Effect of ozone oxidative preconditioning in preventing early radiation-induced lung injury in rats

Ionizing radiation causes its biological effects mainly through oxidative damage induced by reactive oxygen species. Previous studies showed that ozone oxidative preconditioning attenuated pathophysiological events mediated by reactive oxygen species. As inhalation of ozone induces lung injury, the aim of this study was to examine whether ozone oxidative preconditioning potentiates or attenuates the effects of irradiation on the lung. Rats were subjected to total body irradiation, with or without treatment with ozone oxidative preconditioning (0.72 mg/kg). Serum proinflammatory cytokine levels, oxidative damage markers, and histopathological analysis were compared at 6 and 72 h after total body irradiation. Irradiation significantly increased lung malondialdehyde levels as an end-product of lipoperoxidation. Irradiation also significantly decreased lung superoxide dismutase activity, which is an indicator of the generation of oxidative stress and an early protective response to oxidative damage. Ozone oxidative preconditioning plus irradiation significantly decreased malondialdehyde levels and increased the activity of superoxide dismutase, which might indicate protection of the lung from radiation-induced lung injury. Serum tumor necrosis factor alpha and interleukin-1 beta levels, which increased significantly following total body irradiation, were decreased with ozone oxidative preconditioning. Moreover, ozone oxidative preconditioning was able to ameliorate radiation-induced lung injury assessed by histopathological evaluation. In conclusion, ozone oxidative preconditioning, repeated low-dose intraperitoneal administration of ozone, did not exacerbate radiation-induced lung injury, and, on the contrary, it provided protection against radiation-induced lung damage

Investigation of genetic variations of il17 for vitiligo disease

Objective: Vitiligo is a disorder of pigmentation characterized by the presence of depigmented skin macules due to a chronic and progressive loss of melanocytes from the cutaneous epidermis. Among many different etiologic hypotheses that have been suggested so far for vitiligo, the most compelling one involves a combination of environmental and genetic factors that cause autoimmune melanocyte destruction. The purpose of this study is then to determine whether there is any relationship between vitiligo and IL17 gene Glu126Gly, His161Arg and G197A polymorphisms. Design: Controlled prospective study Setting: Department of Molecular Biology and Genetics, Bulent Ecevit University Subjects: Genetic polymorphisms of IL17 gene were detected by using polymerase chain reaction based restriction fragment length polymorphism in 86 vitiligo patients and 90 healthy controls. Intervention: For genetic analysis, 5 ml of venous blood was drawn into tubes containing EDTA from each patient. Main outcome measures: IL17 gene Glu126Gly, His161Arg and G197A polymorphisms in vitiligo patients Results: As a result of our study, we have found a significant relation between His161Arg polymorphism of IL17F gene and vitiligo patients (p = 0.045). Conclusions: Our findings suggest that the IL17F His161Arg gene polymorphism has a protective role in susceptibility to vitiligo. This may be regarded as hypothesis-generating and should further be investigated in independent studies. © 2019, Kuwait Medical Association. All rights reserved.2013-50737594-02This work was supported by grants from the Bulent Ecevit University (Project number: 2013-50737594-02

Effect of ozone oxidative preconditioning in preventing early radiation-induced lung injury in rats

Ionizing radiation causes its biological effects mainly through oxidative damage induced by reactive oxygen species. Previous studies showed that ozone oxidative preconditioning attenuated pathophysiological events mediated by reactive oxygen species. As inhalation of ozone induces lung injury, the aim of this study was to examine whether ozone oxidative preconditioning potentiates or attenuates the effects of irradiation on the lung. Rats were subjected to total body irradiation, with or without treatment with ozone oxidative preconditioning (0.72 mg/kg). Serum proinflammatory cytokine levels, oxidative damage markers, and histopathological analysis were compared at 6 and 72 h after total body irradiation. Irradiation significantly increased lung malondialdehyde levels as an end-product of lipoperoxidation. Irradiation also significantly decreased lung superoxide dismutase activity, which is an indicator of the generation of oxidative stress and an early protective response to oxidative damage. Ozone oxidative preconditioning plus irradiation significantly decreased malondialdehyde levels and increased the activity of superoxide dismutase, which might indicate protection of the lung from radiation-induced lung injury. Serum tumor necrosis factor alpha and interleukin-1 beta levels, which increased significantly following total body irradiation, were decreased with ozone oxidative preconditioning. Moreover, ozone oxidative preconditioning was able to ameliorate radiation-induced lung injury assessed by histopathological evaluation. In conclusion, ozone oxidative preconditioning, repeated low-dose intraperitoneal administration of ozone, did not exacerbate radiation-induced lung injury, and, on the contrary, it provided protection against radiation-induced lung damage

