionally, light microscopic evaluations (H&E staining) revealed degeneration of epithelium and inflammatory cell infiltration in the colonic and rectal tissues in radiation groups. RVT treatment reversed all conducted biochemical parameters and ameliorated histomorphological changes following early and late effects of pelvic radiation in tissues. In conclusion, resveratrol may be a candidate as a radioprotector for normal tissues during and after radiotherapy. [ABSTRACT FROM AUTHOR]

Obesity causes cognitive weakening and increases the risk of neurodegenerative diseases. Myrtus communis extract (MC) has anti-inflammatory and antioxidant properties. In this study, it is aimed to investigate the effects of Myrtus communis on oxidative brain damage caused by a high-fat diet (HFD), using behavioral and biochemical parameters. Twenty-four Wistar albino rats (200-250 g) were divided into three groups. The control group (C) received a standard diet, while HFD groups were received HFD for 16 weeks. MC (100 mg/kg, oral) was given to the HFD + MC group for the last 4 weeks. At the end of the study, the novel object recognition test (NORT) was performed and the hippocampus and blood samples were collected. Acetylcholinesterase (AChE) and Na+/K+- ATPase activities, malondialdehyde (MDA), 8-hydroxy-2'-deoxyguanosine (8-OHdG) and reduced glutathione (GSH) levels were measured in the hippocampal samples and cholesterol levels were analyzed in sera. Findings have shown that NORT performance of the HFD group was reduced, while administration of MC prevents this reduction and in parallel, increased AChE and decreased Na+/K+ -ATPase activities were ameliorated by administration of MC. Increased MDA and 8-OHdG levels observed in the HFD group, were decreased in the MC treated HFD group. Our results point out that MC has ameliorative effects on hippocampal oxidative stress and cognitive impairment in high fat nutritioninduced obesity. [ABSTRACT FROM AUTHOR]

Cisplatin is a chemotherapeutic agent that is the first to enter treatment from organic platinum-derived drugs. Nephrotoxicity and cytotoxicity are major factors that limit its use. The aim of the study is to investigate the possible protective effects of quercetin against cisplatin-induced urogenital organ toxicity. In our study, Sprague Dawley four month old male rats were divided into 4 groups; control + saline (SF), control + quercetin (20 mg/kg for 21 days), cisplatin (7 mg/kg as a single dose) + SF and cisplatin + quercetin groups. After decapitation, the kidney, bladder, testis and corpus cavernosum tissue samples were taken to analyze caspase-3, an index of apoptosis, and oxidative stress parameters such as malondialdehyde (MDA), gluta-thione (GSH), and 8-hydroxy-2' -deoxyguanosine (8-OHdG). Furthermore, tissues were also examined histologically. Cisplatin caused significant increases in MDA and 8-OHdG levels, demonstrating increases in lipid peroxidation and oxidative DNA damage, respectively, in all tissues. In parallel with the oxidant stress increase, the endogenous strong antioxidant GSH levels were decreased. Caspase activity and caspase 3 expressions, which we measured as an indicator of apoptosis, increased significantly with cisplatin treatment. On the other hand, treatment with quercetin, a powerful antioxidant flavonoid, reversed these changes. Histological findings also demonstrated well-preserved tissues due to quercetin treatment. In conclusion, our results suggested that quercetin, when given with cisplatin, can be protective against the chemotherapeutic induced toxicity and thus provide therapeutic benefit. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the effects of calorie restriction (CR) and swimming exercise (SW) on oxidative injury in kidney and bladder tissues, in rats with metabolic syndrome (MS). 3-months old rats were divided into five; Control, MS, MS+CR, MS+SW, MS+CR+SW. The metabolic syndrome model was created using 10% fructose solution in drinking water for three months. Afterwards, SW and 40% CR were applied for six weeks. Blood glucose measurements were performed at the beginning, the third month and the end of experiment. After decapitation, blood, kidney and bladder samples were collected. Cytokine levels, antioxidant and oxidative stress parameters were examined. There was a remarkable change in blood glucose levels in MS+CR+SW group. Fructose-induced increased TNF-a and decreased ADP levels in plasma were reversed in CR, SW, and CR+SW groups. MDA levels were increased, while SOD and ADP levels were decreased in renal and bladder tissues in MS group. CR and SW significantly reversed all parameters in both tissues. Moreover, caspase activity increased in both tissues in MS group. CR decreased the caspase activity in kidney tissue, and in bladder tissues caspase activity significantly decreased with both CR and SW. Western blot analysis showed an increased caspase-3 protein expression in both tissues which was reversed by CR, SW, and CR+SW. The results of our study showed that MS disrupts the balance of pro/anti-inflammatory cytokines in plasma and causes oxidant damage in urinary tissues. Calorie restriction and exercise are protective against the damage caused by MS. [ABSTRACT FROM AUTHOR]

