Effects of colchicine on gingival inflammation, apoptosis, and alveolar bone loss in experimental periodontitis.

BACKGROUND: The aim of the study was to investigate the effects of colchicine on cytokine production, apoptosis, alveolar bone loss, and oxidative stress in an experimental model of periodontitis in rats. METHODS: Forty-eight rats were divided equally into four groups: healthy (H); periodontitis (P); periodontitis+colchicine low dose (CL, 30 µg/kg/day), and periodontitis+colchicine high dose (CH, 100 µg/kg/day). After 11 days, interleukin (IL) -1ß, IL-8, and IL-10 were analyzed in gingival samples using Enzyme-Linked ImmunoSorbent Assay. Receptor activator of nuclear factor kappa-B ligand (RANKL), osteoprotegerin (OPG), total oxidative stress (TOS), total antioxidant status (TAS), and oxidative stress index (OSI) were measured in gingiva and serum. Alveolar bone volume was evaluated via micro-CT. Apoptotic cells were detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay in histological sections. RESULTS: Colchicine treatment significantly reduced IL-1ß, IL-8, RANKL, RANKL/OPG, TOS, OSI, and bone volume ratio levels, and increased TAS levels compared to group P (p < 0.05). High dose colchicine treatment (CH) significantly decreased TUNEL+ cell counts compared to group P (p < 0.05). CONCLUSIONS: These finding suggest that colchicine has a prophylactic potential for the prevention of periodontal tissue destruction through anti-inflammatory, anti-oxidative, anti-apoptotic, and bone-protective effects.

Effects of Cornus mas L. and Morus rubra L. extracts on penicillin-induced epileptiform activity: an electrophysiological and biochemical study.

Traditionally, Morus rubra L. (Moraceae) (red mulberry) and Cornus mas L. (Cornacea) (cornelian cherry) fruits are eaten fresh and are also used in marmalades, juices, jam, natural dyes in Turkey and are believed to have beneficial effects in case of multiple health issues such as antipyretic, diarrhea and intestinal parasites. However, the effects of M. rubra and C. mas on epilepsy has not been known. This study evaluates the effects of M. rubra and C. mas extracts on penicillin-induced epileptiform activity. Sixty Wistar rats randomly divided into ten groups (n=6): control, sham, penicillin, penicillin+M. rubra extract (2.5, 5, 10, 20 mg/kg) and penicillin+C. mas extract (2.5, 5, 10 mg/kg). Epileptiform activity was induced by using penicillin (500 IU, i.c.) and electrocorticogram records (150 min) were obtained. Also, biochemical analysis in blood samples were evaluated. According to the electrocorticogram analysis, the effective dose was detected as 10 mg/kg for both C. mas and M. rubra. This dose decreased the spike frequencies of convulsions while amplitude wasn't changed by both substances. In erythrocyte studies, there were significant differences regarding nitric oxide in the control, sham and penicillin groups. There were significant differences regarding malondialdehyde in all groups. In the plasma, there were significant differences among groups regarding xanthine oxidase in the penicillin­C. mas and penicillin­M. rubra groups. There were differences regarding malondialdehyde in the penicillin-C. mas and M. rubra-C. mas groups. Both extracts reduced the frequency of epileptiform activity. After administration of the extracts malondialdehyde levels decreased also in both erythrocytes and plasma.

Trace metal concentrations in hair and nails from Alzheimer's disease patients: Relations with clinical severity.

