Filtreler
Experimental bile-duct ligation resulted in accumulation of oxidized low-density lipoproteins in BALB/c mice liver

Cömert M. | Tekin I.Ö. | Açikgöz Ş. | Üstundag Y. | Uçan B.H. | Acun Z. | Barut F.

Article | 2004 | Journal of Gastroenterology and Hepatology (Australia)19 ( 9 ) , pp.1052 - 1057

Background and Aim: Oxidized low-density lipoproteins (LDL), which are produced during oxidative stress by the process of lipid peroxidation, have also been proposed to have complex roles in many other immuno-inflammatory mechanisms. It has been shown that bile-duct ligation results in oxidative stress in the liver of animals. The aim of this study was to investigate if oxidized LDL are produced in the liver tissues of bile-duct-ligated mice. Methods: Obstructive jaundice was induced in BALB/c mice by the ligation and division of the common bile duct. Liver concentrations of glutathione and malondialdehyde were measured in the sham- . . .operated (n = 10) and bile-duct-ligated (n = 10) mice on the 10th day of obstructive jaundice. The presence of oxidized LDL in the liver tissue sections was evaluated using a special, novel immunofluorescent staining method. The final step was to explore the existence of oxidized LDL under fluorescent microscopy. Results: Compared with sham-operated mice, jaundiced mice showed significantly higher levels of malondialdehyde and lower concentrations of reduced glutathione in the liver. While there was no staining in the sham-operated group, bile-duct ligation resulted in positive oxidized LDL staining in the liver tissues of mice. The present study testifies that bile-duct ligation results in oxidative stress and enhanced lipid peroxidation in the hepatic tissues of BALB/c mice and moreover, that oxidized LDL accumulate in the liver of mice with experimental obstructive jaundice. Conclusion: Oxidized LDL may be an important and direct indicator of ongoing oxidative stress and enhanced lipid peroxidation in obstructive jaundice. The potential roles of this finding were also discussed, briefly. © 2004 Blackwell Publishing Asia Pty Ltd Daha fazlası Daha az

Oxidized low-density lipoproteins accumulate in rat lung after experimental lung edema induced by alpha- naphthylthiourea (ANTU)

Sipahi E.Y. | Ozel Tekin I. | Comert M. | Barut F. | Ustun H. | Sipahi T.H.

Article | 2004 | Pharmacological Research50 ( 6 ) , pp.585 - 591

Oxidation of the low-density lipoprotein (LDL) results in the production of modified LDLs. Oxidation of LDL cholesterol plays a role on the pathogenesis of endothelial dysfunction. This study was designed to investigate the possible participation of the oxidative modification of low density lipoprotein in the lung edema induced by alpha-naphthylthiourea (ANTU), which is a well-known noxious chemical agent on the lung endothelium. When ANTU injected intraperitoneally into rats (15 mg kg-1), it produced lung edema as indicated by an increase in lung weight/body weight (LW/BW) ratio and pleural effusion (PE) reaching a maximum within 4 . . . h. A significant lung edema was observed 4 h after intraperitoneally injection of alpha-naphthylthiourea when compared with olive oil-injected control rats. On microscopic examination of alpha-naphthylthiourea-treated rats were shown to have severe lung injury, while no change was observed in olive oil-treated control rats. While there were no staining in control lungs, positive oxidized low-density lipoproteins immune-fluorescent staining were observed in lung edema group. Our study showed that oxidized low-density lipoprotein (oxLDL) accumulated in ANTU-induced lung damage. This is the first study in which accumulation of oxLDL molecules in the intact lung tissue were shown by fluorescent immune-staining method in experimental lung edema. The potential role of oxLDL in this pathology are still under investigation. © 2004 Elsevier Ltd. All rights reserved Daha fazlası Daha az

6698 sayılı Kişisel Verilerin Korunması Kanunu kapsamında yükümlülüklerimiz ve çerez politikamız hakkında bilgi sahibi olmak için alttaki bağlantıyı kullanabilirsiniz.

creativecommons
Bu site altında yer alan tüm kaynaklar Creative Commons Alıntı-GayriTicari-Türetilemez 4.0 Uluslararası Lisansı ile lisanslanmıştır.
Platforms