Aging is a progressive and catabolic process by cells of the body are broken down. Study scrutinized the effects of exercise and caloric restriction in cardiovascular hemodynamics and antioxidant system parameters. Rats divided to 5 categories as 1 control group (including 3 months aged animals) and 4 test groups (including 15 months aged animals) named by A-SED (aged-sedentary), A-CR (aged-caloric restricted), A-EX (aged-exercised) and A-CR-EX (aged-(exercised + caloric restricted)) created by adding carbachol (CAR) and phenylephrine (PE) cumulatively and during 6 weeks, 40% caloric restriction and swimming were administered to aged animals. At the beginning and end of study, blood pressure (BP) and ECHO of the animals were measured. After decapitation process, tissue (heart and aorta) samples were collected. In tissue samples, apoptotic and oxidative stress parameters, and in blood samples NO levels were studied. Additionally, tissues were viewed as histologically at light microscopy. GraphPad Prism 5v. program was used for statistics and p<0.05 were considered significantly. Contraction-relaxation responses of aorta improved after CR and EX administrations (p<0.05). In both tissues, oxidative stress parameters (8-OHdG, MDA, SOD, GSH), caspase-3 activity and caspase-3 dansity were recovered meaningfully (p<0.05). Finally, NO levels were significantly recovered with CR and EX administrations in aged animals (p<0.05). To sum up, it is suggested that CR and EX administrations contribute to the recovery of hemodynamic and antioxidant system parameters in aged rats. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Urological Surgery is the property of Galenos Yayinevi Tic. LTD. STI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: This study was designed to determine possible protective effect of betaine treatment against oxidative injury in pulmonary tissue induced with thermal trauma. METHODS: Under ether anesthesia, shaved dorsum of Wistar albino rats was exposed to a 90°C water bath for 10 seconds to induce burn injury. Betaine was administered orally (250 mg/kg) for a period of 21 days before burn injury, and single dose of betaine was administered after thermal injury. Control group rats were exposed to 25°C water bath for 10 seconds. Upon conclusion of experiment, rats were decapitated and blood was collected for analysis of pro-inflammatory cytokines and lactate dehydrogenase (LDH) activity. Lung tissue samples were taken to determine malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO), and Na+K+-ATPase activity, in addition to histological analysis. RESULTS: Burn injury caused significant increase in both cytokine levels and LDH activity. In lung samples, raised MDA levels, MPO activity, and reduced GSH levels and Na+/K+-ATPase activity were found due to burn injury. CONCLUSION: Treatment of rats with betaine significantly restored GSH level and Na+K+-ATPase activity, and decreased MDA level and MPO activity. According to the findings of the present study, betaine significantly diminishes burn-induced damage in tissue. [ABSTRACT FROM AUTHOR]

Copyright of Turkish Journal of Urology is the property of Turkish Association of Urology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Epidemiological studies have shown that regular exercise and increased aerobic fitness are associated with a decrease in allcause mortality and morbidity, including diseases related with high blood pressure. However, whether exercise has an antiinflammatory impact on the pathogenesis of hypertension was not elucidated yet. In the present study, to investigate the potential protective and therapeutic effects of exercise training (swimming for 30 min/day, 5 days/week for 9 weeks) on renovascular hypertension (RVH) 10-week-old male Wistar albino rats were divided into 4 groups as sham-operated sedentary control group, sedentary group with RVH (2-Kidney, 1-Clip Goldblatt) and two exercised RVH groups, which had 9-week training either before the surgery or after the surgery. Systolic blood pressures (SBP) were measured by the tail-cuff method on a weekly basis and at the end of 12 weeks, rats were decapitated to obtain kidneys. SBP were significantly higher in the sedentary RVH group than the control group, whereas in the trained RVH group measurements were not different than those of the control animals. In the renal tissues of the sedentary RVH group, malondialdehyde and myeloperoxidase levels were increased with a concomitant decrease in glutathione levels, while in the trained RVH group the levels were not different than those of the control group. Moreover, in the trained RVH group, superoxide dismutase and catalase levels measured as antioxidant parameters, were also significantly increased as compared with those of the sedentary RVH group. Current results demonstrate that regular moderate training controls high blood pressure in RVH, while RVH-induced oxidative damage in renal tissue is ameliorated through the modulation of oxidant-antioxidant balance. Exercise training does not only improve the circulatory functions, but it also initiates an anti-inflammatory process to defend against the angiotensin-II-induced renal injury. [ABSTRACT FROM AUTHOR]

Oxidative stress plays an important role both in spinal cord injury ( SCI) and erectile dysfunction ( ED). The present study investigated the effects of melatonin and tadalafil treatment alone or in combination on SCI-induced ED., Male Wistar albino rats ( n = 40) were divided into five groups: sham-operated control and SCI-injured rats given either vehicle, melatonin (10 mg/kg, i.p.), tadalafil (10 mg/kg, p.o.) or a combination of melatonin and tadalafil. Spinal cord injury was induced using a standard weight-drop method. On Day 7 after SCI, intracavernosal pressure ( ICP) was measured and all rats were decapitated. Cavernosal tissues were obtained to examine caspase 3, nitric oxide synthase ( NOS), myeloperoxidase ( MPO) and superoxide dismutase ( SOD) activities, as well as cGMP, nerve growth factor ( NGF), malondialdehyde ( MDA) and glutathione ( GSH) levels., Spinal cord injury caused oxidative damage, as evidenced by increases in MDA and cGMP levels. In addition, MPO and caspase 3 activites were increased after SCI, whereas GSH and NGF levels and SOD activity were reduced. Melatonin effectively reversed these oxidative changes. Furthermore, in rats treated with both melatonin and tadalafil, the recoveries were more pronounced than in rats given either melatonin or tadalafil alone. The ICP/mean arterial pressure value in vehicle-treated SCI rats was significantly higher than in the control group, whereas in the tadalafil- and tadalafil + melatonin-treated groups have returned this value had returned to control levels., As an individual treatment, and especially when combined with tadalafil, a well-known agent in the treatment of ED, melatonin prevented SCI-induced oxidative damage to cavernosal tissues and restored ED, most likely due to its anti-oxidant effects. [ABSTRACT FROM AUTHOR]