Effects of ozone oxidative preconditioning on liver regeneration after partial hepatectomy in rats

Aim: Similar protective effect of ischemic and ozone oxidative preconditioning (OzoneOP) in hepatic ischemia-reperfusion (I/R) injury was demonstrated, providing evidences that both preconditioning settings shared similar biochemical mechanisms of protection. We investigated the effects of OzoneOP on liver regeneration after 70% partial hepatectomy (PHx) in rats. Methods: Rats were divided into three groups: PHx, I/R + PHx, and OzoneOP + I/R + PHx groups. Ozone (intraperitoneal, 1.2 mg/kg) was given to rats subjected to I/R and 70% hepatectomy daily five times before operation. At 24 hr and 48 hr after resection, samples were collected for the measurement of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), tumor necrosis factor alpha (TNF-?), and interleukin-6 (IL-6). Moreover, liver regeneration rate, proliferating cell nuclear antigen (PCNA) labeling index, mitotic index, and histopathological examination were evaluated. Results: OzoneOP reduced liver injury determined by liver histology and serum transaminases. There was a rise in serum TNF-? and IL-6 levels in the I/R + PHx group whereas OzoneOP significantly decreased the rise in the level of TNF-? but not IL-6 on the 24 hr and 48 hr of reperfusion. Moreover, liver regeneration in OzoneOP + PHx group, as assessed by the regenerated liver weight, mitotic, and PCNA-labeling index, was significantly improved when compared to I/R + PHx group. Conclusion: These results suggest that OzoneOP ameliorates the hepatic injury associated with I/R and has a stimulatory effect on liver cell regeneration that may make it valuable as a hepatoprotective modality. © 2013 Informa Healthcare USA, Inc.111S306This research was supported by the Scientific and Technological Research Council of Turkey (TUBITAK); project grant no. 111S306

N-acetyl-cysteine improves anastomotic wound healing after radiotherapy in rats

Aim: This study was designed to determine the effects of intraperitoneally or orally administered N-acetylcysteine (NAC) on anastomotic healing of irradiated rats. Methods: Thirty-two male Wistar albino rats were randomized into four groups containing 8 rats each: I; standard resection plus anastomosis, II; radiation plus standard resection plus anastomosis, III; radiation plus standard resection plus anastomosis plus oral NAC, IV; radiation plus standard resection plus anastomosis plus intraperitoneal NAC. Four types of assessment were performed: bursting pressure, hydroxiproline (OHP) content, histopathology, and biochemical evaluation, including serum malondialdehyde (MDA), advanced oxidation protein products (AOPP), reduced glutathione (GSH) and superoxide dismutase (SOD) activities. Results: Group comparisons demonstrated that bursting pressure was significantly higher in NAC treated rats. The mean tissue OHP concentration in the anastomotic tissue was significantly lower in irradiated rats (group II) than in the other groups. NAC treatment caused increased activity of SOD and GSH. In contrast, MDA levels were found to be decreased in groups III and IV. Histopathological analysis revealed that NAC administration, either orally or intraperitoneally, leads to a better anastomotic healing in terms of reepithelialization, perianastomotic fibrosis, ischemic necrosis, and muscle layer destruction. Conclusion: The present study supports the hypothesis that NAC administration alleviates the negative effects of radiotherapy on anastomotic healing. Nevertheless, the underlying mechanisms responsible for this protective effect is unknown today. © 2011 Informa Healthcare USA, Inc

N-acetylcycsteine attenuates the deleterious effects of radiation therapy on incisional wound healing in rats

Background: During preoperative radiotherapy, effective doses of ionizing radiation occasionally cause wound complications after subsequent surgery. This study was designed to determine the effects of intraperitoneally or orally administered N-acetylcysteine (NAC) on anastomotic healing of irradiated rats. Material & Methods: Forty Wistar albino rats were randomized into four groups containing 10 rats each. A 3 cm long surgical full-thickness midline laparotomy was performed to all groups (Groups 1-4). Group 1 was designed as a control group without radiation therapy and NAC treatment. Groups 2, 3 and 4 received a single abdominal dose of 10 Gy irradiation before laparotomy and groups 3 and 4 received oral and intraperitoneal NAC, respectively. Results: Group comparisons demonstrated that breaking strength was significantly higher in NAC treated rats. A statistically significant difference was determined in terms of superoxide dismutase (SOD), malondealdehyde (MDA) and glutation (GSH) values between groups (p<0.001). Nevertheless, advanced oxidation protein products (AOPP) levels were found to be similar between groups (p=0.163). Serum GSH and SOD levels were significantly higher in groups 3 and 4 when compared to group 2 (p < 0.05). Similarly, there was a significant increase in serum MDA concentration, predicting lipid peroxidation, in group 2 when compared to groups 1, 3 and 4 (p < 0.05). There was not a significant difference between Groups 3 and 4 regarding GSH, MDA, SOD, and AOPP levels. Histopathological analysis revealed that NAC administration, either orally or intraperitoneally, leads to a better incisional healing in terms of inflammation, granulation, collagen deposition, reepithelization and neovascularization. Conclusion: The present study supports the hypothesis that NAC administration alleviates the negative effects of radiotherapy on incisional wound healing by means of reducing oxidative stress markers and improving histologic parameters independent of the route of administration

