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Objectives: Nutritional obesity causes oxidant damage in the body and cataract formation in the lenses by increasing the formation of free radicals. Myrtus communis leaf extracts (Myr) have antioxidant properties, and apocynin (Apo) is an effective NADPH-oxidase inhibitor. The data on tissue boron levels are quite lacking. The aim of this novel study was to investigate the effects of Myr and Apo treatment on boron levels and oxidative lens damage in rats fed a high-fat diet (HFD). Materials and Methods: Wistar albino male rats were randomly divided into four groups: the control group, HFD group, HFD + Myr group, and HFD + Apo group. Body weight and blood lipids were determined before and after the experiment. After decapitating the rats, the lenses were removed and homogenized. Catalase (CAT) and superoxide dismutase (SOD) activities and boron, malondialdehyde (MDA), and reduced glutathione (GSH) levels in the lens homogenates were determined. Results: The HFD increased serum triglyceride (p<0.05), total cholesterol level (p<0.001), body weight (p<0.001), and lens MDA levels (p<0.01) and decreased lens GSH (p<0.05) and boron level (p<0.01), SOD (p<0.001), and CAT activity (p<0.001). However, Myr and Apo treatment reduced the rats' body weight (p<0.001), serum triglyceride (p<0.05), and total cholesterol level (p<0.001) and increased lens boron (p<0.01; p<0.001), GSH levels (p<0.05; p<0.01), and CAT activity (p<0.001). Conclusion: Both Myr and Apo may be able to reduce oxidative stress in the lenses of obese rats caused by HFD by increasing boron levels. [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.)

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.)

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]

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.)

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 present study was undertaken to determine whether resveratrol (RVT) could ameliorate ionizing radiation-induced oxidative injury. After a 10-days pre-treatment with RVT (10 mg/kg/day p.o.), rats were exposed to whole-body IR (800 cGy) and the RVT treatment was continued for 10 more days after the irradiation. Irradiation caused a significant decrease in glutathione level, while malondialdehyde levels, myeloperoxidase activity and collagen content were increased in the liver and ileum tissues. Similarly, plasma lactate dehydrogenase and pro-inflammatory cytokine levels, 8-hydroxy-2'-deoxyguanosine and leukocyte apoptosis were elevated, while antioxidant-capacity was reduced in the irradiated rats as compared with the control group. Furthermore, Na+, K+-ATPase activity was inhibited and DNA fragmentation was increased in the ileal tissues. Resveratrol treatment reversed all these biochemical indices, as well as histopathological alterations induced by irradiation. In conclusion, supplementing cancer patients with adjuvant therapy of resveratrol may have some benefit for a more successful radiotherapy. [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.)

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]

Abstract: Sepsis leads to various organ damage and dysfunction. One of the underlying mechanisms is thought to be the oxidative damage due to the generation of free radicals. In this study, we investigated the putative protective role of β-glucan against sepsis-induced oxidative organ damage. Sepsis was induced by caecal ligation and puncture (CLP) in Wistar albino rats. Sham operated (control) and sepsis groups received saline or β-glucan (50 mg/kg, po) once daily for 10 days and 30 min prior to and 6 h after the CLP. Sixteen hours after the surgery, rats were decapitated and the biochemical changes were determined in the brain, diaphragm, kidney, heart, liver and lung tissues using malondialdehyde (MDA) content – an index of lipid peroxidation – glutathione (GSH) levels – a key antioxidant – and myeloperoxidase (MPO) activity – an index of neutrophil infiltration. Serum TNF-α levels were assessed by RIA method. Tissues were also examined under light microscope to evaluate the degree of sepsis-induced damage. The results demonstrate that sepsis significantly decreased GSH levels and increased the MDA levels and MPO activity (p &#60;0.05–p &#60;0.001) causing oxidative damage. Elevated plasma TNF-α levels in septic rats significantly reduced to control levels in β-glucan treated rats. Since β-glucan administration reversed these oxidant responses, it seems likely that β-glucan protects against sepsis-induced oxidative organ injury. [Copyright &y& Elsevier]

Sepsis is commonly associated with enhanced generation of reactive oxygen metabolites, which lead to multiple organ dysfunction. The aim of this study was to examine the role of melatonin, a potent antioxidant, in protecting the intestinal and bladder tissues against damage in a rat model of sepsis. Sepsis was induced by cecal ligation and perforation (CLP) in Wistar Albino rats. Sham operated (control) and CLP group received saline or melatonin (10 mg/kg, ip) 30 minutes prior to and 6 hours after the operation. Sixteen hours after the surgery, rats were decapitated and the intestinal and urinary bladder tissues were used for contractility studies, or stored for the measurement of malondialdehyde (MDA) content -an index of lipid peroxidation-, glutathione (GSH) levels -a key antioxidant- and myeloperoxidase (MPO) activity- an index of neutrophil infiltration-. Ileal and bladder MDA levels in the CLP group were significantly increased (p < 0.001) with concomitant decreases in GSH levels (p < 0.01–p < 0.001) when compared to the control group. Similarly, MPO activity was significantly increased (p < 0.001) in both ileum and bladder tissues. On the other hand, melatonin treatment significantly reversed (p < 0.001) the elevations in MDA and MPO levels, while reduced GSH levels were increased back to the control levels (p < 0.01–p < 0.001). In the CLP group, the contractility of the ileal and bladder tissues decreased significantly compared with controls. Melatonin treatment of the CLP group restored these responses. In this study, CLP induced dysfunction of the ileal and bladder tissue of rats was reversed by melatonin treatment. Moreover, melatonin, as an antioxidant, abolished the elevation in lipid peroxidation products and myeloperoxidase activity, and reduction in the endogenous antioxidant glutathione and thus protected the tissues against sepsis-induced oxidative damage. [Copyright &y& Elsevier]