Objective: The aim was to investigate the putative anti-inflammatory and anti-apoptotic effect of obestatin in a rat model of subarachnoidal haemorrhage (SAH). Methods: To induce SAH, rats were injected with 0.3 mL blood into their cisterna magna. At 48 hours rats were decapitated after neurological examination. Blood-brain barrier (BBB) permeability, brain water content, oxidative stress markers and histological analysis were done in brain tissue. Results: The results showed that neurological examination scores were increased in the SAH group and, moreover, BBB permeability was impaired and oedema formed. SAH resulted in increased levels of plasma tumour necrosis factor (TNF)- α, interleukin (IL)-1 β, IL-6 levels and caspase-3 activity. Lipid peroxidation and protein oxidation levels and myeloperoxidase activity were all increased in the brain tissue, with concomitant decreases in antioxidant enzymes. On the other hand, SAH-induced neurological impairment and oxidative brain injury were ameliorated in the obestatin-treated group. Conclusion: The present study provides the first evidence that peripheral administration of obestatin exerts potent anti-inflammatory and neuroprotective effects in SAH-induced oxidative damage by maintaining a balance in oxidant-antioxidant status through the augmentation of endogenous antioxidants and the inhibition of pro-inflammatory mediators. [ABSTRACT FROM AUTHOR]

Copyright of Marmara Pharmaceutical Journal is the property of Marmara University, Faculty of Pharmacy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Marmara Pharmaceutical Journal is the property of Marmara University, Faculty of Pharmacy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Oxidative stress induced by spinal cord injury (SCI) has deleterious effects on the function of several organ systems including the urinary bladder. In this study, we investigated the possible protective actions of melatonin on SCI-induced oxidative damage and urinary bladder dysfunction. Wistar albino rats (n = 24) were divided randomly as control, vehicle- or melatonin (10 mg/kg, ip)-treated SCI groups. To induce SCI, a standard weight-drop method that induced a moderately severe injury at T10 was used. Injured animals were given either vehicle or melatonin 15 min postinjury. One week postinjury, each rat was neurologically examined and then decapitated; blood samples were taken to evaluate neuron-specific enolase (NSE) and soluble protein 100β (S-100β). Spinal cord (SC) and urinary bladder samples were taken for functional studies and histological examination or stored for the measurement of malondialdehyde (MDA), glutathione (GSH) and nerve growth factor (NGF) levels and caspase-3 activity. Isometric contractions in bladder strips were induced by carbachol. In the SCI rats, decreased contractile responses of the bladder strips were found to be restored by melatonin treatment. Serum S-100β levels and NSE activities and tissue MDA levels and caspase-3 activities, all of which were elevated in the vehicle-treated SCI animals as compared to the control values, were reversed by melatonin treatment. On the other hand, reduced GSH and NGF levels due to SCI were restored by melatonin treatment. Furthermore, melatonin treatment improved histological findings. These findings suggest that melatonin reduces SCI-induced tissue injury and improves bladder functions through its effects on oxidative stress and NGF. [ABSTRACT FROM AUTHOR]

Chronic renal failure (CRF) is associated with oxidative stress that promotes production of reactive oxygen species and cytokine release. We aimed to investigate the possible protective and antioxidant effects of aqueous garlic extract (AGE) in a rat model of CRF. Male Sprague-Dawley rats were randomly assigned as either CRF group with 5/6 reduction in the renal mass or sham-operated control group. CRF group received either saline or AGE (250 mg/kg/day/1 mL) orally for 3 weeks. At the end of the 3 weeks, rats were decapitated and trunk blood was collected. Creatinine, blood urea nitrogen (BUN) and lactate dehydrogenase (LDH) activity, and TNF-αα and IL-1ββ levels were measured in the serum samples, while malondialdehyde (MDA), glutathione (GSH) levels, and myeloperoxidase (MPO) activity were determined in the kidney, lung, and heart samples. CRF caused significant decreases in tissue GSH, which were accompanied with significant increases in MDA levels and MPO activities, while the circulating levels of the LDH activity, creatinine, BUN, TNF-αα, and IL-1ββ were elevated. AGE treatment alleviated CRF-induced oxidative changes in the injured tissues, while CRF-induced elevations in the blood levels of the pro-inflammatory cytokines and LDH were reduced. In conclusion, CRF-induced oxidative tissue injury occurs via the activation of pro-inflammatory mediators and by neutrophil infiltration into tissues and that the protective effects of garlic on CRF-induced injury can be attributed to its ability to inhibit neutrophil infiltration and pro-inflammatory mediators. These findings suggest that garlic, as a supplementary to diet, may have a potential therapeutic use in delimitating the systemic oxidant effects of CRF on remote organs. [ABSTRACT FROM AUTHOR]

Objectives The putative protective effects of resveratrol against oxidative injury in the heart, kidney and brain tissues of rats induced with the two-kidney, one-clip (2K1C) hypertension model were investigated. Methods Wistar albino rats were divided into sham-operated ( n = 8) or 2K1C groups, in which rats received either resveratrol (10 mg/kg per day, i.p., n = 8), or saline ( n = 8) starting at Week 3 after the surgery and continuing for the following 6 weeks. Indirect blood pressure recordings and echocardiographic images were made to evaluate cardiac function. At the end of Week 9 the animals were decapitated and plasma, heart, kidney and brain were taken for biochemical assays, while aortic rings were prepared for vascular reactivity studies. Key findings 2K1C hypertension resulted in increased blood pressure, aortic hypercontractility and reduced left ventricular function, leading to increased lipid peroxidation and myeloperoxidase activity, concomitant with significant reductions in tissue glutathione, superoxide dismutase, Na+/K+-ATPase and catalase activities in the cardiac, renal and brain tissues, indicating the presence of oxidative tissue damage in peripheral target organs. Elevated plasma levels of lactate dehydrogenase, creatine kinase, as well as reduced plasma levels of antioxidant capacity and nitric oxide further verified the severity of oxidative injury. A 6-week treatment with resveratrol reversed all the measured parameters, ameliorated hypertension-induced oxidative injury in the target organs and improved cardiovascular function. Conclusions Resveratrol improved cardiovascular function through the augmentation of endogenous antioxidants and the inhibition of lipid peroxidation by maintaining a balance in oxidant/antioxidant status, which also ameliorated hypertension-induced oxidative injury in the cardiac, renal and cerebral tissues. [ABSTRACT FROM AUTHOR]