BACKGROUND AND OBJECTIVES: Metals, especially transition metals, seem to be important in the pathogenesis of Alzheimer disease. This study aims to determine the relationship of trace metal elements to the pathogenesis and/or course of Alzheimer Disease in terms of clinical severity. METHODS: The hair and nail trace metal levels of 62 Alzheimer Disease patients at different clinical stages (21 mild, 20 moderate, 21 severe) and 60 healthy control subjects were measured by using inductively coupled plasma-mass spectrometry. The statistical comparisons were performed with regards to the study groups, clinical stages, disease duration and age. RESULTS: The patient and control groups were significantly different from each other in regards to Mn, Fe, Cu, Cd, Hg (p<0.001), Zn (p<0.01) in nail concentrations and, Na, Al, Pb, Co (p<0.001), Fe, Mn (p=0.001), Hg, Cu, Cd, K in hair concentrations (p<0.01). No difference was detected in the levels of Mg and Ca. Nail Na level showed differences among different clinical stages of the disease (p<0.01). In comparing the mild degree Alzheimer patients to the control group; significant differences were detected in nail Mn, Fe, Cu, Co (p<0.001), Hg, Zn (p<0.01) and, hair Pb, Al (p<0.001), Na, K levels (p<0.01). CONCLUSIONS: Our results have shown that transition and posttransition metals are especially important metals for the disease process. The relation of nail Na level with clinical stages of AD is an interesting new finding, making someone to think that alkali metals may be important in the progression of the disease.

Therapeutic effects of systemic vitamin k2 and vitamin d3 on gingival inflammation and alveolar bone in rats with experimentally induced periodontitis.

BACKGROUND: The synergistic effects of vitamin D3 and vitamin K2 on bone loss prevention have been reported. This study evaluates the effects of vitamin D3 and vitamin K2 supplementation in conjunction with conventional periodontal therapy (scaling and root planing [SRP]) on gingival interleukin (IL)-1ß and IL-10, serum bone alkaline phosphatase (B-ALP) and tartrate-resistant acid phosphatase 5b (TRAP-5b), and calcium and alveolar bone levels in rats with experimentally induced periodontitis. METHODS: Seventy-two rats were divided into the following groups: 1) healthy; 2) periodontitis; 3) SRP; 4) SRP + vitamin D3; 5) SRP + vitamin K2; and 6) SRP + vitamins K2 and D3. Periodontitis was induced by ligature placement for 7 days, and vitamin K2 (30 mg/kg) and/or vitamin D3 (2 µg/kg) were administered for 10 days in the SRP + vitamin D3, SRP + vitamin K2, and SRP + vitamins K2 and D3 groups by oral gavage. On day 18, the animals were sacrificed, serum B-ALP, TRAP-5b, and calcium levels were measured, gingiva specimens were extracted for IL-1ß and IL-10 analysis, and distances between the cemento-enamel junction and alveolar bone crest were evaluated. RESULTS: Alveolar bone levels in the periodontitis group were significantly greater than those in the other five groups. No significant differences were found in gingival IL-1ß and IL-10, serum B-ALP and TRAP-5b, and calcium and alveolar bone levels between the groups receiving SRP and vitamins and the group receiving SRP alone. CONCLUSION: Within the limitations of this study, vitamin D3 and K2 alone or in combination did not affect gingival IL-1ß and IL-10, serum B-ALP and TRAP-5b levels, or alveolar bone compared with conventional periodontal therapy alone.

The endocrine disruptor bisphenol A may play a role in the aetiopathogenesis of polycystic ovary syndrome in adolescent girls.

AIM: Experimental in vitro studies have shown that bisphenol A affects steroidogenesis, folliculogenesis and ovarian morphology. The aim of this study was to investigate the role of the endocrine disruptor bisphenol A in the aetiopathogenesis of polycystic ovary syndrome (PCOS) in adolescents and its relationship with metabolic parameters, insulin resistance and obesity in this population. METHODS: A total of 112 girls with PCOS and 61 controls between 13 and 19 years of age were enrolled in the study. Serum bisphenol A levels were measured by high-pressure liquid chromatography. An oral glucose tolerance test was also performed. RESULTS: Adolescents with PCOS had markedly increased serum bisphenol A levels (mean: 1.1 ng/mL 95% CI: 1.0-1.2) than controls (mean: 0.8 ng/mL 95% CI: 0.6-0.9, p = 0.001). When we compared the subgroups according to obesity, the main factor determining the significant increase in bisphenol A was the presence of PCOS, but not obesity (p = 0.029). Bisphenol A was significantly correlated with total testosterone (r = 0.52), free testosterone (r = 0.44), dehydroepiandrosterone sulphate (r = 0.37) and Ferriman-Gallwey score (r = 0.43) (p < 0.05). CONCLUSION: Adolescents with PCOS had higher serum bisphenol A levels than controls, independent of obesity. Bisphenol A concentrations were significantly correlated with androgen levels, leading us to consider that bisphenol A might play a role in the aetiopathogenesis of PCOS in adolescents.