Ulcerative colitis (UC) which has a global impact on the health care system with its recurrent and incompletely curable characteristics, affects the patients' quality of life. Gilaburu (GB; Viburnum opulus L.) is a fruit with rich polyphenol ingredient which is used ethnobotanically in Türkiye for medicinal purposes (for example, to pass kidney stones, to treat stomach, heart, and liver diseases, hemorrhages, hypertension, ulcers, common cold, tuberculosis, rheumatic and menstrual pain, and diabetes). On the other hand, the effects of GB in the experimental UC model have not been studied. This study aimed to explore the potential antioxidant and anti-inflammatory effects of GB fruit extract in improving acetic acid (AA)-induced UC. Starting immediately after (AA + GB group) or 1 week before (GB + AA + GB group) the colitis induced by intrarectal AA (5%; v/v) administration, the rats orally received GB (100 mg/kg) once per day for 3 days. The control and AA groups were administered orally saline (1 ml), while the AA + SS group were administered sulfasalazine (SS; 100 mg/kg; orally) as a positive control once per day for 3 days. Distal colonic tissue specimens were obtained for the histological and biochemical [myeloperoxidase (MPO), malondialdehyde (MDA), glutathione (GSH), chemiluminescence (CL), caspase-3, 8-hydroxy-2'-deoxyguanosine (8-OHdG), matrix metalloproteinase (MMP)-9, transforming growth factor (TGF)-β 1 , smad-3 and cytokine (tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, IL-8, interferon (IFN)-γ), measurements] evaluations on the 3rd day. Elevated macroscopic and microscopic damage scores, high tissue wet weight values, increased tissue-associated MPO, MDA, CL, caspase-3, 8-OHdG, cytokines (TNF-α, IL-1β, IL-6, IL-8), MMP-9, TGF-β 1 , smad-3 levels, and decreased GSH values of the AA group were all reversed by GB treatments (AA + GB and GB + AA + GB groups) (p < 0.05–0.001). However, sulfasalazine treatment (AA + SS group) did not change the IL-8, 8-OHdG, MMP-9, and TGF-β 1 measurements significantly. Gilaburu shows both anti-inflammatory and antioxidant effects against AA-induced colonic damage by suppressing neutrophil infiltration, regulating inflammatory mediators, inhibiting reactive species production, lipid peroxidation, and apoptosis, conserving endogenous antioxidant glutathione, and ameliorating oxidative DNA damage. Since the current ulcerative colitis drugs display limited benefits and adverse side effects, potential therapeutic and/or prophylactic role of gilaburu can be evaluated in ulcerative colitis. [Display omitted] • Gilaburu (GB) suppresses neutrophil infiltration to the inflamed colonic tissue. • GB prevents lipid peroxidation and endogenous antioxidant glutathione depletion. • GB reduces toxic oxygen and nitrogen metabolites in the acetic acid-induced colitis. • GB improves oxidative DNA damage and inhibits apoptosis in tissues of colitic rats. • GB exerts anti-inflammatory activity by reducing/inhibiting proinflammatory cytokines. [ABSTRACT FROM AUTHOR]

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: The potential protective effect of OT on a stress-aggravated colitis model in rats and the involvement of OT receptors were evaluated. Holeboard test performances of Sprague–Dawley rats were videotaped for 5min to evaluate their exploratory behavior as indices of anxiety levels. A subgroup of rats was exposed to a 30-min psychological stress procedure, “water avoidance stress”, for 5 consecutive days. Colitis was induced by intracolonic administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS, 30mg/ml), while the sham group was administered with intracolonic saline. Either OT (0.5mg/kg/day; subcutaneously) or OT + OT receptor antagonist atosiban, was given (1mg/kg/day; intraperitoneally) for 3 consecutive days after colitis induction. On the third day, holeboard tests were performed again and the rats were decapitated. Macroscopic lesions were scored and the degree of oxidant damage was evaluated by colonic myeloperoxidase activity (MPO), malondialdehyde (MDA) and glutathione (GSH) levels, and by histological analysis. Colitis induction inhibited exploratory behavior, indicating increased anxiety level, while exposure to stress further exaggerated the degree of anxiety. Macroscopic scores as well as MDA and MPO levels revealed that tissue damage is aggravated in the stressed group with colitis while antioxidant GSH levels were decreased in both colitis and stressed colitis groups. Oxytocin treatment decreased the exacerbated anxiety, MPO and MDA levels and inflammatory cell infiltration and submucosal edema while atosiban abolished all the protective effects of OT. Thus, the results showed that the anxiolytic and antioxidant effects of OT are mediated via its receptors, since atosiban reversed the protective impact of OT on colonic injury while blocking its stress-relieving effect. [Copyright &y& Elsevier]