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1.
Article in English | MEDLINE | ID: mdl-17507267

ABSTRACT

Ligneous periodontitis (LP) is a rare periodontal disease in which plasminogen deficiency and fibrin deposition both play a part, resulting in characteristic gingival enlargement and periodontal breakdown. Recent data suggest that oxidant/antioxidant changes are significant in the pathology of oral diseases. This study examines the gingival histopathology in 2 cases with LP. To examine the antioxidant (AO) status, the activity of the major AOs glutathione (GSH), catalase (CAT), and glutathione S-transferase (GST) and the malondialdehyde (MDA) levels, a product of lipid peroxidation, were measured and compared with healthy control subjects. The histopathologic examination of the gingiva revealed subepithelial fibrin accumulation and irregular extensive downward proliferation of the epithelium. Biochemical analysis showed that the CAT, GST, and MDA levels were higher in LP patients than in the control subjects, and the GSH level was lower. Our preliminary findings show that in LP, the AO capacity of the gingiva changes or decreases and lipid peroxidation increases, which suggests that oxidative stress is involved in the pathology of the periodontal breakdown observed in this disease.


Subject(s)
Antioxidants/analysis , Gingiva/chemistry , Gingival Overgrowth/surgery , Periodontitis/surgery , Adolescent , Case-Control Studies , Catalase/analysis , Conjunctivitis/complications , Conjunctivitis/drug therapy , Cyclosporine/adverse effects , Dermatologic Agents/adverse effects , Female , Fibrin/biosynthesis , Gingival Overgrowth/chemically induced , Gingival Overgrowth/pathology , Glutathione/analysis , Glutathione Transferase/analysis , Humans , Malondialdehyde/analysis , Periodontitis/diagnostic imaging , Plasminogen/deficiency , Radiography
2.
Exp Lung Res ; 32(7): 287-303, 2006 Aug.
Article in English | MEDLINE | ID: mdl-17060173

ABSTRACT

Recent studies suggest that ischemic preconditioning (IP) of the lung may have a protective effect in ischemia-reperfusion (I/R) injury. The purpose of the present study was to investigate the preconditioning hypothesis in rat pulmonary vascular bed and to examine the role of nitric oxide (NO) in IP. Isolated rat lung was perfused with Krebs-Henseleit solution containing indomethacin at a constant flow rate and perfusion pressure changes was recorded by a pressure transducer. In rat pulmonary vascular bed, 2 hours of hypothermic ischemia significantly attenuated histamine-induced vasodilator responses without affecting sodium nitroprusside (SNP) vasodilation when compared to sham values. However, 2 cycles of 5 minutes of ischemia and reperfusion that were applied prior to 2 hours of ischemia (IP protocol) prevented the attenuation of histamine-induced vasodilation. On the other hand, IP failed to prevent pulmonary edema after ischemia. Histopathological examination of rat lungs demonstrated that IP was able to protect endothelial cells and type II pneumocytes in lung. Moreover, in IP group, malondialdehyde (MDA) contents of the lung tissue were significantly lower and tissue glutathione (GSH) contents were significantly higher than those in I/R group. Administration of NO synthase inhibitor, N(G)-nitro-L-arginine-methyl ester (L-NAME) prior to the IP protocol abolished the protective effects of IP, but not affected the tissue malondialdehyde and glutathione levels. These results suggest that I/R impaired endothelium-dependent vasodilatory response, whereas endothelium-independent SNP-induced responses were preserved in rat pulmonary vascular bed. IP prevented the impairment of pulmonary vascular endothelium-dependent responses, and these effects may be partially mediated by NO.


Subject(s)
Ischemic Preconditioning , Lung/physiopathology , Nitric Oxide/physiology , Reperfusion Injury/prevention & control , Animals , Endothelium, Vascular/drug effects , Endothelium, Vascular/metabolism , Endothelium, Vascular/pathology , Enzyme Inhibitors/pharmacology , Glutathione/metabolism , Ischemic Preconditioning/methods , Lipid Peroxidation/physiology , Lung/blood supply , Lung/drug effects , Lung/pathology , Male , Malondialdehyde/metabolism , NG-Nitroarginine Methyl Ester/pharmacology , Nitric Oxide Synthase/antagonists & inhibitors , Nitric Oxide Synthase/metabolism , Rats , Rats, Wistar , Reperfusion Injury/pathology , Reperfusion Injury/physiopathology , Thiobarbituric Acid Reactive Substances/metabolism
3.
Life Sci ; 78(4): 421-7, 2005 Dec 12.
Article in English | MEDLINE | ID: mdl-16111719

