Turgay M, Turgay F, Devrim E, Kucuksahin O, Caydere M, Durak I
Rheumatology Department, Ankara University Faculty of Medicine, Ankara, Turkey.
Bratisl Lek Listy. 2012;113(1):10-3. doi: 10.4149/bll_2012_002.
The study was aimed to evaluate the possible effects of dexamethasone on oxidant/antioxidant status in kidney tissues of rats administered mercuric chloride (HgCl2). Thirty male Wistar-albino rats were enrolled in this study. Rats were divided into 4 groups: G1 (n=7) underwent no therapy (control group), G2 (n=8) received HgCl2 + physiological saline, G3 (n=7) dexamethasone (DM) + physiological saline and G4 (n=8) received HgCl2 + DM. HgCl2 was injected subcutaneously into rats in the G2 and G4 on the first day of the study. Dexamethasone was injected intraperitoneally into rats in the G3 and G4 for 3 days. Malondialdehyde (MDA) levels, catalase (CAT), glutathione peroxidase (GSH-Px), xanthine oxidase (XO) and superoxide dismutase (SOD) activities were evaluated in the kidney tissues. Serum creatinine levels were also measured. Xanthine oxidase activity was increased in the G2 compared to the control group. Catalase activity in the control group was significantly higher compared to the other groups. In the histopathological examination of kidneys, there was a tubular degeneration in G2 and G4. It was concluded that HgCl2 administration may cause oxidative stress through increasing XO and decreasing CAT activities. Dexamethasone injection may partially protect the rat kidneys against oxidative reactions by preventing the increase in XO activity (Tab. 1, Ref. 33).
本研究旨在评估地塞米松对给予氯化汞（HgCl2）的大鼠肾组织中氧化/抗氧化状态的可能影响。30只雄性Wistar白化大鼠参与了本研究。大鼠被分为4组：G1（n = 7）未接受治疗（对照组），G2（n = 8）接受HgCl2 + 生理盐水，G3（n = 7）接受地塞米松（DM）+ 生理盐水，G4（n = 8）接受HgCl2 + DM。在研究的第一天，对G2和G4组的大鼠皮下注射HgCl2。对G3和G4组的大鼠腹腔注射地塞米松，持续3天。评估肾组织中的丙二醛（MDA）水平、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GSH-Px）、黄嘌呤氧化酶（XO）和超氧化物歧化酶（SOD）活性。还测量了血清肌酐水平。与对照组相比，G2组的黄嘌呤氧化酶活性增加。与其他组相比，对照组的过氧化氢酶活性显著更高。在肾脏的组织病理学检查中，G2和G4组出现肾小管变性。得出的结论是，给予HgCl2可能通过增加XO活性和降低CAT活性而导致氧化应激。注射地塞米松可能通过防止XO活性增加而部分保护大鼠肾脏免受氧化反应的影响（表1，参考文献33）。