In this study the role of free radicals in naphthalene-induced toxicity and the protection by erdosteine are investigated. Female Sprague-Dawley rats were treated with a single oral dose of 1100 mg naphthalene/kg in corn oil. Erdosteine was given 50 mg/kg/day orally for 3 days before naphthalene treatment and rats were decapitated 24 hours after naphthalene administration. Liver and kidney tissue samples were taken for determination of malondialdehyde (MDA), glutathione (GSH), Na+, K+-ATPase and myeloperoxidase (MPO) activities. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN) and creatinine levels and lactate dehydrogenase (LDH) activity were measured in the serum samples, while TNF-α, IL-1β, IL-6, 8-hydroxy-2'-deoxyguanosine (8- OHdG) and total antioxidant capacity (AOC) were assayed in plasma samples. Naphthalene administration caused a significant decrease in tissue GSH levels, Na+, K+-ATPase activity and plasma AOC levels, which was accompanied with significant increases in tissue MDA levels and MPO activity. Moreover the pro-inflammatory mediators (TNF-α, IL-β, IL-6), 8- OHdG, LDH activity, AST, ALT, creatinine and BUN levels were significantly increased in the naphthalene group. On the other hand erdosteine treatment prevented all these biochemical changes induced by naphthalene. In conclusion, it seems likely that erdostein protects tissues by inhibiting neutrophil infiltration, balancing the oxidant-antioxidant status and regulating the generation of inflammatory mediators. [ABSTRACT FROM AUTHOR]

The neuroprotective effect of alpha lipoic acid (ALA; 100 mg/kg, po), a dithiol antioxidant, on experimentally induced subarachnoid hemorrhage (SAH) was assessed in Wistar albino rats. Neurological examination scores recorded at the 48th h of SAH induction were increased in SAH groups, which were accompanied with significant increases in the formation of reactive oxygen species, DNA fragmentation ratios, malondialdehyde levels and myeloperoxidase activity, while significant decreases in the brain glutathione content and Na+, K+-ATPase activity were observed. On the other hand, ALA treatment reversed all these biochemical indices as well as SAH-induced histopathological alterations. Increased brain edema, impaired blood-brain-barrier permeability and neurological scores were also improved by ALA treatment. The results demonstrate that ALA exerts neuroprotective effects via the enhancement of endogenous antioxidant enzyme activity, the inhibition of neutrophil accumulation and free radical generation, suggesting a therapeutic potential in reducing secondary injury after SAH in patients. [ABSTRACT FROM AUTHOR]

Copyright of Marmara Pharmaceutical Journal is the property of Marmara University, Faculty of Pharmacy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The effect of melatonin was investigated in an angiotensin II-dependent renovascular hypertension model in Wistar albino rats by placing a renal artery clip (two-kidney, one-clip; 2K1C), while sham rats did not have clip placement. Starting either on the operation day or 3 wk after the operation, the rats received melatonin (10 mg/kg/day) or vehicle for the following 6 wk. At the end of the nineth week, after blood pressure (BP) and echocardiographic recordings were obtained, plasma samples were obtained to assay lactate dehydrogenase (LDH), creatine kinase (CK), antioxidant capacity (AOC), asymmetric dimethylarginine (ADMA), and nitric oxide (NOx) levels. In the kidney, heart and brain tissues, malondialdehyde (MDA) and glutathione (GSH) levels, superoxide dismutase (SOD), catalase (CAT), myeloperoxidase (MPO) and Na+-K+ ATPase activities were determined. 2K1C caused an increase in BP and left ventricular (LV) dysfunction. In hypertensive animals LDH, CK, ADMA levels were increased in plasma with a concomitant reduction in AOC and NOx. Moreover, hypertension caused a significant decrease in tissue SOD, CAT, and Na+, K+-ATPase activities and glutathione content, while MDA levels and MPO activity were increased in all studied tissues. On the other hand, both melatonin regimens significantly reduced BP, alleviated oxidative injury and improved LV function. In conclusion, melatonin protected against renovascular hypertension-induced tissue damage and improved cardiac function presumably due to both its direct antioxidant and receptor-dependent actions, suggesting that melatonin may be of therapeutic use in preventing oxidative stress due to hypertension. [ABSTRACT FROM AUTHOR]

Sprague Dawley rats of both sexes were injected with either saline or RVT (10 mg/kg) either before or after acetic acid ulcer induction and decapitated 3, 5 or 10 days after ulcer. In the saline-treated ulcer groups, macroscopically evident ulcers were observed, while RVT-pretreated or RVT-treated groups had lower macroscopic ulcer scores. Likewise, the microscopic damage scores were lower for the RVT-administered groups. Gastric myeloperoxidase activity, malondialdehyde, collagen and tumour necrosis factor-alpha levels, as well as luminol- and lucigenin-enhanced chemiluminescence levels that were elevated in the saline-administered ulcer groups, were depressed with both RVT-pretreatment and RVT-treatment. Moreover, depleted glutathione levels in the ulcer groups were increased back to control levels by both pre- and post-treatments of RVT. Results demonstrate that resveratrol has both protective and therapeutic effects on oxidative gastric damage by suppressing pro-inflammatory cascades, including the activation of pro-inflammatory cytokines, accumulation of neutrophils and release of oxygen-derived free radicals. [ABSTRACT FROM AUTHOR]