The protective effects of grape seed extract on MDA, AOPP, apoptosis and eNOS expression in testicular torsion: an experimental study.

OBJECTIVES: Grape seed proanthocyanidin extract (GSPE) is a potent antioxidant and a free radical scavenger. This study was designed to determine whether GSPE could protect against dysfunction and oxidative stress induced by torsion-detorsion injury in rat testis. METHODS: A total of 45 male Wistar albino rats were divided into five groups: control group, sham group, torsion-detorsion (T/D) group, T/D + GSPE group, GSPE group. GSPE was administrated 100 mg/kg/day with oral gavage over seven days before torsion. Testicular torsion was performed for 2 h, and afterward, detorsion was performed for 2 h. The rats were decapitated under ketamine anesthesia, and their testes tissues were removed. Tissue malondialdehyde, advanced oxidation protein products levels, eNOS expression, apoptosis and histopathological damage scores were then compared. RESULTS: Testicular torsion-detorsion caused significant increases in malondialdehyde level, apoptosis and eNOS expression level and caused a significant decrease in advanced oxidation protein product levels and testicular spermatogenesis in ipsilateral testes. GSPE prevented the rise in malondialdehyde, apoptosis and eNOS expression and improved testicular morphology and Johnsen's score. CONCLUSIONS: As a result, testicular torsion gives rise to serious damage in testes and GSPE is a potent antioxidant agent in preventing testicular injury.

Prognostic value of tumor growth factor levels during chemotherapy in patients with metastatic colorectal cancer.

Tumor growth and angiogenic factors are usually overexpressed in colorectal carcinomas. We aimed to assess the prognostic role of VEGF, bFGF, PDGF-AA, EGF, HGF, and E-selectin in patients with metastatic colorectal cancer treated with capecitabine and oxaliplatin (XELOX) chemotherapy protocol. Thirty-eight colorectal cancer patients who had evidence of distant metastasis were enrolled in the study. Angiogenic factors were measured before and after third cycle of chemotherapy. Patients were randomized into three groups, partial response (PR), stable disease (SD), and progressive disease (PD) groups, according to their clinical and radiologic evaluation after three cycles of XELOX chemotherapy. Eighteen patients (47.3 %) achieved partial response, 10 (26.3 %) stable disease, and 10 (26.3 %) progressive disease. VEGF (63.20 Pg/ml vs. 19,79 Pg/ml; p < 0.001), EGF (7.29 ± 3.08 Pg/ml vs. 4.79 ± 2.05 Pg/ml; p < 0.011), HGF (618.16 ± 340.39 Pg/ml vs. 452.02 ± 217.18 Pg/ml; p < 0.049), and PDGF-AA (691.68 ± 187.10 Pg/ml vs. 404.89 ± 168.47 Pg/ml; p < 0.001) were significantly decreased in PR group. PDGF-AA levels were also decreased in SD group (706.66 ± 206.66 Pg/ml vs. 389.79 ± 143.16 Pg/ml; p < 0,001). HGF levels were significantly increased in PD disease group (449.99 Pg/ml vs. 682.22 Pg/ml; p < 0.046). The baseline E-selectin levels were inversely proportional with overall survival that could be an important prognostic factor at the time of diagnosis. This study demonstrated that tumor growth factors can be helpful to determine colorectal cancer prognosis and overall survival in patients with metastatic disease. VEGF, HGF, EGF, and PDGF-AA levels were decreased in PR group. However, meaningful increment was seen HGF levels in PD group. Angiogenic factors and E-selectin provided unique prognostic information in advanced colorectal carcinoma patients.

Efficacy of royal jelly on methotrexate-induced systemic oxidative stress and damage to small intestine in rats.