ABSTRACT

Ischemic preconditioning (IP) has been shown to protect the lung against ischemia-reperfusion (I/R) injury. Although the production of reactive oxygen species (ROS) has been postulated to play a crucial role in I/R injury, the sources of these radicals in I/R and the mechanisms of protection in IP remain unknown. Since it was postulated that deamination of endogenous and exogenous amines by semicarbazide-sensitive amine oxidase (SSAO) in tissue damage leads to the overproduction of hydrogen peroxide (H2O2), we investigated the possible contribution of tissue SSAO to excess ROS generation and lipid peroxidation during I/R and IP of the lung. Male Wistar rats were randomized into 6 groups: control lungs were subjected to 30 min of perfusion in absence and presence of SSAO inhibitor, whereas the lungs of the I/R group were subjected to 2 h of cold ischemia following the 30 min of perfusion in absence and presence of SSAO inhibitor. IP was performed by two cycles of 5 min ischemia followed by 5 min of reperfusion prior to 2 h of hypothermic ischemia in absence and presence of SSAO inhibitor. Lipid peroxidation, reduced (GSH) and oxidized (GSSG) glutathione levels, antioxidant enzyme activities, SSAO activity, and H2O2 release were determined in tissue samples of the study groups. Lipid peroxidation, glutathione disulfide (GSSG) content, SSAO activity and H2O2 release were increased in the I/R group, whereas GSH content, GSH/GSSG ratio and antioxidant enzyme activities were decreased. SSAO activity, H2O2 release, GSSG content and lipid peroxidation were markedly decreased in the IP group, whereas GSH content, GSH/GSSG ratio and antioxidant enzyme activities were significantly increased. SSAO activity was found to be positively correlated with H2O2 production in all study groups. Increased lipid peroxidation, SSAO activity, GSSG and H2O2 contents as well as decreased GSH and antioxidant enzyme levels in I/R returned to their basal levels when IP and SSAO inhibition were applied together. The present study suggests that application of IP and SSAO inhibition together may be more effective than IP alone against I/R injury in the lung.


Subject(s)
Amine Oxidase (Copper-Containing)/antagonists & inhibitors , Amine Oxidase (Copper-Containing)/metabolism , Ischemic Preconditioning , Lung/enzymology , Animals , Antioxidants/metabolism , Catalase/metabolism , Glutathione/metabolism , Glutathione Disulfide/metabolism , Glutathione Peroxidase/metabolism , Glutathione Reductase/metabolism , Glutathione Transferase/metabolism , Hydrogen Peroxide/metabolism , In Vitro Techniques , Lipid Peroxidation , Lung/pathology , Male , Perfusion , Rats , Rats, Wistar , Reactive Oxygen Species/metabolism , Reperfusion Injury , Superoxide Dismutase/metabolism
4.
Clin Biochem ; 38(7): 681-4, 2005 Jul.
Article in English | MEDLINE | ID: mdl-15882860

ABSTRACT

OBJECTIVE: To investigate the protective effect of ischemic preconditioning (IP) in the early phase of reperfusion injury. DESIGN AND METHODS: Control rat lungs were subjected to 3 h of perfusion, whereas the lungs of the ischemia-then-reperfusion (I/R) group were subjected to 2 h of cold ischemia following 30 min of perfusion. IP was performed by two cycles of 5-min ischemia followed by 5 min of reperfusion prior to 2-h cold ischemia. Lipid peroxidation and antioxidant status were determined in tissue samples. RESULTS: Lipid peroxidation and reduced/oxidized glutathione (GSH/GSSG) ratio were increased; antioxidant enzyme activities were decreased in the I/R group whereas lipid peroxidation and GSH/GSSG ratio were decreased; antioxidant enzyme activities were increased in the IP group. CONCLUSION: IP appeared to have a protective effect against reactive oxygen species-mediated I/R injury in isolated rat lung.


Subject(s)
Ischemic Preconditioning , Lung/pathology , Reactive Oxygen Species/pharmacology , Reperfusion Injury/physiopathology , Animals , Glutathione/metabolism , In Vitro Techniques , Lipid Peroxidation , Lung/drug effects , Male , Peroxidases/metabolism , Rats , Rats, Wistar
5.
J Surg Res ; 124(1): 139-45, 2005 Mar.
Article in English | MEDLINE | ID: mdl-15734492

ABSTRACT

BACKGROUND: For adequate control of excess bleeding during liver resection, total vascular exclusion (TVE) is preferred by surgeons, especially when the tumor is located in the posterior liver lobes or near the cava. To the authors' knowledge, the effects of TVE technique on the postoperative liver regeneration process have not thus far been evaluated yet in the literature. This study was planned to compare the effects of liver resections performed either with portal pedicle clamping or with TVE on the regeneration process. MATERIALS AND METHODS: Seventy percent hepatectomy was performed with portal pedicle clamping (n=10, Group A) or with TVE (n=10, Group B) in rats. At 48 h after resection, sampling was performed for the measurement of serum transaminase, alkaline phosphatase (ALP), tissue malondialdehyde (MDA), and glutathione (GSH) levels. Liver regeneration rate, proliferating cell nuclear antigen (PCNA) labeling, and mitotic indices were also evaluated. RESULTS: Liver injury determinants (serum transaminases, ALP, and tissue MDA levels) were found significantly higher in group B than in group A. Liver regeneration rate, liver GSH levels, PCNA labeling index, and mitotic index were significantly lower in group B than in group A. CONCLUSIONS: The injury during TVE seems to be greater than during resection with portal pedicle clamping. The negative effect of this oxidative damage may influence the regenerative capacity of the remnant liver tissue.


Subject(s)
Hepatectomy/methods , Ischemia/etiology , Liver Regeneration , Liver/blood supply , Vascular Surgical Procedures/adverse effects , Animals , Constriction , Hepatic Artery/surgery , Hepatic Veins/surgery , Liver/metabolism , Liver/pathology , Male , Models, Animal , Necrosis , Oxidative Stress , Portal Vein/surgery , Rats , Rats, Wistar , Vascular Surgical Procedures/methods
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