Effects of diode laser irradiation on dental pulps in rats.

OBJECTIVES: To evaluate the effects of different power densities of diode laser on dental pulps in rats. BACKGROUND: In this study, we used the maxillary central incisors (n=80) of the 40 adult male Wistar albino rats. METHODS: Rats were randomly divided into four groups according to power densities of diode laser (n=10). Histopathological changes in pulp and height of odontoblast layer were examined . All data were compared statistically using Mann‒Whitney U (Bonferroni) test, p<0.05. RESULTS: G2 displayed slight histolopathologic alterations such as odontoblast cell disorganization and irregularities in cell extensions. Alterations were more prominent in the G3 than G2. Although the lowest odontoblast layer was measured in the G4, the difference in height of odontoblast layer among the groups was not found to be statistically significant. CONCLUSION: It was concluded that the use of diode laser caused changes at the cellular level in histological examination and may induce the formation of tertiary dentin by influencing the secretory activity of odontoblasts. As long as used in accordance with the recommended procedure, the diode laser can be safely used in dental hard tissues (Tab. 1, Fig. 4, Ref. 15).

Harmful effects of formaldehyde and possible protective effect of Nigella sativa on the trachea of rats.

OBJECTIVE: We aimed in this study to investigate the harmful effects of formaldehyde (FA) inhalation and possible protective effects of Nigella sativa (NS) on rats' trachea. MATERIALS AND METHODS: In this study, 63 adult male rats were used. Animals were divided into nine groups. Group I was used as control group. All other groups were exposed to FA inhalation. Group III, V, VII, and IX were administered NS by gavage. Tissues were examined histologically, and immunohistochemical examination for Bax and caspase-3 immunoreactivity was carried out. RESULTS: Our study demonstrated that FA caused apoptosis in the tracheal epithelial cells. The most apoptotic activity occurred at a 10 ppm dose in a 13-week exposure. Distortion of tracheal epithelium and cilia loss on epithelial surface was present in all groups. However, NS treated Groups VII and IX had decreased apoptotic activity and lymphoid infiltration and protected the epithelial structure, despite some shedded areas. Difference of tracheal epithelial thickness and histological score was statistically significant between Group VI-VII and VIII-IX. CONCLUSION: FA induces apoptosis and tracheal epithelial damage in rats, and chronic administration of NS can be used to prevent FA-induced apoptosis and epithelial damage.

The protective effects of apocynin on ionizing radiation-induced intestinal damage in rats.

BACKGROUND AND AIMS: Radiation colitis typically emerges during radiotherapy of intra-abdominal malignancies. While the underlying mechanism remains unclear, it is considered that free oxygen radicals act like cellular mediators to cause colonic damage. Apocynin (APO) prevents oxidative stress and apoptotic cell death by inhibiting NADPH oxidase, and preventing the formation of free oxygen radicals. The aim of the present study was to investigate the protective effect of APO, a strong antioxidant and antiinflammatory agent, on radiation induced colonic oxidative damage in rats. MATERIALS AND METHODS: Rats were randomly divided into four groups (n = 8/group). Group I (control group); Group II (Group RAD) received a single dose of 800 cGy ionizing radiation to the whole abdomen with a linear accelerator (LINAC); Group III (Group APO) received a single dose of 20 mg/kg of APO intraperitoneally for five days; Group IV (Group APO+RAD) received APO for five days before radiation exposure (similar to Group III), (similar to Group II). RESULTS: APO treatment prior to radiation led to protection in the biochemical and histopathological parameters. CONCLUSIONS: Our study shows that APO treatment before radiation improves radiation induced colonic injury in rats, by decreasing oxidative stress and apoptosis.

The effects of caffeic acid phenethyl ester on streptozotocin-induced diabetic liver injury.

