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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.)

Objectives: Alzheimer's disease is a neurodegenerative disorder characterized by progressive loss of memory followed by complete dementia. Furthermore it is the commonest form of dementia affecting older people. In this study we investigated the role of agmatine (Agm) on learning and memory and on parameters of oxidative stress in intracerebroventricular (i.c.v) streptozotocin (STZ) model of Alzheimer's disease in rats. Materials and Methods: We grouped rats as: naive control, sham operated, STZ and STZ+agmatine. Rats were injected bilaterally i.c.v STZ (3mg/kg) using stereotaxic frame on day 1 and 3 to induce experimental Alzheimer's disease. After 14 days from 1st STZ injection, learning and memory impairment of rats were observed in passive avoidance. Following this test, agmatine administered intraperitoneal (i.p.) 40mg/kg twice daily for 7 days. These animals were again subjected to these behavioral tests after 7 days agmatine treatment. On the 21st day after 1st STZ injection all groups were sacrificed by decapitation and brain tissues were collected for oxidative stress measurement. Malondialdehyde (MDA), glutathione (GSH) levels and myeloperoxidase (MPO) activity were measured for estimation of oxidative stress. Results: In this study it has been demonstrated that i.c.v STZ in Alzheimer model can cause disorder in cognitive functions and oxidative damage. Agmatine treatment is found to be effective to prevent both cognitive deficits as well as the oxidative damage. Conclusion: According to results of the current study agmatine, as an endogenous molecule, might be an important modulator in alzheimer's etiopathogenesis. [ABSTRACT FROM AUTHOR]

Objectives: Alzheimer's disease is a neurodegenerative disorder characterized by progressive loss of memory followed by complete dementia. Furthermore it is the commonest form of dementia affecting older people. In this study we investigated the role of agmatine (Agm) on learning and memory and on parameters of oxidative stress in intracerebroventricular (i.c.v) streptozotocin (STZ) model of Alzheimer's disease in rats. Materials and Methods: We grouped rats as: naive control, sham operated, STZ and STZ+agmatine. Rats were injected bilaterally i.c.v STZ (3mg/kg) using stereotaxic frame on day 1 and 3 to induce experimental Alzheimer's disease. After 14 days from 1st STZ injection, learning and memory impairment of rats were observed in passive avoidance. Following this test, agmatine administered intraperitoneal (i.p.) 40mg/kg twice daily for 7 days. These animals were again subjected to these behavioral tests after 7 days agmatine treatment. On the 21st day after 1st STZ injection all groups were sacrificed by decapitation and brain tissues were collected for oxidative stress measurement. Malondialdehyde (MDA), glutathione (GSH) levels and myeloperoxidase (MPO) activity were measured for estimation of oxidative stress. Results: In this study it has been demonstrated that i.c.v STZ in Alzheimer model can cause disorder in cognitive functions and oxidative damage. Agmatine treatment is found to be effective to prevent both cognitive deficits as well as the oxidative damage. Conclusion: According to results of the current study agmatine, as an endogenous molecule, might be an important modulator in alzheimer's etiopathogenesis. [ABSTRACT FROM AUTHOR]

We investigated the protective effect of Nigella sativa against oxidative injury in the heart and kidney tissues of rats with renovascular hypertension (RVH). RVH model was induced by placing a renal artery clip (2-kidney-1-clip, 2K1C) in Wistar albino rats (n= 8), while sham rats (n= 8) had no clip placement. Starting on the 3rd week after the operation, rats received Nigella sativa (0.2 ml/kg/day, intraperitoneally) or vehicle for the following 6 weeks. Blood pressures (BP) were recorded at the beginning of the study and at the end of the 3rd and 9th weeks. Cardiac functions were assessed using transthoracic echocardiography before the rats were decapitated. Plasma samples were obtained to assay asymmetric dimethylarginine (ADMA), nitric oxide (NO), creatine kinase (CK) and lactate dehydrogenase (LDH) levels. Production of reactive oxidants was monitored by chemiluminescence (CL) assay in the cardiac and renal tissues. Moreover oxidative injury was examined through malondialdehyde (MDA) and glutathione (GSH) levels and Na+,K+-ATPase activity in these tissues. 2K1C caused increased BP and left ventricular (LV) dysfunction, while plasma ADMA, CK, and LDH levels were increased (p<0.05-0.001). Moreover, hypertension caused significant decreases in plasma NO levels, as well as in tissue Na+,K+-ATPase activities and GSH contents, while MDA levels in both tissues were increased (p<0.05-0.001). On the other hand, Nigella sativa treatment significantly reduced BP, attenuated oxidative injury and improved LV function. Nigella sativa protected against hypertension-induced tissue damage and improved cardiovascular function via its antioxidant and antihypertensive actions, suggesting a therapeutic potential of Nigella sativa in renovascular hypertension. [ABSTRACT FROM AUTHOR]

