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Ahmet Korkmaz

Publications and source records attributed to Ahmet Korkmaz.

At least 19 recordsLinked to original sources
PubMed2007

Antioxidant effects of melatonin in rats during chronic exposure to hyperbaric oxygen.

In addition to its beneficial effects, hyperbaric oxygen (HBO) exposure causes some detrimental effects via oxidative stress. Previous experimental studies showed that melatonin is a useful agent to block single session HBO-induced oxidative stress. In the present study, we investigated the antioxidant effect of exogenously administered as well as endogenously produced melatonin in lung and brain tissues of rats exposed to long term HBO. The HBO procedure was set as daily exposures to 2.5 ATA of oxygen for 1 hr and a total of 10 sessions. Twenty-eight male Sprague-Dawley rats were divided into four groups as follows: control, daytime HBO, daytime HBO plus melatonin (5 mg/kg), nighttime HBO. Tissue oxidative/antioxidant status was examined by determining the protein carbonyl content as a criteria for oxidative stress and the activities of the antioxidant enzymes, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). HBO exposure for 10 days caused significant increases in protein carbonyl content and SOD levels of lung and brain, but GSH-Px activities remained unaffected. The increases in protein carbonyls were blocked by exogenously administered melatonin and in part by nighttime exposure to darkness whereas the increase of SOD activity was only impeded by endogenously produced melatonin in brain tissue. Lung SOD activity was augmented by endogenous melatonin. In conclusion, melatonin blocks long-term HBO-induced cumulative oxidative stress as indicated changes in protein carbonyls. Both exogenously injected and physiologically secreted melatonin has this potential. The effects of HBO-exposure and melatonin on the activities of the antioxidative enzymes are less clear.

Animals↗
PubMed2006

Lung toxicity of nitrogen mustard may be mediated by nitric oxide and peroxynitrite in rats.

Nitric oxide (NO) has previously been shown to be responsible for nitrogen mustard (NM)-induced tissue toxicity. Excessive amounts of NO are known to be able to produce peroxynitrite, an important reactive nitrogen compound, by reacting with superoxide. Previous studies reported that NO synthase inhibitors are able to prevent NM toxicity. The aim of this study was to evaluate whether peroxynitrite is also responsible for NM-induced lung tissue damage in rats. Wistar rats were divided into four groups. NM was injected intratracheally and was treated with the selective inducible nitric oxide synthase (iNOS) inhibitor aminoguanidine (AG) (intraperitoneal) or the peroxynitrite scavenger ebselen (intragastric). Control animals were exposed to saline only. NM injection caused both oxidative and nitrosative stress, reflected by dramatically increased levels of the lipid peroxidation end product malondialdehyde (MDA), iNOS activation and urine nitrite-nitrate (NOx) values. Histopathological evaluation demonstrated lung damage with NM exposure. AG blocked iNOS activation and decreased urine NOx levels, and resulted in less histopathological changes in the lung. Although the histopathological outcome was found to be similar to AG, ebselen did not change urinary NOx or lung iNOS levels. Furthermore, ebselen was more able than AG to protect against MDA accumulation. In conclusion, the ability of ebselen to prevent against lung damage without blocking NO synthesis suggests that peroxynitrites may have an important role in the pathogenesis of NM toxicity in addition to NO.

Alkylating Agents↗
PubMed2006

Hyperbaric oxygen treatment augments the efficacy of a losartan regime in an experimental nephrotic syndrome model.