The aim of the present study was to clarify the role of oxidative stress in streptozotocin induced liver injury and the possible protective effect of caffeic acid phenethyl ester (CAPE) using histological and biochemical parameters. 32 male Wistar rats were divided into 4 groups as follows: Group 1: Control animals, Group 2: Control animals given CAPE Group 3: STZ-induced diabetic animals (DM group), Group 4: STZ-induced diabetic rats given CAPE (DM+CAPE group). All the injections started on the same day of single-dose STZ injection and continued for 20 days. At the end of this period, livers were removed and processed for routine histological procedures. Biochemical parameters and morphological changes were examined. In DM group, blood glucose levels were significantly increased compared with the control group. Significant increases in tissue malondialdehyde (MDA) level and decreases in superoxide dismutase (SOD) and total glutathione (GSH) activities were detected in DM group. Administration of CAPE significantly reduced these values. STZ-induced histopathological alterations including inflammatory cell infiltration around portal triad, congestion, loss of glycogen in the hepatocytes. Additionally, degenerative cellular alterations, such as numerous vacuolizations including myelinic figure formation, pyknotic nuclei with peripheral localization of heterochromatin condensation and mitochondrial elongation were observed in cytoplasm of hepatocytes. CAPE significantly reduced these histopathological changes. Our results indicate that CAPE should be considered in the prevention of oxidative stress in diabetic liver.

The protective effect of N-acetylcysteine against acrylamide toxicity in liver and small and large intestine tissues.

The aim of this study was to investigate the protective effects of N-acetylcysteine against acrylamide toxicity in liver and small and large intestine tissues in rats.The rats were divided into four groups. Acrylamide administration increased MDA levels in all tissues significantly (p < 0.05). But acrylamide+NAC administration decreased MDA levels significantly as compared to the acrylamide group, and lowered it to a level close to the control group values (p < 0.05). GSH levels in liver and small intestine tissues reduced significantly in the acrylamide group (p < 0.05). But acrylamide+NAC administration increased GSH levels significantly in all tissues. Whereas GST activity decreased significantly in the acrylamide group in liver and small intestine tissues as compared to the other groups (p < 0.05), the GST activity increased significantly in the acrylamide+NAC group in all tissues as compared to the acrylamide group (p < 0.05). Liver histopathology showed that the liver epithelial cells were damaged significantly in the acrylamide group. Small intestine histopathology showed that the intestinal villous epithelial cells were damaged significantly in the acrylamide group.Our results indicate that a high level of acrylamide causes oxidative damage in liver and small and large intestine tissues, while N-acetylcysteine administration in a pharmacological dose shows to have an antioxidant effect in preventing this damage (Tab. 2, Fig. 2, Ref. 66).

Combined usage of estrogen and melatonin restores bladder contractility and reduces kidney and bladder damage in ovariectomized and pinealectomized rat.

OBJECTIVE: The incidence of urinary bladder disturbances and renal structural changes and functional decline are found to increase with age. METHODS: We investigated the effect of melatonin treatment in addition to estrogen replacement therapy in pinealectomized (Px) and ovariectomized (Ovx) rats. 56 female Wistar rats were divided into seven groups, each containing eight animals: Sham, (Ovx), (Px), Px+Ovx, Px+Ovx receiving estrogen (Px+Ovx+E), Px+Ovx receiving melatonin (Px+Ovx+M) and Px+Ovx estrogen and melatonin supplemented (Px+Ovx+EM) group (EM group). We evaluated reduced glutathione (GSH) levels and malondialdehyde (MDA) levels. The mean collagen fiber (CF)/smooth muscle (SM) ratio in the bladder wall and structure of the kidney were examined histolologically. We also recorded response of the bladder contractility to acetylcholine (Ach). RESULTS: Px and Ovx groups showed statistically significant reductions of antioxidant defenses, impaired Ach-evoked contraction, histological changes compared with the control group. Also, these changes were prominent in Px+Ovx group compared with all other groups. Both estrogen and melatonin reversed these changes however best restoration was observed in the EM group. CONCLUSIONS: Px performed in addition to Ovx led to a distinct increase in oxidative damage in bladder and renal tissue and deteriorate of the detrussor function. Either estradiol or melatonin replacement alone or in combination prevents significant alterations of tissue histology and bladder contractility following Ovx and Px. Thus, combination treatment appears to be the best method to restore both contractility and histomorphology of bladder and kidney tissues after Ovx and Px (Tab. 3, Fig. 4, Ref. 44).

