Tsamouri Maria-Malvina, Rapti Maria, Kouka Paraskevi, Nepka Charitini, Tsarouhas Konstantinos, Soumelidis Anestis, Koukoulis George, Tsatsakis Aristides, Kouretas Demetrios, Tsitsimpikou Christina
Department of Biochemistry-Biotechnology, School of Health Sciences, University of Thessaly, Viopolis, Larissa, 41500, Greece.
Department of Pathology, University Hospital of Larissa, Mezourlo, Larissa, 41110, Greece.
Food Chem Toxicol. 2017 Oct;108(Pt A):186-193. doi: 10.1016/j.fct.2017.07.058. Epub 2017 Jul 31.
Contrast-induced nephropathy (CIN) is a leading cause of hospital-acquired acute kidney injury as a result of iodinated contrast-media use for diagnostic purposes. Pathophysiology remains unclear. In the present study iopromide was administered to New Zealand white rabbits without any prior intervention. Oxidative stress was assessed in blood and tissue level at three anatomical kidney areas (medullary, cortical, juxtamedullary). Histopathological evaluation was also performed. Serum creatinine and urea increased in the CIN groups over 25% at two hours after administration and returned to baseline at 48 h. In kidney tissues, a significant reduction (40%) of catalase in renal cortexes of the CIN groups was observed. Necrosis and tubular vacuolization was also noted that correlated with urea and creatinine levels. Lipid peroxidation decreased at 10 h after administration (>45%) and remained low even at 48 h. Plasma protein carbonyls were significantly increased (67%) in 2 h and dropped later. Serum levels of creatinine and urea at 24 and 48 h significantly correlated with the Total Antioxidant Activity and lipid peroxidation, respectively. Oxidative stress is shown to be involved in CIN development in the rabbit, with more pronounced effects to be confined to the cortex and outer stripe of the outer medulla.
对比剂肾病（CIN）是因使用碘化造影剂进行诊断而导致医院获得性急性肾损伤的主要原因。其病理生理学仍不清楚。在本研究中，对新西兰白兔在未进行任何预先干预的情况下给予碘普罗胺。在三个肾脏解剖区域（髓质、皮质、近髓质）的血液和组织水平评估氧化应激。还进行了组织病理学评估。CIN组在给药后两小时血清肌酐和尿素升高超过25%，并在48小时恢复至基线水平。在肾脏组织中，观察到CIN组肾皮质中的过氧化氢酶显著降低（40%）。还注意到坏死和肾小管空泡化与尿素和肌酐水平相关。脂质过氧化在给药后10小时下降（>45%），甚至在48小时仍保持在低水平。血浆蛋白羰基在2小时显著增加（67%），随后下降。24小时和48小时的血清肌酐和尿素水平分别与总抗氧化活性和脂质过氧化显著相关。氧化应激被证明参与了兔CIN的发展，更明显的影响局限于皮质和外髓质的外带。