BACKGROUND/AIMS: Proteinuria is associated with oxidant stress and inflammation. Hyperbaric oxygen (HBO) treatment has anti-inflammatory and anti-oxidant effects. The aim of the study was to investigate the benefits of HBO treatment on an experimental nephrotic syndrome model. METHODS: 50 male Sprague-Dawley rats weighing 255 +/- 39 g were housed. Forty rats were injected 6 mg/kg adriamycin into tail veins under anesthesia to induce nephrosis, while 10 rats were spared as sham control. After the stabilization of proteinuria at the sixth week, the rats were treated for 6 weeks by losartan (n = 10, 30 mg/kg/day), HBO (n = 10, 2.8 atmosphere absolute, 90 min/day), HBO + losartan (n = 10) and vehicle (n = 10). Protein carbonyl (PCO), superoxide dismutase (SOD) and glutathione peroxidase (GPx) were analyzed from tissue specimens. Biochemical markers were studied from venous samples and 24-hour urine was collected for proteinuria. The surviving animals at 12 weeks (vehicle group (n = 6), HBO (n = 6), losartan (n = 8), HBO + losartan (n = 10) were sacrificed. Glomerular sclerosis, tubulointerstitial and blood vessel changes were determined by semiquantitative scoring. RESULTS: The PCO levels increased (p < 0.001), and the GPx and SOD levels decreased (p < 0.001 for both) in the nephrotic rats. In losartan and HBO groups GPx levels increased (p = 0.001, p = 0.002 respectively), but PCO and SOD levels did not change. The combination of HBO with losartan significantly increased the GPx and SOD levels (p = 0.001 for both) and decreased PCO levels (p = 0.005). HBO but not losartan significantly reduced proteinuria (p < 0.001). The combination of HBO and losartan reduced proteinuria better than the single losartan regime (p < 0.001). The effect of the combination was also noticed on the histological examination of the kidneys. The activities, appetites, weight gains, and improvement of edema were better in the HBO combined with losartan regime. CONCLUSIONS: These results indicate that the addition of HBO therapy to a conventional regime, angiotensin receptor blockers, has significant benefits in the management of proteinuria. Future clinical studies are needed to elucidate the role of HBO and other antioxidant strategies in the treatment of proteinuria.

Animals↗
PubMed2006

Molecular targets against mustard toxicity: implication of cell surface receptors, peroxynitrite production, and PARP activation.

Despite many years of research into chemical warfare agents, cytotoxic mechanisms induced by mustards are not well understood. Reactive oxygen and nitrogen species (ROS and RNS) are likely to be involved in chemical warfare agents induced toxicity. These species lead to lipid peroxidation, protein oxidation, and DNA injury, and trigger many pathophysiological processes that harm the organism. In this article, several steps of pathophysiological mechanisms and possible ways of protection against chemical warfare agents have been discussed. In summary, pathogenesis of mustard toxicity is explained by three steps: (1) mustard binds target cell surface receptor, (2) activates intracellular ROS and RNS leading to peroxynitrite (ONOO(-)) production, and (3) the increased ONOO(-) level damages organic molecules (lipids, proteins, and DNA) leading to poly(adenosine diphosphate-ribose) polymerase (PARP) activation. Therefore, protection against mustard toxicity could also be performed in these ways: (1) blocking of cell surface receptor, (2) inhibiting the ONOO(-) production or scavenging the ONOO(-) produced, and (3) inhibiting the PARP, activated by ONOO(-) and hydroxyl radical (OH(*)) induced DNA damage. As conclusion, to be really effective, treatment against mustards must take all molecular mechanisms of cytotoxicity into account. Combination of several individual potent agents, each blocking one of the toxic mechanisms induced by mustards, would be interesting. Therefore, variations of combination of cell membrane receptor blockers, antioxidants, nitric oxide synthase inhibitors, ONOO(-) scavengers, and PARP inhibitors should be investigated.

Animals↗
PubMed2005

Effects of hyperbaric oxygen treatment on liver functions, oxidative status and histology in septic rats.