Adjuvant aromatase inhibitor therapy in patients with stage I breast cancer at a regional oncology center in Israel: implementation of a 'switching' policy in postmenopausal patients after initial tamoxifen.

OBJECTIVE: To analyze the implementation of a switching policy of adjuvant aromatase inhibitor (AI) therapy sequentially after tamoxifen in consecutively treated stage I (T1N0M0) hormone receptor (HR)-positive breast cancer (BC) patients. METHODS: The records of 279 consecutive HR-positive BC patients diagnosed between 2002 and 2006 and followed at the Soroka Medical Center were reviewed. RESULTS: Two-hundred-seventeen patients who initially received tamoxifen were suitable for switching and 28 received an AI as initial adjuvant treatment. The switch was accomplished in 82.5% of the 217 patients. Those who switched to an AI had a higher proportion of T1c stage than patients eligible who were not switched, but did not differ in age, histologic grade, or having received chemotherapy. Of the 179 patients who switched, 155 (86.6%) completed at least 4.5-5 years of adjuvant tamoxifen/AI therapy. Eighteen patients discontinued AI therapy prematurely because of toxicity. CONCLUSIONS: In this stage I BC population, despite the toxicities of AI therapy, >84% of eligible patients received an AI as adjuvant therapy. Measures to improve the management of AI toxicity, such as changing to a different AI, may reduce early stopping.

Effects of molsidomine against doxorubicin-induced cardiotoxicity in rats.

PURPOSE: To explore the protective and curative effects of molsidomine (MOL) on doxorubicin (DOX)-induced cardiac damage in the in vivo rat heart. METHODS: Forty rats were randomized into five groups (n = 8): (1) the control group; (2) the MOL group (10 mg/kg for 21 days); (3) the DOX group (a single dose of 20 mg/kg); (4) the DOX + MOL group (3 days after the single dose of DOX, 10 mg/kg MOL continued for 21 days), and (5) the MOL + DOX group (24 h after a 21-day regimen of 10 mg/kg MOL, a single dose of DOX). The rats were monitored for mean arterial blood pressure, heart rate, O2 saturation, and electrocardiography. Heart tissue levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), and nitric oxide (NO) were determined. RESULTS: Blood pressure and O2 saturation values indicated a significant decrease in the DOX group compared with the control group. T negativity was observed in 4 of 8 rats in the DOX group, in 1 of 8 rats in the DOX + MOL group, and in 4 of 8 rats in the MOL + DOX group. MDA levels were significantly higher in the DOX group. SOD, GSH, and NO levels were significantly lower in the DOX group compared with the other groups. There was no statistically significant difference in the CAT levels in any of the study groups compared with controls. DOX treatment induced morphological alterations, such as disorganization of cardiomyocytes, loss of myofibrils, and cytoplasmic vacuolization in the heart. On the other hand, histological damage was significantly reduced in the DOX + MOL and MOL + DOX groups. CONCLUSION: This study implies that there are cardioprotective effects of MOL on DOX-induced cardiotoxicity.

Effects of agomelatine on rat liver regeneration following partial hepatectomy.

Primary or metastatic hepatic malignancies are common. Partial hepatectomy (PH) is the primary treatment for both benign and malignant hepatic neoplasms; it also is used for living donor liver transplantation. The regenerative potential of the liver after PH is 70-80% in humans. We investigated the protective and therapeutic effects of agomelatine (AGM) on rat liver regeneration following PH. We used 32 rats distributed equally into four groups: group 1, sham control; group 2, PH group; group 3, administered 20 mg/kg AGM orally once/day for 7 days following PH; group 4, administered 20 mg/kg AGM orally once/day 3 days before and 7 days following PH for 10 days. Liver samples were analyzed for antioxidants and free radicals. Tissue samples were processed and stained with hematoxylin and eosin to assess histopathological status and stained immunohistochemically for Ki-67. We found that PH reduced antioxidant enzymes and increased tissue reactive oxygen species, whereas AGM treatment had the opposite effect on these parameters. Our biochemical and histopathological findings were consistent. PH caused sinusoid congestion and dilation. Intensity of Ki-67 immunostaining of hepatocytes was increased in group 2, whereas these were reduced in group 4. Intensity of Ki-67 immunostaining of hepatocytes was increased in group 2, whereas it was reduced in the group 4 compared to group 1. We found that AGM was hepatoprotective following PH due to its antioxidant and free radical scavenger properties.