The aim of this present study is to investigate the mucositis caused by methotrexate (MTX), as well as whether the application of royal jelly (RJ) has a protective effect on oxidative stress. This present study included six groups each consisted of 12 Wistar rats. Distilled water (po: peroral) was given to the 1st group as placebo for 10 days and MTX (20 mg/kg, intraperitoneal: ip) on the 7th day. The 2nd group received RJ (50mg/kg, po) for 10 days and normal saline (NS) instead of MTX. RJ (50mg/kg) was given to the 3rd group for 10 days and MTX on the 7th day. The 4th group received RJ (100 mg/kg, po) for 10 days and NS was given intraperitoneally. RJ (100mg/kg) was given to the 5th group for 10 days and a single dose of MTX. Distilled water was given to the 6th (control) group for 10 days and intraperitoneal NS on the 7th day. Malondialdehyde (MDA), glutathione peroxidase and superoxide dismutase were analyzed in blood samples on the 11th day. Morphological and histopathological changes were examined in the intestinal tissue samples. Villus length and mucosal thickness, as well as the villus length/crypt ratio, were significantly decreased with MTX administration, and the semi-quantitative histological evaluation (SQHE) score was measured high (p<0.001). In addition, a decrease in the antioxidant parameters and an increase in the MDA levels were identified. The villus length and SQHE were significantly different in the groups receiving RJ (p<0.001) as compared to the MTX group. Although RJ addition had no effect on the decreased mucosal thickness and villus/crypt ratio in MTX groups, it caused an improvement in the antioxidant levels and a remarkable decrease in MDA levels. Adding RJ has a decreasing effect on the MTX-induced intestinal damage and it has a suppressive effect on MTX-induced oxidative stress by means of increasing antioxidant enzyme activity and decreasing lipid peroxidation.

Increased lipid peroxidation and impaired enzymatic antioxidant defense mechanism in thyroid tissue with multinodular goiter and papillary carcinoma.

OBJECTIVES: We aimed to evaluate the oxidant/antioxidant status of thyroid tissue in patients with multinodular goiter, papillary carcinoma and to compare with their nonpathologic tissues. METHODS: We studied 41 patients with multinodular goiter who underwent surgical treatment. The patients were divided into three groups according to clinical diagnosis. Malondialdehyde, selenium, total superoxide dismutase and glutathione peroxidase of thyroid tissue samples were determined in 14 toxic multinodular goiters, 18 non-toxic multinodular goiters, and 9 papillary carcinomas. RESULT: Superoxide dismutase and glutathione peroxidase and selenium were found lower but malondialdehyde was higher in both nodule and cancerous tissues compared with those of control ones. The level of malondialdehyde in non-toxic multinodular goiters group was higher than toxic multinodular goiters group in nodule tissues. CONCLUSIONS: It can be stated that the lipid peroxidation is increased and enzymatic free radical defense system was significantly impaired in patients with both multinodular goiters and papillary carcinomas.

The protective effects of propofol and citicoline combination in experimental head injury in rats.

AIM: Lipid peroxidation (LP) is an important factor in tissue damage following head injury. Reactive oxygen radicals which damage cellular components play an important role in ischemic or hypoxic tissue. They initiate the lipid peroxidation process after head trauma. However, antioxidant agents may protect brain tissue against oxidative damage MATERIAL AND METHODS: 39 male Swiss Albino rats (200-250 g) were used in this experimental study. These animals were divided into 3 groups: 1) control group, 2) propofol group (100 mg/kg) and, 3) citicoline (250 mg/kg) and propofol (100 mg/kg) combination group. Oxidant effect in brain tissue content was assessed by measuring the Malonyldialdehyde (MDA), Superoxide Dismutase (SOD) and Gluthatione Peroxidase (GPx) activities. RESULTS: There was no statistically meaningful difference among the groups regarding GPx levels. MDA levels were significantly lower in the citicoline and combination group than those of the control group. As for the levels of SOD, there was an increase both in the propofol and combination groups. CONCLUSION: Atherapeutic benefit of the propofol and citicolin combination in head trauma has not been previously demonstrated. We examined the possible potential protective effect of propofol and citicolin against oxidative damage in experimental head trauma in the present study.

Effects of melatonin and phospholipid on adhesion formation and correlation with vascular endothelial growth factor expression in rats.