Oxidative stress has detrimental effects in several models of neurodegenerative diseases, including subarachnoid hemorrhage (SAH). This study investigated the putative neuroprotective effect of melatonin, a powerful antioxidant, in a rat model of SAH. Male Wistar albino rats were divided as control, vehicle-treated SAH, and melatonin-treated (10 mg/kg, i.p.) SAH groups. To induce SAH, 0.3 mL blood was injected into cisterna magna of rats. Forty-eight hours after SAH induction, neurological examination scores were measured and the rats were decapitated. Brain tissue samples were taken for blood–brain barrier (BBB) permeability, brain water content, histological examination, or determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO), and Na+-K+-ATPase activities. Formation of reactive oxygen species in brain tissue samples was monitored by using a chemiluminescence (CL) technique. The neurological examination scores were increased in SAH groups on the second day of SAH induction and SAH caused a significant decrease in brain GSH content and Na+-K+-ATPase activity, which was accompanied with significant increases in CL, MDA levels, and MPO activity. On the other hand, melatonin treatment reversed all these biochemical indices as well as SAH-induced histopathological alterations, while increased brain water content and impaired BBB were also reversed by melatonin treatment. This study suggests that melatonin, which can easily cross BBB, alleviates SAH-induced oxidative stress and exerts neuroprotection by preserving BBB permeability and by reducing brain edema. [ABSTRACT FROM AUTHOR]

Copyright of Erciyes Medical Journal / Erciyes Tip Dergisi is the property of KARE Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The possible protective effects of resveratrol (RVT) against cardiotoxicity were investigated in Wistar albino rats treated with saline, saline+doxorubicin (DOX; 20 mg/kg) or RVT (10 mg/kg)+DOX. Blood pressure and heart rate were recorded on the 1st week and on the 7th week, while cardiomyopathy was assessed using transthoracic echocardiography before the rats were decapitated. DOX-induced cardiotoxicity resulted in decreased blood pressure and heart rate, but lactate dehydrogenase, creatine phosphokinase, total cholesterol, triglyceride, aspartate aminotransferase and 8-OHdG levels were increased in plasma. Moreover, DOX caused a significant decrease in plasma total antioxidant capacity along with a reduction in cardiac superoxide dismutase, catalase and Na+,K+-ATPase activities and glutathione contents, while malondialdehyde, myelopreoxidase activity and the generation of reactive oxygen species were increased in the cardiac tissue. On the other hand, RVT markedly ameliorated the severity of cardiac dysfunction, while all oxidant responses were prevented; implicating that RVT may be of therapeutic use in preventing oxidative stress due to DOX toxicity. [ABSTRACT FROM AUTHOR]

Abstract: Objective: This investigation confirms the role of free radicals in naphthalene-induced toxicity and elucidates the mechanism of resveratrol (RVT). Methods: Both male and female BALB-c mice were administered with naphthalene (100mg/kg, i.p.) for 30 days, either along with saline or along with RVT (10mg/kg, orally). At the end of the experiment, following treatment and sacrifice of animals by decapitation, lung, liver and kidney tissue samples were taken for histological examination or determination of malondialdehyde (MDA), glutathione (GSH), myeloperoxidase (MPO) activity and collagen contents. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN) and creatinine levels and lactate dehydrogenase (LDH) activity were measured in the serum samples, while TNF-α, IL-β, IL-6 and total antioxidant capacity (AOC) were assayed in plasma samples. Results: Naphthalene administration caused a significant decrease in tissue GSH and plasma AOC, which was accompanied with significant increases in tissue MDA and collagen levels and MPO activity. Moreover, the pro-inflammatory mediators (TNF-α, IL-β, IL-6), LDH activity, AST, ALT, creatinine and BUN levels were significantly increased in the naphthalene group. On the other hand, RVT treatment reversed all these biochemical indices as well as histopathological alterations induced by naphthalene. Conclusions: Oxidative mechanisms play an important role in naphthalene-induced tissue damage, and RVT, by inhibiting neutrophil infiltration, balancing oxidant–antioxidant status, and regulating the generation of inflammatory mediators, ameliorates oxidative organ injury due to naphthalene toxicity. [Copyright &y& Elsevier]

Endosulfan is a chlorinated cyclodiene insecticide which induces oxidative stress. In this study, we investigated the possible protective effect of melatonin, an antioxidant agent, against endosulfan (Endo)-induced toxicity in rats. Wistar albino rats (n = 8) were administered endosulfan (22 mg/kg/day orally) followed by either saline (Endo group) or melatonin (10 mg/kg/day, Endo + Mel group) for 5 days. In other rats, saline (control group) or melatonin (10 mg/kg/day, Mel group) was injected for 5 days, following corn oil administration (vehicle of endosulfan). Measurement of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen content were performed in liver and kidney. Furthermore, aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN), and creatinine levels, lactate dehydrogenase (LDH) activity were measured in the serum samples, while tumor necrosis factor-α (TNF-α), interleukin-β (IL-β) and total antioxidant capacity (AOC) were assayed in plasma samples. Endosulfan administration caused a significant decrease in tissue GSH and plasma AOC, which was accompanied with significant rises in tissue MDA and collagen levels and MPO activity. Moreover, the proinflammatory mediators (TNF-α and IL-β), LDH activity, AST, ALT, creatinine and BUN levels were significantly elevated in the endosulfan-treated rats. On the other hand, melatonin treatment reversed all these biochemical alterations induced by endosulfan. Our results suggest that oxidative mechanisms play an important role in endosulfan-induced tissue damage and melatonin, by inhibiting neutrophil infiltration, balancing oxidant–antioxidant status and regulating the generation of inflammatory mediators, ameliorates oxidative organ injury as a result of endosulfan toxicity. [ABSTRACT FROM AUTHOR]