The effects of montelukast against amikacin-induced acute renal damage.

BACKGROUND AND OBJECTIVES: The therapeutic and protective effects of montelukast against amikacin-induced acute renal damage were investigated. MATERIAL AND METHODS: 35 Wistar albino female rats were divided into 5 groups as follows: Group I: Control; Group II: Control+montelukast; Group III: Amikacin; Group IV: Amikacin+montelukast; Group V: Montelukast+amikacin. At the end of the experiment, the kidney tissues and the blood of rats were collected. Malondialdehyde (MDA), myeloperoxidase (MPO), and reduced glutathione (GSH) levels were determined from kidney tissues. Blood urea nitrogen (BUN), creatinine (Cr), TNF-alpha, and IL-1beta levels were assessed in the serum. In addition the kidney tissues were examined histologically. RESULTS AND DISCUSSION: The MDA, MPO, BUN, and Cr levels of group III significantly increased when compared to groups I and II. These parameters of group IV decreased when compared to group III. In addition, GSH levels significantly increased when compared to the first three groups. MDA, BUN and Cr levels of group V did not reach significant level in comparison with the control group. The most significant histological damage was observed in the group III followed by the groups IV and V. Immunohistochemically, group III showed a significantly increased apoptotic staining. In group IV, it was observed that montelukast treatment reduced the expression of apoptotic cells. CONCLUSIONS: Montelukast treatment after amikacin injection could reduce the amikacin-induced kidney damage.

Quercetin prevents 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced testicular damage in rats.

The protective effect of quercetin on 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced testicular damage in rats was investigated. Twenty-two rats were equally divided into four groups; first group was kept as control and given corn oil as carrier. In second group, TCDD was orally administered at the dose of 2 µ (kg week)(-1) for 60 days. In third group, quercetin was orally administered at the dose of 20 mg (kg day)(-1) by gavages, and in fourth group TCDD and quercetin were given together at the same doses. Although TCDD increased the formation of thiobarbituric acid reactive substances (TBARS) significantly, it caused a significant decline in the levels of glutathione (GSH), catalase (CAT), GSH-Px and CuZn-Superoxide Dismutase (CuZn-SOD) in rats. In contrast, quercetin significantly increased the GSH, CAT, GSH-Px and CuZn-SOD levels but decreased the formation of TBARS. In addition, sperm motility, sperm concentration and serum testosterone levels were significantly decreased but abnormal sperm rate and testicular damage were increased with TCDD treatment. However, these effects of TCDD on sperm parameters, histological changes and hormone levels were eliminated by quercetin treatment. Our results show that administration of TCDD induces testicular damage (oxidative stress, testes tissue damage, serum hormone level and sperm parameters), and quercetin prevents TCDD-induced testicular damage in rats. Thus, quercetin may be useful for the prevention and treatment of TCDD-induced testicular damage.

Cardioprotective potential of melatonin, quercetin and resveratrol in an experimental model of diabetes.