BACKGROUND: The aim of this experimental study was to investigate the effects of melatonin and phospholipid on adhesion formation and the correlation with vascular endothelial growth factor (VEGF) expression in rats. METHODS: Sixty Wistar-Albino rats were divided into four groups as sham, control and two study groups, each including 15 rats. In the sham group, laparotomy was the only procedure. Left lower parietal peritoneum was abraded after laparotomy and serosal defects formed on the cecum, ileum and right uterine horn in the study and control groups. Ringer lactate was then applied to the control group, while melatonin and phospholipid suspension were applied separately in the two study groups. Relaparotomy was performed in all groups on the 15th day to score and evaluate the adhesion formation. RESULTS: Adhesion formation was significantly lower in the sham, melatonin and phospholipid groups than in the control group (p<0.05). VEGF staining was significantly higher in the control group with adhesion areas compared to the other groups (p<0.05). When VEGF staining was compared, there was no significant difference between VEGF- stained and normal areas in the melatonin and phospholipid groups. CONCLUSION: Melatonin and phospholipid decreased the adhesion formation in an experimental adhesion model in rats. There is a correlation between adhesion severity and VEGF expression.

Assessment of DNA damage and plasma catalase activity in healthy term hyperbilirubinemic infants receiving phototherapy.

Phototherapy (PT) is the most widely used form of treatment for unconjugated hyperbilirubinemia. One possible harmful consequence of PT is of a genetic nature. High levels of bilirubin may lead to oxidative damage in newborns: photochemical reactions may produce toxic photoproducts, probably peroxides. In order to investigate this hypothesis further under in vivo conditions, DNA strand-break frequency was examined by means of the comet assay in peripheral lymphocytes of icteric newborns undergoing PT treatment, and the levels of catalase, an antioxidant enzyme, were determined. We analyzed 20 term non-hemolitic hyperbilirubinemic jaundiced neonates before PT ('before PT' group) and just prior to ending PT ('after PT' group) and compared comet scores of these patients with those of 20 healthy term neonates who all had bilirubin levels in the physiological range. Comet scores (tail length, tail moment and %DNA in tail) of the group 'before phototherapy' were 23.5 +/- 16.3, 7.41 (0.97-40.7), 33.0 +/- 12.1, respectively and scores of after phototherapy group were 3.2 +/- 1.8, 0.29 (0.3-3.2), 10.7 +/- 3.7, respectively. Comet scores of the control group were 3.0 +/- 2.9, 0.25 (0.03-3.22), 10.9 +/- 4.5, respectively. Comet scores and plasma catalase activities in hyperbilirubinemic newborns were significantly higher before phototherapy, compared with the values after phototherapy and in the control groups (p < 0.001). There was no statistical difference between the 'after phototherapy' group and the controls (p > 0.05). These results indicate that high serum bilirubin level has genotoxic effects as is evident from the high rate of DNA strand-breaks in jaundiced newborns. Also PT does not cause an increase in DNA oxidation or induce the genotoxic effects of bilirubin. The counteracting effect of higher catalase activities in hyperbilirubinemic newborns may be responsible for the inactivating toxic and DNA-damaging effects of PT.

The effect of grape seed extract on radiation-induced oxidative stress in the rat liver.

BACKGROUND/AIMS: The tolerance of the liver is considerably low when an effective radiation (RTx) dose needs to be delivered in patients in whom either their liver or whole body area has to be irradiated. The aim of this study was to evaluate the possible protective effect of grape seed extract on liver toxicity induced by RTx in the rat liver. METHODS: We used four groups, each consisting of 12 healthy male Wistar rats. RTx-grape seed extract group: rats were given grape seed extract (100 mg/kg) orally for seven days, following 8 Gy whole body irradiation, and grape seed extract was maintained for four days. RTx group: the same protocol was applied in this group; however, they received distilled water instead of grape seed extract. Grape seed extract group: only grape seed extract solution was administered for 11 consecutive days in the same fashion. CONTROL GROUP: only distilled water (orally) was administered in a similar manner. The level of malondialdehyde, an end product of lipid peroxidation, and the activities of superoxide dismutase and catalase, two important endogenous antioxidants, were evaluated in tissue homogenates. RESULTS: Grape seed extract was seen to protect the cellular membrane from oxidative damage and consequently from protein and lipid oxidation. In the RTx group, malondialdehyde levels were extremely higher than those of the grape seed extract-RTx group (p<0.001). Grape seed extract administration moderately reserved the malondialdehyde levels. RTx therapy decreased superoxide dismutase and catalase activities in the liver homogenates (p<0.001), and these alterations were significantly reversed by grape seed extract treatment (p<0.001). There were no differences between the grape seed extract- RTx, grape seed extract and control groups with regard to antioxidant activity (p>0.05). CONCLUSIONS: The levels of antioxidant parameters on RTx-induced liver toxicity were restored to control values with grape seed extract therapy. Grape seed extract may be promising as a therapeutic option in RTx-induced oxidative stress in the rat liver.