Abstract: Mercury(II) is a highly toxic metal which induces oxidative stress in the body. In this study we aimed to investigate the possible protective effect of Ginkgo biloba (EGb), an antioxidant agent, against experimental mercury toxicity in rat model. Following a single dose of 5mg/kg mercuric chloride (HgCl2; Hg group) either saline or EGb (150mg/kg) was administered for 5days. After decapitation of the rats trunk blood was obtained and the tissue samples from the brain, lung, liver, and kidney were taken for the determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen contents. Formation of reactive oxygen species in the tissue samples was monitored by chemiluminescence (CL) technique. BUN, creatinin, ALT, and AST levels and tumor necrosis factor-α (TNF-α) and lactate dehydrogenase (LDH) activity were assayed in serum samples. The results revealed that HgCl2 induced oxidative damage caused significant decrease in GSH level, significant increase in MDA level, MPO activity and collagen content of the tissues. Treatment of rats with EGb significantly increased the GSH level and decreased the MDA level, MPO activity, and collagen contents. Similarly, serum ALT, AST and BUN levels, as well as LDH and TNF-α, were elevated in the Hg group as compared to control group. On the other hand, EGb treatment reversed all these biochemical indices. Our results implicate that mercury-induced oxidative damage in brain, lung, liver, and kidney tissues protected by G. biloba extract, with its antioxidant effects. [Copyright &y& Elsevier]

Oxidative stress, in particular lipid peroxidation, induces collagen synthesis and causes fibrosis. The aim of this study was to assess the antioxidant and antifibrotic effects of erdosteine on liver fibrosis induced by biliary obstruction in rats. Liver fibrosis was induced in Wistar albino rats by bile duct ligation (BDL). Erdosteine (10 mg/kg, orally) or saline was administered for 28 days. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) levels were determined to assess liver functions and tissue damage, respectively. Pro-inflammatory cytokines, TNF-α, IL-1β and IL-6 and antioxidant capacity (AOC) were assayed in plasma samples. Liver tissues were taken for determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen content. Production of reactive oxidants was monitored by chemiluminescence assay. Serum AST, ALT, LDH, and plasma cytokines were elevated in the BDL group as compared to controls and were significantly decreased by erdosteine treatment. Hepatic GSH level and plasma AOC, depressed by BDL, were elevated back to control level with erdosteine treatment. Furthermore, hepatic luminol and lucigenin chemiluminescence (CL), MDA level, MPO activity and collagen content in BDL group increased dramatically compared to control and reduced by erdosteine treatment. Since erdosteine administration alleviated the BDL-induced oxidative injury of the liver and improved the hepatic functions, it seems likely that erdosteine with its antioxidant and antifibrotic properties, may be of potential therapeutic value in protecting the liver fibrosis and oxidative injury due to biliary obstruction. [ABSTRACT FROM AUTHOR]

Background: The present study was designed to examine whether resveratrol, a potent antioxidant, protects against renal ischemia-reperfusion (I/R) injury. Methods: Wistar albino rats were unilaterally nephrectomized and subjected to 45 min of renal pedicle occlusion followed by 6 h of reperfusion. Resveratrol (RVT, 30 mg/kg, i.p.) or vehicle was administered twice, at 30 min prior to ischemia and immediately before the reperfusion period. At the end of the reperfusion period, rats were decapitated and kidney samples were taken for histological examination or determination of levels of renal malondialdehyde (MDA), an end product of lipid peroxidation; glutathione (GSH), a key antioxidant; and myeloperoxidase (MPO) activity, an index of tissue neutrophil infiltration. Formation of reactive oxygen species in hepatic tissue samples was monitored by using chemiluminescence (CL) technique with luminol and lucigenin probes. Renal tissue collagen content as a fibrosis marker was also determined, while serum creatinine and urea concentrations were measured for the evaluation of renal function. Tumor necrosis factor- (TNF-) and lactate dehydrogenase (LDH) were also assayed in serum samples. Results: Ischemia/reperfusion caused a significant decrease in tissue GSH level, which was accompanied by significant increases in the renal luminol and lucigenin CL values, MDA level, MPO activity and collagen content. Similarly, serum creatinine and BUN levels, as well as LDH and TNF-α, were elevated in the I/R group as compared to control group. On the other hand, resveratrol treatment reversed all these biochemical indices, as well as histopathological alterations that were induced by I/R. Conclusions: Findings of the present study suggest that resveratrol exerts renoprotective effects via its radical scavenging and antioxidant activities, which appear to involve the inhibition of tissue neutrophil infiltration. [Copyright &y& Elsevier]

Abstract: There is increasing evidence that oxidative stress has an important role in the development of multiorgan failure after major burn injury. In the present study, we investigated whether the leukotriene receptor blocker montelukast is protective against burn-induced injury of the gut. Under brief ether anaesthesia, shaved dorsum of the rats was exposed to 90°C (burn group) or 25°C (control group) water bath for 10s. Montelukast (10mg/kg) or saline was administered intraperitoneally immediately after and at the 12th hour of the burn injury. Rats were decapitated 24h after burn injury and the skin samples, as well as tissue samples from stomach, ileum and colon, were taken for the determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen contents. Tissues were also examined microscopically. Tumor necrosis factor-α (TNF-α) and lactate dehydrogenase (LDH) were assayed in serum samples. Severe skin scald injury (30% of total body surface area) caused a significant decrease in GSH level, which was accompanied with significant increases in MDA level, MPO activity and collagen content of tissues. Similarly, serum TNF-α and LDH were elevated in the burn group as compared to control group. On the other hand, montelukast treatment reversed all these biochemical indices, as well as histopathological alterations, which were induced by thermal trauma. Findings of the present study suggest that montelukast possesses an anti-inflammatory effect on burn-induced gastrointestinal damage and protects against oxidative injury by a neutrophil-dependent mechanism. [Copyright &y& Elsevier]