Oxygen radicals participate in the pathogenesis of heart damage. Diabetes accelerates the formation of reactive oxygen species (ROS). We investigated the effects of the antioxidants, melatonin, quercetin and resveratrol, on cardiomyopathy and apoptosis in rats with streptozotocin (STZ) induced diabetes mellitus (DM). Rats were divided into five groups of seven: control, DM, DM + melatonin, DM + quercetin and DM + resveratrol. All treatments were begun with a single dose of STZ to induce diabetes and experimental treatments were continued daily for 30 days. Morphologic and apoptotic changes were analyzed by histological assessment. The heart tissue of the control group exhibited normal histology, whereas the heart tissue of the DM group exhibited vacuolization, necrosis, congestion, infiltration and myofibril loss. The DM group exhibited significantly increased apoptosis compared to the control group. Differences in anti-apoptotic effects were statistically significant for all three antioxidant treatment groups; the anti-apoptotic effects of quercetin and resveratrol were similar. Melatonin, resveratrol and quercetin exhibited protective effects against diabetic heart damage.

Protective effect of short-term thymoquinone administration on the central nervous system in cisplatin-induced neurotoxicity.

OBJECTIVE: This study was performed to investigate the potential beneficial effects of thymoquinone (TQ) on brain tissue based on biochemical and histopathological analyses in cisplatin (CIS) treated rats with central nervous system (CNS) neurotoxicity. MATERIALS AND METHODS: The rats were randomly divided into 4 groups with 8 rats in each group (n:8). Group 1: (Control), saline was administered for 3 days at a volume of 0.5 ml per day intraperitoneal (i.p.). Group 2: (CIS Group), one dose of CIS was administered (7 mg/kg i.p.). Group 3: (TQ Group), TQ was given at a dose of 5 mg/kg per day for 3 days (i.p.). Group 4: (CIS+TQ Group), one dose of 7 mg/kg was initiated half an hour before administration of CIS and one dose of 5 mg/kg per day was administered TQ i.p. for 3 days. RESULTS: Malondialdehyde levels were found to be statistically significantly higher in the CIS group compared to the control group. Degenerative changes observed in the CIS+TQ group were found to be milder than in the CIS group. In the CIS+TQ group, a statistically significant decrease in the severity of caspase-3 immunoreactivity was found when compared to the CIS group. It was found that the severity of neurofilament immunoreactivity monitored in neuronal extensions was similar in all groups. In the CIS+TQ group, the severity of tau protein's immunoreactivity was similar to that of the CIS-group. CONCLUSIONS: According to the results obtained in our study, beneficial effects were obtained in reducing neurotoxicity with short-term TQ application in rats treated with CIS treatment.

Dexpanthenol reduces diabetic nephropathy and renal oxidative stress in rats.

Hyperglycemia increases reactive oxygen species (ROS) and the resulting oxidative stress contributes to the development of diabetic complications. Dexpanthenol (Dxp) is the biological active form of pantothenic acid. We investigated whether Dxp administration could decrease oxidative stress as a way to treat renal complications of diabetes mellitus (DM). Thirty-two male Wistar albino rats were divided into four groups: control, Dxp, DM and DM + Dxp. Experimental diabetes was induced by a single dose of streptozotocin (STZ). After administration of STZ, the DM + Dxp group was administered 500 mg/kg Dxp intraperitoneally every day for 6 weeks. At the end of the study, blood glucose levels were measured and rats were sacrificed. Kidneys were embedded in paraffin, sectioned and stained with hematoxylin and eosin, and periodic acid-Schiff. The mean malondialdehyde levels, glutathione peroxidase, superoxide dismutase and catalase activities, and total antioxidant and total oxidant status also were measured. The control group was normal in histological appearance. We observed congestion, inflammation, glomerulosclerosis, tubular desquamation, loss of villi and hydropic degeneration in tubule cells in the DM group. Indicators of oxidative stress were elevated and antioxidant activity was reduced in the DM group compared to controls. In the DM + Dxp group, oxidative stress was decreased, antioxidant activity was increased and histopathological changes were reduced compared to the DM group. We found that Dxp exhibited ameliorative effects on STZ induced diabetic nephropathy by increasing antioxidant activity.

Protective Effect of Dexpanthenol on Ischemia-Reperfusion-Induced Liver Injury.