Role of grape seed extract on methotrexate induced oxidative stress in rat liver.

UNLABELLED: The efficacy of methotrexate (MTX), a widely used cytotoxic chemotherapeutic agent, is often limited by its severe hepatotoxicity. Regarding the mechanisms of these adverse effects, several hypotheses have been put forward, among which oxidative stress is noticeable. The present study was undertaken to determine whether grape seed extract (GSE), a new natural free radical scavenger, could ameliorate the MTX-induced oxidative injury in the rat liver. The animals were divided into 3 groups. Each group consisted of 12 animals. MTX-GSE group: rats were given GSE (100mg/kg body weight) orally for 15 days, and a single dose of MTX (20 mg/kg, intraperitoneally) was added on the 10th day. MTX group: these received placebo distilled water (orally) instead of GSE for 15 days and the same MTX protocol applied to this group on the 10th day. CONTROL GROUP: rats were given distilled water (orally) through 15 days and physiological saline (intraperitoneally) instead of MTX was administered on the 10th day in a similar manner. On the 16th day, liver tissue samples were obtained under deep anaesthesia. The level of malondialdehyde (MDA), an end product of lipid peroxidation, and the activities of süperoxide dismutase (SOD) and catalase (CAT), two important endogenous antioxidants, were evaluated in the tissue homogenates. MTX administration increased the MDA level and decreased the SOD and CAT activities in the liver homogenates (p < 0.001), while these alterations were significantly reversed by GSE treatment (p < 0.001). MTX led to significantly reduced whole blood count parameters (p < 0.05). When GSE was supplemented, no significant changes in blood count parameters were noted. It appears that GSE protects the rat liver and inhibits methotrexate-induced oxidative stress. These data indicate that GSE may be of therapeutic benefit when used with MTX.

Protective effects of caffeic acid phenethyl ester on radiation induced lung injury in rats.

PURPOSE: The prevention of radiation-induced pulmonary toxicity may help to improve radiation therapy in the cancer patient. The aim of this study was to investigate the pulmonary protective effects of caffeic acid phenethyl ester (CAPE), an antioxidant, on radiation-induced lung injury in rats. METHODS: 30 Wistar albino rats were divided into three groups and treated with saline, Radiation (RT) and RT + CAPE respectively. All rats were treated with CAPE (50 ?mol/kg i.p.) or saline. The first dose of CAPE was injected 24 h before radiation and application continued daily, with radiation in second day and 2 days more after the radiation treatment. Radiation dose was 800 cGy for total body. At 72 hr after the last radiation application, under general anesthesia using ip ketamine, the lungs were removed immediately after decapitation. After sacrification, antioxidant enzymes catalase (CAT), superoxide dismutase (SOD) activities and malondiadehyde (MDA) levels were evaluated in lung tissue. RESULTS: The level of malondialdehyde (MDA) was higher in the RT group (233.4+/-1.5 nmol/g protein) than in both the control (131.8+/-0.92) and the RT + CAPE (151.4+/-1.8) groups (P < 0.001). However, CAT activity was decreased in the RT group (7.26+/-0.27 U mg protein) compared with control (8.49+/-0.51) and increased again in the RT + CAPE group (8.31+/-0.56; P < 0.001). In accord with CAT activity, SOD activity in the RT group (0.42+/-0.07 nmol MDA/g wet tissue) was different from the control (0.78+/-0.02) and RT + CAPE (0.86+/-0.06) groups (P < 0.001). CONCLUSION: CAPE application with radiation therapy attenuated radiation induced pulmonary injury in vivo, possibly by its antioxidant effect.