Mercury exerts a variety of toxic effects in the body. Lipid peroxidation, DNA damage and depletion of reduced glutathione by Hg(II) suggest an oxidative stress-like mechanism for Hg(II) toxicity. Melatonin, the main secretory product of the pineal gland, was recently found to be a potent free radical scavenger and antioxidant. N-Acetylcysteine, a precursor of reduced glutathione and an antioxidant, is used in the therapy of acute heavy metal poisoning. In this study the protective effects of melatonin in comparison to that of N-acetylcysteine against Hg-induced oxidative damage in the kidney, liver, lung and brain tissues were investigated. Wistar albino rats of either sex (200–250 g) were divided into six groups, each consisting of 8 animals. Rats were intraperitoneally injected with 1) 0.9% NaCl, control (C) group; 2) a single dose of 5 mg/kg mercuric chloride (HgCl2), Hg group; 3) melatonin in a dose of 10 mg/kg, 1 hr after HgCl2 injection, Hg-melatonin group; 4) melatonin in a dose of 10 mg/kg one day before and 1 hr after HgCl2 injection, melatonin-Hg-melatonin group; 5) N-acetylcysteine in a dose of 150 mg/kg, 1 hr after HgCl2 injection, Hg-N-acetylcysteine group, and 6) N-acetylcysteine in a dose of 150 mg/kg one day before and 1 hr after HgCl2 injection, N-acetylcysteine-Hg-N-acetylcysteine group. Animals were killed by decapitation 24 hr after the injection of HgCl2. Tissue samples were taken for determination of malondialdehyde, an end-product of lipid peroxidation; glutathione (GSH), a key antioxidant, and myeloperoxidase activity, an index of neutrophil infiltration. The results revealed that HgCl2 induced oxidative tissue damage, as evidenced by increases in malondialdehyde levels. Myeloperoxidase activity was also increased, and GSH levels were decreased in the liver, kidney and the lungs. All of these effects were reversed by melatonin or N-acetylcysteine treatment. Since melatonin or N-acetylcysteine administration reversed these responses, it seems likely that melatonin or N-acetylcysteine can protect all these tissues against HgCl2-induced oxidative damage. [ABSTRACT FROM AUTHOR]

AbstractIntroductionMethodsResultsConclusionPostmenopausal diabetes is a condition that affects millions of women and their quality of life. Also, kidney and small intestine tissues are damaged due to diabetes. The present study aimed to examine the protective effects of an extract prepared from Myrtus communis leaves on kidney and small intestine tissues against experimentally created postmenopausal diabetes.For this purpose, experimental rats were randomly divided into six groups (Control; ovariectomy:OVX, diabetic:D, ovariectomy + diabetic:OVX + D, ovariectomy + diabetic + oestrogen:OVX + D+E2, ovariectomy + diabetic + MC: OVX + D+MC) and kidney and small intestine tissues were taken after the experimental procedure.Evaluations of biochemical parameters (glutathione and glutathione-related enzymes, antioxidant enzymes, etc.) showed that MC had a protective effect on kidney and small intestine tissues in diabetes and ovariectomy groups.It can be suggested that MC extract has a protective effect on small intestine and kidney tissues in postmenopausal diabetes and may be a good herbal source for this purpose. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate possible protective effects of apocynin (APO), an NADPH oxidase (NOX2) inhibitor, on cisplatin (CIS)‐induced testicular damage. Four groups of Sprague Dawley rats were used: control, APO, CIS and CIS+APO. Following a single intraperitoneal dose of CIS (7 mg/kg), either dimethyl sulfoxide or APO (25 mg/kg) was administered orally for 5 days. Testis samples were evaluated microscopically for general histopathology and ultrastructure, proliferating and apoptotic cells, and NOX2 localization. Sperm parameters were evaluated. Malondialdehyde (MDA) and glutathione (GSH) levels and superoxide dismutase (SOD), myeloperoxidase (MPO) and 8‐hydroxy‐2‐deoxyguanosine (8‐OHdG) activities were analysed biochemically. The CIS group had a greater number of abnormal spermatozoa, atrophic seminiferous tubules, apoptotic and NOX2‐immunoreactive cells; numerous large vacuole formations in the cytoplasm of germinal epithelial cells; degenerated intercellular tight junctions; higher MDA, 8‐OHdG and MPO levels; decreased numbers of spermatozoa; and lower proliferative index and GSH and SOD levels. All these histologic and biochemical results were better in the CIS+APO group. CIS causes testicular damage by decreasing spermatogenic cell lines and increasing NOX2 activity and apoptosis through oxidative stress. APO prevents testicular damage, possibly by its antioxidant effects. [ABSTRACT FROM AUTHOR]

Abstract: Mechanisms of burn-induced skin and remote organ injury involve oxidant generation and the release of pro-inflammatory cytokines. In this study the possible antioxidant and anti-inflammatory effects of ghrelin were evaluated in a rat model of thermal trauma. Wistar albino rats were exposed to 90°C bath for 10s to induce thermal trauma. Ghrelin, was administered subcutaneously (10ng/kg/day) after the burn injury and repeated twice daily. Rats were decapitated at 6h and 48h after burn injury and blood was collected for the analysis of pro-inflammatory cytokines (TNF-α and IL-1β), lactate dehydrogenase (LDH) activity and antioxidant capacity (AOC). In skin, lung and stomach tissue samples malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) and Na+–K+-ATPase activity were measured in addition to the histological analysis. DNA fragmentation ratio in the gastric mucosa was also evaluated. Burn injury caused significant increase in both cytokine levels, and LDH activity, while plasma AOC was found to be depleted after thermal trauma. On the other hand, in tissue samples the raised MDA levels, MPO activity and reduced GSH levels, Na+–K+-ATPase activity due to burn injury were found at control levels in ghrelin-treated groups, while DNA fragmentation in the gastric tissue was also reduced. According to the findings of the present study, ghrelin possesses a neutrophil-dependent anti-inflammatory effect that prevents burn-induced damage in skin and remote organs and protects against oxidative organ damage. [Copyright &y& Elsevier]