Thermal injury may lead to systemic inflammatory response, and multiple organ failure. This study was designed to determine the possible protective effect of etanercept treatment against oxidative damage in the lung tissue induced by burn injury. Under ether anaesthesia, the shaved dorsum of rats was exposed to a 90°C bath for 10 s to induce burn injury. Etanercept (1 mg/kg) or saline was administered intraperitoneally immediately after and at 24th hour burn injury. Rats were decapitated at 6 h and 48 h following burn injury and trunk blood was collected to assay pro-inflammatory cytokines (TNF-α and IL-1β), lactate dehydrogenase (LDH) activity. In order to evaluate the presence of oxidant injury lung tissue samples were taken for the determination of malondialdehyde (MDA) and glutathione levels, myelopreoxidase (MPO) and Na+-K+ ATPase activities. Tissues were also examined microscopically. Severe skin scald injury (30% of total body surface area) caused a significant decrease in GSH level and Na+-K+ ATPase activity, which was accompanied with significant increases in MDA level, MPO activity. Similarly, serum TNF-α, IL-1β and LDH were elevated in the burn group as compared to control group. On the other hand, etanercept treatment reversed all these biochemical indices, as well as histopathological alterations, which were induced by thermal trauma. Findings of the present study suggest that etanercept possesses an anti-inflammatory effect on burn-induced pulmonary damage and may be beneficial in thermal trauma [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 protective effect of resveratrol against nicotine induced oxidative damage on urogenital tissues was evaluated by biochemical, histological and functional studies. Wistar Albino rats were injected with either nicotine hydrogen bitartarate (0.6 mg/kg/day, ip) or saline. Resveratrol (10 mg/kg, po) was administered along with saline or nicotine injections for 28 days. After decapitation, the urinary bladder, corpus cavernosum and kidney tissues were excised. Corpus cavernosum and bladder tissues were used for in vitro contractility studies, or stored at -80 ºC along with kidney tissue for the measurement of malondialdehyde (MDA), glutathione (GSH), and luminol-lucigenin chemiluminescence (CL) levels. Tissue samples were also examined histologically. Chronic nicotine administration caused a significant decrease in GSH levels and increases in MDA levels, and luminol-lucigenin CL in kidney, urinary bladder and corpus cavernosum tissues, suggesting oxidative organ damage, which was also verified histologically. In serum samples increased blood urea nitrogen (BUN), creatinine, proinflammatory cytokines (TNF-α and IL-1β), lactate dehydrogenase (LDH) activity, oxidative DNA damage (8-OHdG) and decreased antioxidant capacity (AOC) due to nicotine administration were reversed with resveratrol. Furthermore, chronic nicotine administration impaired the contractile activity of the bladder and corpus cavernosum strips while resveratrol supplementation to nicotine-treated animals reversed these effects in both tissues. Resveratrol treatment to the nicotine group restored the endogenous GSH levels and decreased oxidative damage parameters in all studied tissues. These data suggest that resveratrol supplementation effectively counteracts the deleterious effect of chronic nicotine administration on bladder, corpus cavernosum and kidney functions and attenuates oxidative damage possibly by its antioxidant effects. [ABSTRACT FROM AUTHOR]

This study was designed to determine the possible protective effect of grape seed extract (GSE), a widely used antioxidant dietary supplement, on hepatic ischemia/reperfusion (I/R) injury. Wistar albino rats were subjected to 45 min of hepatic ischemia, followed by a 60 min reperfusion period. GSE was administered in a dose of 50 mg/kg/day orally for 15 days before I/R injury and repeated before the reperfusion period. Liver samples were taken for histological examination or determination of hepatic malondialdehyde (MDA), glutathione (GSH) and myeloperoxidase (MPO) activity. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were determined to assess liver functions. Lactate dehydrogenase (LDH) and cytokines (TNF- α and IL-1 β) were also assayed in serum samples for the evaluation of generalized tissue damage. Ischemia/reperfusion caused a significant decrease in hepatic GSH, and significant increases in MDA level, and MPO activity. Serum AST and ALT levels, as well as LDH activity and plasma TNF- α and IL-1 β levels were also elevated in the I/R group. Treatment with GSE reversed all these biochemical parameters as well as histological alterations induced by I/R. In conclusion, GSE reduced I/R-induced organ injury through its ability to balance the oxidant-antioxidant status, to inhibit neutrophil infiltration and to regulate the release of inflammatory mediators. Copyright © 2007 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