OBJECTIVE: The liver is thought to be responsible for multiple organ failure during sepsis. Increase in tissue oxygen consumption is a major component of the septic response. Hyperbaric oxygen (HBO) therapy provides more oxygenation in the whole body. This study examined the effect of HBO alone or in combination with cefepime (CEF) on the liver in septic rats. DESIGN AND INTERVENTIONS: We divided 90 male rats into six groups; control, HBO, sepsis (SEP), SEP+HBO, SEP+CEF, and SEP+CEF+HBO. Sepsis was induced with an intraperitoneal injection of Escherichia coli (2.1 x 10(9) cfu). A total of six HBO sessions were performed at 2 atm absolute for 90 min at 6-h intervals. CEF was administered intraperitoneally at a dose of 50 mg/kg twice daily. Animals were killed 48 h after sepsis induction. Their liver and blood were removed for biochemical and histopathological analysis. MEASUREMENTS AND RESULTS: Liver thiobarbituric acid reactive substances as well as serum alanine transaminase, aspartate transaminase and alkaline phosphatase levels increased while the activity of the antioxidant enzymes superoxide dismutase and catalase decreased significantly in septic rats. These parameters returned to nearly control levels in the SEP+CEF+HBO group. Histological observations supported these findings: Hepatocellular degeneration was observed and intensive polymorphonuclear cell infiltration appeared in all fields of septic animal livers. HBO alone could not sufficiently reverse these histopathological changes, but most liver sections presented normal histology when it was combined with CEF. CONCLUSIONS: HBO may be a useful adjuvant therapy modality to improve the efficacy of sepsis treatment.

Animals↗
PubMed2005

Contribution of flavonoid antioxidants to the preventive effect of mesna in cyclophosphamide-induced cystitis in rats.

Cyclophosphamide (CP) is widely used, alone or in combination with other chemotherapeutic agents, for treatment of neoplastic diseases. Its urotoxicity may cause dose-limiting side-effects, for example hemorrhagic cystitis. The agent most often used to prevent this side-effect is mesna (2-mercaptoethane sulfonate). Overproduction of reactive oxygen species during inflammation is one reason for possible urothelial injury. The aim of this study was to evaluate whether combinations of quercetin and epigallocatechin 3-gallate (EGCG), flavonoid antioxidants and mesna could prevent cystitis induced by cyclophosphamide, better than mesna alone. A total of 38 male Sprague-Dawley rats were divided into five groups. Four groups received single dose of CP (100 mg kg(-1)) intraperitoneally at the same time. Group 2 received CP only, group 3 received mesna (3 x 21.5 mg kg(-1)), group 4 received a single dose of mesna+EGCG (2 x 20 mg kg(-1)), and group 5 received a single dose of mesna+quercetin (2 x 20 mg kg(-1)), before and after CP injection. Group 1 (not treated) served as control. CP injection alone resulted in severe cystitis. Mesna resulted in some, but not full, protection against CP toxicity. Quercetin and catechine, together with mesna, resulted in full protection against CP toxicity, on the basis of histopathology of the urinary bladder. It was concluded that oxidants might be important in the pathogenesis of CP-induced cystitis, and that flavonoid antioxidants, used in addition to mesna, may help to ameliorate bladder damage.

Animals↗
PubMed2005

The effect of hyperbaric oxygen treatment on the renal functions in septic rats: relation to oxidative damage.

PURPOSE: To investigate the effects of hyperbaric oxygen (HBO) treatment on renal functions and damage in septic rats. METHODS: The animals were divided into four groups, each containing ten animals: control, hyperbaric oxygen, sepsis, and sepsis/hyperbaric oxygen. One milliliter of saline containing live Escherichia coli cells (2.1 x 10(9)) was injected intraperitoneally to induce sepsis. The groups treated with HBO were given five sessions of 2 atmospheres absolute of 100% oxygen at intervals of 6 h. Blood, urine, and tissue samples were then collected, and the functional renal parameters, malondialdehyde (MDA) levels, and superoxide dismutase (SOD) and catalase activities were examined. RESULTS: The reduced glomerular filtration rate and urine flow returned to normal levels after HBO treatment; however, the increase in fractionated sodium excretion continued. The increased MDA levels in the renal cortex and medulla also decreased to the level of the control group. In the sepsis group, both the SOD and catalase activities decreased in the renal cortex, while a reduction was observed only in the catalase activity in the medulla. The reduced enzyme activities significantly increased in the sepsis/hyperbaric oxygen group. CONCLUSION: HBO treatment has a beneficial effect on renal dysfunction in sepsis. The probable reason for this effect is the reduction in oxidative damage because of the increase in antioxidative capacity.