OBJECTIVE: We aimed to investigate the protective and therapeutic effects of dexpanthenol (DXP) on liver injuries induced by ischemia-reperfusion (IR) in an in vivo rat model. METHODS: Thirty-two rats were randomly divided into 4 experimental groups (n = 8 in each group: Sham, IR, DXP, and DXP+IR. DXP (500 mg/kg) was intraperitoneally administered for 30 min before 60 min of ischemia, followed by 60 min of reperfusion to rats in the DXP and DXP+IR groups. All rats were euthanized on day 10 to evaluate immunohistopathological changes as well as tissue levels of oxidants and antioxidants. RESULTS: IR decreased total glutathione (tGSH) levels in IR group when compared to the Sham group. DXP supplementation to IR group significantly ameliorated tGSH levels (P < .05). IR also elevated myeloperoxidase production compared to the Sham group, whereas DXP treatment prevented these hazardous effects. However, plasma superoxidedismutase, catalase, and malondialdehyde levels did not differ between the DXP+IR than the IR rats. Histologic tissue damage was reduced in the DXP and DXP+IR group. CONCLUSION: Liver IR is an inevitable problem during liver surgery. Our results suggested that DXP pretreatment suppressed oxidative stress and increased antioxidant levels in a rat model of liver IR.

The protective effect of melatonin in lungs of newborn rats exposed to maternal nicotine.

We investigated possible healing effects of melatonin (MEL) on biochemical and histological changes in the lungs of rat offspring caused by exposure to nicotine (NT) in utero. Pregnant rats were divided randomly into five groups. The SP group was treated with physiological saline. The EA group was treated with ethyl alcohol. The MEL group was treated with MEL. The NT group was treated with NT. The NT + MEL group was treated with NT and MEL. At the end of the study, the biochemistry and histopathology of lung tissue of the offspring were examined. Reduced alveolar development and increased numbers of alveolar macrophages and mast cells were observed in the NT group compared to the SP, EA and MEL groups. We also found increased malondialdehyde (MDA) levels and decreased total glutathione (GSH) levels in the NT group. Application of MEL ameliorated the histological and biochemical damage caused by NT. The number of alveoli was greater in the NT + MEL group than in the NT group. Also, the increased numbers of alveolar macrophages and mast cells resulting from exposure to NT were decreased following MEL treatment. We found that MEL caused a significant decrease in the level of MDA. Maternal exposure to NT caused significant structural and biochemical changes in the lungs of the offspring and administration of MEL ameliorated the changes.

Effects of melatonin on acetylsalicylic acid induced gastroduodenal and jejunal mucosal injury.

We evaluated the effects of melatonin on acetylsalicylic acid (ASA) induced gastroduodenal and jejunal mucosal injury. We used 40 postpubertal rats divided randomly into five groups of eight animals. The control group consisted of untreated animals. The Mel group was injected intraperitoneally (i.p.) with 5 mg/kg melatonin. The ASA group was injected i.p. with 200 mg/kg ASA. The ASA + Mel group was injected i.p. with 5 mg/kg melatonin 45 min after administering 200 mg/kg ASA i.p. The Mel + ASA group was injected i.p. with 5 mg/kg melatonin 45 min before administering 200 mg/kg ASA i.p. We found no statistically significant differences in mean histopathological scores in the ASA + Mel group compared to the ASA group. ASA caused shortened villi and loss of the apical villus in the duodenum. The histopathological score was increased and villus height was decreased in the ASA group compared to untreated controls. Treatment with melatonin attenuated the histological damage. In the ASA group, occasional areas showed erosion of villi in the jejunum; however, differences in mean histopathological score in ASA group compared to the other groups were not statistically significant. Malondialdehyde (MDA), glutathione (GSH) and superoxide dismutase (SOD) activities were measured in stomach, duodenal and jejunum tissue. We found increased MDA activity in both stomach and duodenal tissues in the ASA group compared to the control group (p < 0.05). We found no statistically significant changes in MDA levels in jejunal tissue in the ASA group compared to the control group. We found no change in SOD activity in either stomach or duodenal tissues in the ASA group compared to the control group. We observed decreased SOD activity in jejunal tissue in the ASA group compared to the control group (p < 0.05). We detected no change in GSH activity in stomach, duodenal or jejunal tissues in the ASA group compared to the control group. The stomach damage was less in melatonin treated groups, but the lesions were not completely eliminated. The jejunum in the ASA group retained a nearly normal appearance. We found that melatonin exhibited some healing effects on ASA induced duodenal mucosal injury.