This investigation elucidated the role of free radicals in naphthalene-induced toxicity and protection by Ginkgo biloba extract (EGb). BALB-c mice of either sex were administered with naphthalene (100 mg/kg; i.p.) for 30 days, along with either saline or EGb (150 mg/kg, orally). At the end of the experiment, following 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. In addition, proinflammatory cytokines (TNF- α and IL- β) and total antioxidant capacity (AOC) were assayed in the plasma, while lactate dehydrogenase (LDH) activity was assayed in serum samples. The results revealed that naphthalene caused a significant decrease in GSH level, and significant increases in MDA level, MPO activity and collagen content of tissues. Similarly, plasma cytokines, as well as serum LDH activity, were elevated while AOC was decreased in the naphthalene group compared with the control group. On the other hand, EGb treatment reversed all these biochemical indices. The results demonstrate that EGb extract, by balancing the oxidant-antioxidant status and inhibiting the generation of proinflammatory cytokines and neutrophil infiltration, protects against naphthalene-induced oxidative organ injury. Copyright © 2006 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Experiments have shown that chronic nicotine administration caused oxidative damage in various organs by increasing lipid peroxidation products and decreasing the activity of endogenous antioxidants. The aim of this study was to investigate the effects of taurine treatment on nicotine-induced oxidative changes in rat thoracic aorta and heart and to explore the possible mechanisms of action. Male Wistar albino rats (200–250 g) were injected with nicotine hydrogen bitartrate (0.6 mg/kg; i.p.) or saline for 21 days. Taurine was administered (50 mg/kg; i.p.) alone or along with nicotine injections. After decapitation, the thoracic aorta and heart tissues were excised. The aorta was used for in vitro contractility studies or stored along with the heart samples for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen content. Tissue samples were also examined histologically. Serum samples were stored for the measurement of MDA, GSH and lactate dehydrogenase (LDH) activity. Chronic nicotine treatment impaired both the contraction and relaxation responses of the aortic rings to phenylephrine and acetylcholine, respectively. It increased lipid peroxidation, MPO levels and tissue collagen content of both aorta and heart samples. Taurine supplementation to nicotine-treated animals reversed the contractile dysfunction and restored the endogenous GSH levels and decreased high lipid peroxidation and MPO activities in both tissues. These data suggest that taurine supplementation effectively attenuates the oxidative damage because of chronic nicotine administration possibly by its antioxidant effects. [ABSTRACT FROM AUTHOR]

Oxygen free radicals are involved in pathophysiology of ischemia/reperfusion (I/R) injury. This study was designed to assess the possible protective effect of pycnogenol, against I/R-induced oxidative renal damage. Wistar albino rats were unilaterally nephrectomized and subjected to 45 min of renal pedicle occlusion followed by 3 h of reperfusion. PYC (10 mg kg-1, i.p.) or saline was administered at 15 min prior to ischemia and immediately before the reperfusion period. At the end of the 3 h, rats were decapitated and trunk blood was collected. Creatinine, blood urea nitrogen (BUN) and lactate dehydrogenase (LDH) activity were measured in the serum samples, while proinflammatory cytokines, TNF-α, IL-1β, IL-6 levels were assayed in plasma samples. Kidney samples were taken for the determination of tissue malondialdehyde (MDA), glutathione (GSH) levels, Na+, K+ ATPase and myeloperoxidase (MPO) activity and the extent of tissue injury was analyzed microscopically. Ischemia/reperfusion caused a significant decrease in tissue GSH level and Na+, K+ ATPase activity, which was accompanied with significant increases in the renal MDA level and MPO activity. Similarly, serum creatinine and BUN levels, as well as LDH and IL-1β IL-6, and TNF-α levels were elevated in the I/R group as compared to control group. On the other hand, pycnogenol treatment reversed all these biochemical indices, as well as histopathological alterations that were induced by I/R. Findings of the present study suggest that pycnogenol exerts renoprotective effects via its free radical scavenging and antioxidant activities, that appear to involve the inhibition of tissue neutrophil infiltration. [ABSTRACT FROM AUTHOR]