Animals↗
PubMed2005

The oxidative and morphological effects of high concentration chronic toluene exposure on rat sciatic nerves.

This study was designed to investigate the effects of chronic toluene inhalation in high concentration on lipid peroxidation, antioxidant enzyme activities and ultrastructural changes in the sciatic nerves of rats. Male Wistar albino rats (150-250 g) were divided in two experimental groups: the control and the toluene treated group (n = 10 for each). Toluene treatment was performed by inhalation of 3000 ppm toluene, in a 8 h/day and 6 day/week order for 16 weeks. Blood and tissue samples were obtained for biochemical and histopathological investigation. The blood and sciatic nerves were assayed for toluene by gas chromatography. Toluene significantly increased blood and tissue malondialdehyde (MDA), and decreased tissue superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), but not tissue catalase (CAT) levels when compared with controls. Electron micrographs of sciatic nerve in the toluene group shows myelin destructions with onion-bulb and bubble form protrusion on the myelin sheath and axolemma border of myelinated axons. The area of injury on the myelin sheath were measured by Image-Pro Plus. Mean of the injury area were estimated 34% each myelin. These findings indicate that chronic toluene inhalation might be involved with free radical processes.

Animals↗
PubMed2005

Correlation between hyperbaric oxygen exposure pressures and oxidative parameters in rat lung, brain, and erythrocytes.

OBJECTIVES: The oxygen toxicity risk of hyperbaric oxygen (HBO) treatment has long been of interest. However, there are no comprehensive articles describing the relationship between HBO protocols and oxidative parameters used clinically. The purpose of this study was to determine the effects of various HBO pressure modalities on the oxidative values of rat lung, brain, and erythrocytes. DESIGN AND METHODS: A total of 64 male Sprague-Dawley rats was randomly divided into 7 groups. Group A was used as a control. Groups C to G were subjected to 100% oxygen at a pressure of 1, 1.5, 2, 2.5, and 3 ATA (atmosphere absolute), respectively, for 2 h. Group B was exposed to normal atmospheric air at 3 ATA for the same duration. The rat's lung, brain, and blood were taken immediately after the exposure and thiobarbituric acid reactive substances (TBARS) and superoxide dismutase (SOD) levels were determined. RESULTS: Both TBARS levels and SOD activity increased concordantly with the pressure increase. Although a statistically significant change in TBARS levels started from 100% oxygen exposure at 1 ATA (normobaric), SOD activity was affected after 2 ATA. A significant correlation exists between exposure pressure and the aforementioned parameters. Ambient air exposure at 3 ATA did not affect any parameters besides the brain TBARS levels. CONCLUSIONS: It is clear that HBO exposure causes oxidative stress. The main reason for this effect seems to be exposure to pure oxygen, since pure high pressure has no significant effect on the aforementioned parameters. However, clinicians should use as low pressures as possible since all oxidative parameters appear to be directly proportional to the extent of HBO exposure.

Animals↗
PubMed2005

Quercetin, a flavonoid antioxidant, prevents and protects streptozotocin-induced oxidative stress and beta-cell damage in rat pancreas.