The effect of erythropoietin on anastomotic healing of irradiated rats

Aim: The aim of the present study is to evaluate the possible protective effects of erythropoietin (EPO) on anastomotic wound healing after preoperative radiotherapy according to its pleiotropic mechanism of action. Methods: Thirty-two male Wistar albino rats were randomized into four groups containing eight rats each: ANAS group, standard resection plus anastomosis; RT+ANAS group, radiation plus standard resection plus anastomosis; ANAS+EPO group, standard resection plus anastomosis plus EPO; RT+ANAS+EPO, radiation plus standard resection plus anastomosis plus EPO. All animals were sacrificed by cardiac puncture, and anastomotic healing was measured by bursting pressure, hydroxyproline (OHP) levels, myeloperoxidase (MPO) activity and histopathological evaluations. Malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-?), and matrix metalloproteinase-9 (MMP-9) were also measured in serum specimens. Results: OHP levels in the RT+ANAS + EPO group were significantly increased compared with other groups (p <.05). In contrast, MPO activity in the RT+ANAS+EPO group was significantly decreased compared with other groups (p <.05). Serum MDA levels were found to be decreased in the ANAS+EPO and RT+ANAS+EPO groups (p <.05). Group comparisons demonstrated that bursting pressure was significantly higher in EPO treated rats (p <.05). The histopathology results revealed that EPO treatment improves anastomotic wound healing though decreased necrosis and inflammatory cell infiltration and increased fibroblast activity. Conclusion: The findings of the present study indicate that EPO contributes to wound healing and the strength of colon anastomosis following radiation due to its antioxidant and anti-inflammatory effects, but further studies are needed to explore the significance of these effects. © 2012 Informa Healthcare USA, Inc.Oct.34This study was supported by the Research Fund of the Mugla University (No: 10/34)

Effects of humanin on experimental colitis induced by 2,4,6-trinitrobenzene sulphonic acid in rats

Background/Aim: The excessive apoptosis of intestinal epithelial cells (IECs) partly accounts for the development of colonic inflammation and eventually results in ulcerative colitis (UC). Humanin, an endogenous anti-apoptotic peptide, has previously been shown to protect against Alzheimer's disease and a variety of cellular insults. The present study aimed to investigate the effects of glysin variant of humanin (HNG) on 2,4,6-trinitrobenzene sulphonic acid (TNBS)-induced colitis in rats. Materials and Methods: Rats were divided into four groups as follows: Group 1 (n = 8): control; isotonic saline solution 0.1 ml/rat rectally, Group 2 (n = 8): TNBS colitis; 0.1 ml of a 2.5% (w/v) TNBS solution in 50% ethanol rectally, Group 3 (n = 8): 10 µM HNG, and Group 4 (n = 8): 20 µM HNG intraperitoneal (ip) on day 2 and 6 after rectal TNBS administration. Rats were sacrificed 7 days after the induction of colitis. Blood and tissue samples were harvested for biochemical and histopathological analysis. Results: HNG treatment significantly ameliorated weight loss and macroscopic and microscopic scores. TNBS-induced colitis significantly increased the colonic mRNA expression of tumor necrosis factor-alpha (TNF-?), interleukin-1beta (IL-1ß), and caspase-3 activities in group II in comparison to the group I. HNG treatment was associated with an inhibition of mRNA expression of TNF-? and IL-1ß, and a decrease in caspase-3 activities in colon tissues in group III and IV when compared to group II. Conclusion: The results of this study indicate that HNG treatment may exert beneficial effects in UC by decreasing inflammatory reactions and apoptosis. © 2017 Saudi Journal of Gastroenterology (Official journal of The Saudi Gastroenterology Association) | Published by Wolters Kluwer - Medknow