Aminoguanidine ameliorates radiation-induced oxidative lung damage in rats.

PURPOSE: To investigate the possible protective effects of aminoguanidine (AG ) on lung damage in whole body irradiated rats. METHODS: To evaluate the biological damage of radiation on rat lung tissue, lipid peroxidation products were measured using biochemical parameters. Thirty Wistar albino rats were divided into three subgroups: control (C) , irradiation alone (RT), and RT + AG combined. After sacrificing the rats, antioxidant enzymes catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSHPx) activities and malondiadehyde (MDA), nitric oxide (NO) levels were evaluated in lung tissue. RESULTS: Administration of AG resulted in an increase in the activities of CAT, SOD and GSHPx in the lungs. All were reduced after radiation. In addition, AG administration resulted in a decrease in both NO and MDA levels in lung compared with the irradiated group. CONCLUSION: Amnoguanidine increased the endogenous antioxidant defence mechanism in rats and protected the animals from radiation-induced lung toxicity. Moreover, AG may protect against ionizing radiation-induced lung damage because of its antioxidant effect.

The protective effect of melatonin on nicotine-induced myocardial injury in newborn rats whose mothers received nicotine.

OBJECTIVE: Nicotine, one of the most dangerous substances in tobacco, can pass the placenta and affect the fetal hemodynamics. The aim of this study was to evaluate the protective effects of melatonin on hearts of nicotine exposed newborn rats whose mothers received nicotine. METHODS: This is an experimental, randomized, controlled study. Study groups were composed of five groups of rats; high-dose nicotine (HDN), HDN+melatonin (HDNM), low-dose nicotine (LDN), LDN+melatonin (LDNM), control. Myocardial and plasma malondialdehyde (MDA), nitric oxide(NO), glutathione peroxidase (GSHPx) and superoxide dismutase (SOD) were analyzed and myocardial tissue was examined histopathologically. Comparisons of groups were done with Kruskal-Wallis one-way analysis test. All pairwise multiple comparisons and the comparisons between control and other groups were done with Dunn's nonparametric multiple comparison test. RESULTS: Plasma and tissue MDA levels among groups were different (p=0.001 for plasma MDA and p=0.001 for tissue MDA). Plasma MDA levels of HDN, HDNM, LDN, and tissue MDA levels of HDN and LDN were significantly higher than in control group (p<0.05 for plasma MDA and for tissue MDA). Plasma and tissue NO levels among groups were also different (p=0.011 for plasma NO and p=0.001 for tissue NO). Plasma NO of LDN group was higher than of LDNM group, and plasma NO of LDNM group was lower than in control group (p<0.05). Tissue NO levels of HDN and LDN groups were higher than of control group (p<0.05). There was no difference between plasma GSHPx levels among groups (p=0.221) but statistically significant different was detected between tissue GSHPx levels among groups (p=0.001). Tissue GSHPx level was found lower in HDN group than in control group (p<0.05). Tissue GSHPx level of LDNM group was higher than of LDN group, and tissue GSHPx level of HDNM group was higher than of HDN group (p<0.05). A difference was found between plasma and tissue SOD among groups (p=0.005 for plasma SOD and p=0.001 for tissue SOD). Plasma SOD of LDN group was significantly lower than of HDNM and LDNM groups (p<0.05). Tissue SOD analyzes revealed lower levels in HDN and LDN groups than in control group (p<0.05). Severe cardiomyopathy was determined in HDN and LDN groups (p<0.05). CONCLUSION: Nicotine exposure depletes myocardial antioxidant enzymes and increases free radicals and lipid peroxidation products. Melatonin particularly prevents the nicotine-induced cardiac injury as an antioxidant.

Effects of age and anxiety on learning and memory.