The aim of the present study was the evaluation of possible protective effects of quercetin (QE) against beta-cell damage in experimental streptozotocin (STZ)-induced diabetes in rats. STZ was injected intraperitoneally at a single dose of 50 mg kg(-1) for diabetes induction. QE (15 mg kg(-1) day, intraperitoneal (i.p.) injection) was injected for 3 days prior to STZ administration; these injections were continued to the end of the study (for 4 weeks). It has been believed that oxidative stress plays a role in the pathogenesis of diabetes mellitus (DM). In order to determine the changes of cellular antioxidant defense system, antioxidant enzymes such as glutathione peroxidase (GSHPx), superoxide dismutase (SOD) and catalase (CAT) activities were measured in pancreatic homogenates. Moreover we also measured serum nitric oxide (NO) and erythrocyte and pancreatic tissue malondialdehyde (MDA) levels, a marker of lipid peroxidation, if there is an imbalance between oxidant and antioxidant status. Pancreatic beta-cells were examined by immunohistochemical methods. STZ induced a significant increase lipid peroxidation, serum NO concentrations and decreased the antioxidant enzyme activity. Erythrocyte MDA, serum NO and pancreatic tissue MDA significantly increased (P < 0.05) and also the antioxidant levels significantly decreased (P < 0.05) in diabetic group. QE treatment significantly decreased the elevated MDA and NO (P < 0.05), and also increased the antioxidant enzyme activities (P < 0.05). QE treatment has shown protective effect possibly through decreasing lipid peroxidation, NO production and increasing antioxidant enzyme activity. Islet cells degeneration and weak insulin immunohistochemical staining was observed in STZ induced diabetic rats. Increased staining of insulin and preservation of islet cells were apparent in the QE-treated diabetic rats. These findings suggest that QE treatment has protective effect in diabetes by decreasing oxidative stress and preservation of pancreatic beta-cell integrity.

Animals↗
PubMed2005

Peroxynitrite may be involved in bladder damage caused by cyclophosphamide in rats.

PURPOSE: It was previously shown that nitric oxide (NO) produced by inducible NO synthase (iNOS) is responsible for cyclophosphamide (CP) induced cystitis. In this study we evaluated whether peroxynitrite is also responsible for CP induced bladder damage in rats. MATERIALS AND METHODS: A total of 38 male albino Wistar rats were divided into 4 groups. Group 1 served as controls and was given 2 ml saline, while 3 groups received a single dose of CP (200 mg/kg) at the same intervals. Group 2 received CP only, group 3 received the selective iNOS inhibitor aminoguanidine (AG) (100 mg/kg) and group 4 received the peroxynitrite scavenger ebselen (2-phenyl-1,2-benzisoselenazol-3[2H]-one) (20 mg/kg). RESULTS: CP injection resulted in severe cystitis with continuous macroscopic hemorrhage, strong edema, inflammation and ulceration. Moreover, bladder tissue malondialdehyde levels, iNOS activation and urine nitrite-nitrate levels were dramatically increased. AG histologically protected bladder against CP damage and decreased urine nitrite-nitrate levels, bladder malondialdehyde and iNOS induction. Ebselen showed results similar to those of AG without changing the urinary nitrite-nitrate level and iNOS activity. CONCLUSIONS: These results suggest that not only nitric oxide, but also peroxynitrite may be important in the pathogenesis of CP induced cystitis.

Animals↗
PubMed2005

Protective effects of exogenously administered or endogenously produced melatonin on hyperbaric oxygen-induced oxidative stress in the rat brain.

1. Hyperbaric oxygen (HBO) is a widely used treatment modality in many diseases. A known side-effect of HBO is the production of reactive oxygen species (ROS). Many anti-oxidants, such as vitamins C and E, riboflavin and selenium, have been used successfully to scavenge the ROS produced by HBO administration. 2. The aim of the present study was to determine whether melatonin, a newly discovered anti-oxidant, has a protective effect against the overproduction of ROS produced by HBO in rat brain tissue. 3. Seventy male Sprague-Dawley rats were divided into seven groups as follows: 1, daytime control; 2, daytime HBO; 3, melatonin; 4, daytime HBO plus melatonin; 5, night-time control; 6, night-time HBO; and 7, night-time HBO under light exposure. 4. Hyperbaric oxygen was administered at 303 kPa for 120 min. Melatonin was injected at a dose of 10 mg/kg, i.p. Brain malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GPx) levels were measured to elucidate oxidant status. 4. The MDA and SOD levels of groups 2 and 7 increased significantly. Exogenous (group 4) and endogenous (group 6) melatonin protected against HBO-induced lipid peroxidation. Exogenously administered melatonin (groups 3 and 4) had increased levels of the anti-oxidant enzymes SOD and GPx. 5. In conclusion, HBO caused oxidative stress and melatonin exhibited protective effects. Both endogenously produced and exogenously administered melatonin were found to be effective.