Effects of molsidomine on retinal ischemia/reperfusion injury in rabbits.

We investigated the effect of molsidomine (MOL) on ischemia/reperfusion (I/R) injury. Rabbits were assigned to four groups: group 1, sham; group 2, I/R; group 3, MOL treatment for 4 days after I/R; group 4, MOL treatment for 1 day before I/R and 3 days after I/R. Retinal I/R was produced by elevating the intraocular pressure to 150 mm Hg for 60 min. Seven days after I/R, the eyes were enucleated. Retinal changes were examined using histochemistry. The levels of malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) also were measured. We found a significant increase in the thickness of the outer nuclear layer of group 3 compared to the other groups. In groups 3 and 4, caspase-3 stained cells in the ganglion cell layer were decreased compared to group 2. We found a significant increase in caspase-3 stained cells in the inner nuclear layer (INL) of group 2 compared to the other groups. We found a significant increase in caspase-3 stained cells in group 3 compared to group 4 in the INL. The MDA level in group 2 was significantly higher than group 1 and MOL significantly decreased MDA levels in groups 3 and 4. We found that MOL protected the retina from I/R injury by enhancing antioxidative effects and inhibiting apoptosis of retinal cells.

Protective effects of chronic melatonin treatment against renal ischemia/reperfusion injury in streptozotocin-induced diabetic rats.

AIMS: The purpose of this study was to investigate the effects of chronic administration of melatonin on renal ischemia/reperfusion (IR) injury in streptozotocin (STZ)-induced diabetic rats. METHODOLOGY: Male Sprague-Dawley rats were divided into six groups: control (C), diabetes mellitus (DM), control+IR (C+IR), DM+IR, Melatonin+IR (Mel+IR), DM+Mel+IR. Diabetic and non-diabetic rats were given melatonin 4 mg/kg/day, i.p., for 15 days. The left renal artery and vein of rats were occluded for 30 min at the 18th day, followed by 24 h of reperfusion. RESULTS: In comparison with control group, the levels of malondialdehyde (MDA), protein carbonyl (PC) and and nitric oxide (NO) were determined to be higher in the renal homogenates of DM, DM+IR and C+IR groups. MDA and NO levels were found to be similar in the DM+melatonin+IR and control groups. The most significant histological damage was found in the DM+IR group and this damage was significantly reduced by melatonin. CONCLUSION: Chronic melatonin treatment reduces renal injury by reducing lipid oxidation and NO production in STZ-induced diabetic rats exposed to IR.

Protective and therapeutic effects of molsidomine on radiation induced neural injury in rats.

We investigated the protective and therapeutic effects of molsidomine (MOL) in a rat model of whole brain radiotherapy (RT). Forty female rats were divided into five groups of eight: group 1, control; group 2, 15 Gy single dose RT (RT); group 3, 4 mg/kg MOL treated for 5 days (MOL); group 4, 4 mg/kg MOL for 5 days, 10 days after RT treatment (RT + MOL); group 5, 4 mg/kg MOL treatment for 5 days before RT treatment and for 5 days after RT treatment (MOL + RT). All rats were sacrificed on day 16. Neurodegenerative changes in the brain and tissue levels of oxidants and antioxidants were evaluated. The oxidative parameters were increased and antioxidant status was decreased in group RT compared to groups MOL + RT and RT + MOL. Histopathological examination showed that treatment with MOL after RT application and treatment with MOL before RT treatment decreased neuronal degeneration. No difference in neuronal appearance was found between groups RT + MOL and MOL + RT. MOL treatment protected the nervous system of rats and may be a treatment option for preventing RT induced neural injury.