This study aims to investigate the effects of age and anxiety on behavior, learning and memory in rats. Before and after the anxiety and learning tests, locomotor activity, exploratory activity and autonomic functions of the rats were tested in open field area. At the beginning and at the end of behavior tests, urines were collected so as to determine 5-hydroxyindolaceticacid (5-HIAA) levels. Following these tests, rats were anesthetized and their serum corticosteron (CORT) levels were analyzed. After anxiety, except for defecation, all parameters in open field such as line crossing, rearing, sitting and number of grooming were decreased in both young and aged animals. 5-Hydroxyindolaceticacid levels were decreased and serum CORT levels were increased, it is supported that especially the aged rats were much more affected from anxiety compared to the young ones. Elevated T-maze results show that emotional learning did not change while conditioned performance was tested in the closed arm and unconditioned performance was tested in the open arm. Nevertheless, it is observed that aging leaded to extensions in avoidance responses and thus caused difficulty in learning. In water maze test, rats showed higher performance in reaching the platform in repetitive trials; this demonstrates that they have learned by environmental cues. Experimental group had not better performance in reaching the platform according to control group, so this supports that anxiety affects spatial learning. As a conclusion, it could be stated that especially in aged rats, anxiety that is created by elevated T-maze and cat odor and supported with 5-hydroxyindoleacetic acid and serum corticosterone, causes difficulty in emotional and spatial learning.

Disturbance of pro-oxidative/antioxidative balance in allogeneic peripheral blood stem cell transplantation.

High dose chemotherapy causes increased free radical formation and depletion of tissue antioxidants. Whether allogeneic hematopoietic stem cell transplantation (HSCT) has an effect on oxidative stress is uncertain. The aims of the study were to determine the effect of allogeneic HSCT on plasma concentrations of antioxidants and oxidative stress biomarkers, and to investigate their relationships with graft-versus-host disease (GVHD), conditioning regimens, and transplant-related mortality (TRM) in patients with hematological malignancies. Patients (n=25) undergoing allogeneic HSCT from HLA-matched sibling donors were enrolled in the study. Plasma oxidant and antioxidant status were measured at day -1 before transplantation and 30 days after HSCT. In both myeloablative (n=14) and non-myeloablative (n=11) transplant groups, the mean levels of plasma malondialdehyde (MDA) and nitric oxide (NO) increased after allogeneic HSCT (p <0.01), whereas superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) activities decreased compared with baseline values (p <0.01). No significant relationships were found between either the pretransplant or post-transplant mean levels of the oxidative stress parameters and the existence of graft-versus-host disease (GVHD), the type of conditioning regimen, or transplant related mortality (TRM). This study documents a significant disturbance of pro-oxidative/antioxidative balance in the plasma of patients undergoing allogeneic HSCT regardless of the intensity of the conditioning regimen.

The role of lipoxin A4 in exercise-induced bronchoconstriction in asthma.

BACKGROUND: The pathogenesis of exercise-induced bronchoconstriction in asthma is incompletely understood, and the role of lipoxin A4 has not been investigated. OBJECTIVE: To investigate the involvement of lipoxin A4 in exercise-induced bronchoconstriction. METHODS: Two groups of children were enrolled in the study: asthmatic children with positive (n = 12) and negative (n = 8) responses to exercise. Levels of lipoxin A4 were determined in plasma before and immediately after exercise challenge using enzyme-linked immunosorbent assay. RESULTS: No significant difference was observed in the pre-exercise lipoxin A4 levels among the groups (p > 0.05). A significant difference was observed in the postexercise lipoxin A4 levels between the two groups (p = 0.041). We also observed significant decreases in plasma lipoxin A4 levels immediately after exercise challenge both in asthmatic children with positive responses to exercise (p = 0.013) and negative responses to exercise (p = 0.05). But these levels were significantly higher in asthmatic children with negative responses to exercise (p = 0.041). There was an inverse correlation between lipoxin A4 levels and a reduction in forced expiratory volume at one second percent after exercise (p = 0.045, r = -0.465). CONCLUSION: Our results are the first demonstration of the lower levels of lipoxin A4 associated with exercise-induced bronchoconstriction in asthma. We hypothesize that the development of exercise-induced bronchoconstriction in asthmatic children may be in relation to a reduced endogenous lipoxin biosynthetic capability. Lipoxin mimetics and related compounds could provide novel therapeutic approaches to the treatment of exercise-induced bronchoconstriction in asthma.