Animals↗
PubMed2005

Melatonin ameliorates bladder damage induced by cyclophosphamide in rats.

Cyclophosphamide (CP), an alkylating antineoplastic agent, has potential urotoxicity including causing hemorrhagic cystitis (HC). HC is now accepted as a non-infectious inflammation and the pathogenesis of HC includes cytokine production which leads to inducible nitric oxide synthase (iNOS) induction. Moreover, overproduction of reactive oxygen species (ROS) during inflammation leads to extensive oxidative stress, cellular injury and apoptosis/necrosis via several mechanisms. Based on these facts, the aim of this study was to evaluate the protective effects of melatonin as an antioxidant, iNOS inhibitor and peroxynitrite scavenger against CP-induced urinary bladder damage. A total of 30 male Sprague-Dawley rats were divided into four groups. Three groups received a single dose of CP (100 mg/kg) intraperitoneally with the same times. Group 2 received CP only, group 3 received 5 mg/kg/day and group 4 received 10 mg/kg/day melatonin before and the day after CP administration. Group 1 served as the control. Increased iNOS induction, bladder malonyldialdehyde (MDA) levels and urinary nitrite-nitrate excretion were encountered in the CP-only group leading to severe cystitis. Melatonin exhibited significant protection against CP-induced cystitis by diminishing bladder oxidative stress and blocking iNOS and peroxynitrite production. Oxidants may have a major role in the pathogenesis of CP-induced cystitis and iNOS is an important mediator leading to peroxynitrite production. Melatonin ameliorates bladder damage induced by CP.

Animals↗
PubMed2004

Contribution of antioxidants to preventive effect of mesna in cyclophosphamide-induced hemorrhagic cystitis in rats.

PURPOSE: The aim of this study was to evaluate whether combination of antioxidants and mesna may prevent cystitis induced by cyclophosphamide better than mesna alone. MATERIALS AND METHODS: A total of 46 male Sprague-Dawley rats were divided into six groups. Five groups received single dose of cyclophosphamide (CP, 100 mg/kg) intraperitoneally with the same time intervals: group 2 received CP only, group 3 received mesna (21.5 mg/kg for three times), group 4 beta-carotene (20 mg/kg for two times) and mesna, group 5 received alpha-tocopherol (20 mg/kg for two times) and mesna, and group 6 received melatonin (5 mg/kg for two times) and mesna on the day of CP injection. Group 1 served as control. RESULTS: CP injection resulted in severe cystitis. Mesna has showed meaningful but not full protection against CP toxicity. Although beta-carotene did not show any additional beneficial effect when combined with mesna, alpha-tocopherol and especially melatonin with mesna resulted full protection that the pathologist, blinded to the slides, could not differ from sham control. CONCLUSION: Oxidants may be important in the pathogenesis of CP-induced cystitis. Melatonin and alpha-tocopherol may help to ameliorate bladder damage along with other drugs such as mesna and diuretics.

Animals↗
PubMed2004

Exogenously administered and endogenously produced melatonin reduce hyperbaric oxygen-induced oxidative stress in rat lung.