Abstract: Spinal cord injury (SCI) induced oxidative stress affects multiple organ systems including the kidney. We studied the possible protective effects of melatonin on SCI-induced oxidative damage in renal tissues of rats. Wistar albino rats (n =24) were exposed to SCI and divided into vehicle- or melatonin-treated SCI groups. Melatonin was administred intraperitoneally at a dose of 10mg/kg for seven days. Renal tissues were investigated by light and electron microscopy. Furthermore, tissue malondialdehyde (MDA) and glutathione (GSH) levels and myeloperoxidase (MPO) and superoxide dismutase (SOD) activities were also determined. In the vehicle-treated SCI group, the renal histology was disturbed compared to controls, whereas the melatonin-treated SCI group showed significantly reduced degeneration of renal tissue as seen by both light and electron microscopy. MDA levels, MPO and SOD activities were increased and GSH levels were decreased in the vehicle-treated SCI group compared to controls. On the other hand, decreased MDA levels and MPO activities and increased GSH levels were observed in the melatonin-treated SCI group compared to vehicle-treated SCI group. These results showed that experimentally induced SCI caused oxidative stress in the rat kidney, whereas melatonin treatment reduced oxidative stress, suggesting that it may be used as a complementary therapy of renal problems occurring following SCI. [Copyright &y& Elsevier]

Abstract: Background: Spinal cord injury (SCI) leads to an inflammatory response and generates oxidative stress, which has deleterious effects on the function of several organ systems, including the urinary bladder. The present study was designed to investigate the putative beneficial effect of quercetin against SCI-induced bladder damage. Materials and methods: In order to induce SCI, a standard weight-drop method that induced a moderately severe injury (100 g/cm force) at T10 was used. Injured animals were given either 20 mg/kg quercetin or vehicle 15 min post injury and repeated twice daily for 7 d. After decapitation, bladder strips were placed in organ bath and isometric contractions to carbachol (10−8 to10−4 M) were recorded. In order to examine oxidative tissue injury, luminol chemiluminescence, nitric oxide, malondialdehyde, and glutathione levels and superoxide dismutase, myeloperoxidase, and caspase 3 activities of bladder tissues were measured along with histologic evaluations. Proinflammatory cytokines tumor necrosis factor α, interleukin 1β, and interleukin 6 were also assayed in blood samples. Results: In the injured animals, the contractile responses of the bladder strips were lower than those of the control group and were reversed by treatment with quercetin. On the other hand, increase in nitric oxide, malondialdehyde, luminol chemiluminescence levels, and myeloperoxidase and caspase 3 activities of tissues in the SCI group were significantly reversed by quercetin treatment. Similarly, plasma cytokine levels, which were elevated in the vehicle-treated SCI group, were reduced with quercetin treatment. Furthermore, treatment with quercetin also prevented the depletion of tissue glutathione levels and superoxide dismutase activity seen in the SCI group. Conclusions: According to the results, quercetin exerts beneficial effects against SCI-induced oxidative damage through its anti-inflammatory and antioxidant effects. [Copyright &y& Elsevier]

Abstract: Spinal cord injury (SCI) leads to an inflammatory response that generates substantial secondary damage within the tissue besides the primary damage. Leukotrienes are biologically active 5-lipoxygenase products of arachidonic acid metabolism that are involved in the mediation of various inflammatory disorders including SCI. In this study, we investigated the possible protective effects of montelukast, a leukotriene receptor blocker, on SCI-induced oxidative damage. Wistar albino rats (n =24) were divided randomly as control, vehicle- or montelukast (10mg/kg, ip)-treated SCI groups. To induce SCI, a standard weight-drop method that induced a moderately severe injury at T10 was used. Vehicle or montelukast were administered to the injured animals 15min after injury. At seven days post-injury, neurological examination was performed and rats were decapitated. Blood samples were taken to evaluate leukotriene B4 levels, and pro-inflmamatory cytokines (TNF-α, IL-1β) while in spinal cord and urinary bladder samples malondialdehyde (MDA), glutathione (GSH), luminol chemiluminescence (CL) levels and myeloperoxidase (MPO) and caspase-3 activities were determined. Tissues were also evaluated histologically. SCI caused significant decreases in tissue GSH, which were accompanied with significant increases in luminol CL and MDA levels and MPO and caspase-3 activities, while pro-inflammatory cytokines in the plasma were elevated. On the other hand, montelukast treatment reversed these parameters and improved histological findings. In conclusion, SCI caused oxidative tissue injury through the activation of pro-inflammatory mediators and by neutrophil infiltration into tissues, and the neuroprotective and antiapoptotic effects of montelukast are mediated by the inhibition of lipid peroxidation, neutrophil accumulation and pro-inflammatory cytokine release. Moreover, montelukast does not only exert antioxidant and antiapoptotic effects on the spinal cord, but it has a significant impact on the bladder tissue damage secondary to SCI. [Copyright &y& Elsevier]

Abstract: Oxidative stress has been implicated in various pathological processes including burn induced multiple organ damage. This study investigated the effects of lycopene treatment against oxidative injury in rats with thermal trauma. Under ether anesthesia, shaved dorsum of the rats was exposed to 90°C bath for 10s to induce burn and treated either vehicle (olive oil) or lycopene (50mg/kg orally). Rats were decapitated 48h after injury and the tissue samples from lung and kidney were taken for histological analysis and the determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO), superoxide dismutase (SOD), catalase (CAT) and caspase-3 activities. Proinflammatory cytokines, TNF-α and IL-1β, were assayed in blood samples. Severe skin scald injury caused a significant decrease in GSH levels, SOD and CAT activities, and significant increases in MDA levels, MPO and caspase-3 activities of tissues. Similarly, plasma TNF-α and IL-1β were elevated in the burn group as compared to the control group. Lycopene treatment reversed all these biochemical indices. According to the findings of the present study, lycopene possesses antiinflammatory, antiapoptotic and antioxidant effects that prevents burn-induced oxidative damage in remote organs. [Copyright &y& Elsevier]