Hyperbaric oxygen (HBO) is a widely used treatment modality in many diseases. A known side effect of HBO is the production of reactive oxygen species. Many antioxidants such as vitamins C and E, riboflavin and selenium have been used successfully to scavenge the reactive oxygen species caused by HBO administration. In this study, we aimed to see if melatonin, a newly discovered antioxidant, has a protective effect against the overproduction of reactive oxygen species produced by HBO in rat lung tissue. Sixty male Sprague-Dawley rats were divided into 5 groups as follows: control, daytime HBO (3 ATA, 120 min), daytime HBO plus melatonin (10 mg/kg), nighttime HBO and nighttime HBO (under light exposure). The MDA, SOD and CAT levels of daytime and nighttime HBO (under light exposure) increased significantly. This significance was not found in the daytime HBO plus melatonin and nighttime HBO groups when compared with the control. In this study, HBO caused oxidant stress, and melatonin decreased the levels of MDA, SOD and CAT. Moreover, endogenous melatonin was found to be a more effective antioxidant than exogenous 10 mg/kg melatonin.

Animals↗
PubMed2004

Inducible nitric oxide synthase inhibition in cyclophosphamide induced hemorrhagic cystitis in rats.

Cyclophosphamide (CP) is an antineoplastic agent used alone or in combination with other chemotherapeutic agents for the treatment of many neoplastic diseases. Hemorrhagic cystitis (HC) is a major potential toxicity and dose limiting side effect of CP. Recently, it has been shown that endogenous inflammatory mediators are involved in cystitis by increasing nitric oxide (NO) production in target tissue. The aim of this study was to evaluate the relationship between NO and CP induced hemorrhagic cystitis HC in rats. A total of 30 female Spraque-Dawley rats were divided into 4 groups. Group 1 served as control, three groups received single dose of CP (100 mg/kg) intraperitoneally (i.p.): group 2 received CP only. Group 3 received the NO precursor L-arginine (80 mg/kg/day), and group 4 received the selective inducible NO synthase (iNOS) inhibitor S-methylisothiourea (SMT; 20 mg/kg/day) before and the day after cyclophosphamide injection. CP injection resulted in severe cystitis. SMT but not L-arginine produced marked inhibition of CP induced bladder damage. We concluded that NO produced by iNOS, is an important mediator in the pathogenesis of CP induced cystitis.

Animals↗
PubMed2004

Effects of Nigella sativa on oxidative stress and beta-cell damage in streptozotocin-induced diabetic rats.

The aim of the present study was to evaluate the possible protective effects of Nigella sativa L. (NS) against beta-cell damage from streptozotocin (STZ)-induced diabetes in rats. STZ was injected intraperitoneally at a single dose of 50 mg/kg to induce diabetes. NS (0.2 ml/kg/day, i.p.) was injected for 3 days prior to STZ administration, and these injections were continued throughout the 4-week study. Oxidative stress is believed to play a role in the pathogenesis of diabetes mellitus (DM). To assess changes in the cellular antioxidant defense system, we measured the activities of antioxidant enzymes (such as glutathione peroxidase (GSHPx), superoxide dismutase (SOD), and catalase (CAT)) in pancreatic homogenates. We also measured serum nitric oxide (NO) and erythrocyte and pancreatic tissue malondialdehyde (MDA) levels, a marker of lipid peroxidation, to determine whether there is an imbalance between oxidant and antioxidant status. Pancreatic beta-cells were examined by immunohistochemical methods. STZ induced a significant increase in lipid peroxidation and serum NO concentrations, and decreased antioxidant enzyme activity. NS treatment has been shown to provide a protective effect by decreasing lipid peroxidation and serum NO, and increasing antioxidant enzyme activity. Islet cell degeneration and weak insulin immunohistochemical staining was observed in rats with STZ-induced diabetes. Increased intensity of staining for insulin, and preservation of beta-cell numbers were apparent in the NS-treated diabetic rats. These findings suggest that NS treatment exerts a therapeutic protective effect in diabetes by decreasing oxidative stress and preserving pancreatic beta-cell integrity. Consequently, NS may be clinically useful for protecting beta-cells against oxidative stress.

Animals↗