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Journal of Environmental Pathology, Toxicology and Oncology
Factor de Impacto: 1.241 Factor de Impacto de 5 años: 1.349 SJR: 0.356 SNIP: 0.613 CiteScore™: 1.61

ISSN Imprimir: 0731-8898
ISSN En Línea: 2162-6537

Journal of Environmental Pathology, Toxicology and Oncology

DOI: 10.1615/JEnvironPatholToxicolOncol.2015012424
pages 53-61

Zoledronic Acid Aggravates Kidney Damage During Ischemia Reperfusion Injury in Rat

Ibrahim Sehitoglu
Department of Pathology, Faculty of Medicine, RecepTayyip Erdogan University, Rize, Turkey
Levent Tumkaya
Department of Histology and Embryology, Faculty of Medicine, RecepTayyip Erdogan University, Rize, Turkey
Recep Bedir
Department of Pathology, Faculty of Medicine, RecepTayyip Erdogan University, Rize, Turkey
Yildiray Kalkan
Department of Histology and Embryology, Faculty of Medicine, RecepTayyip Erdogan University, Rize, Turkey
Medine Cumhur Cure
Department of Biochemistry, Faculty of Medicine, RecepTayyip Erdogan University, Rize, Turkey
Ahmet Fikret Yucel
Department of Surgery, Faculty of Medicine, RecepTayyip Erdogan University, Rize, Turkey
Orhan Unal Zorba
Department of Urology, Faculty of Medicine, RecepTayyip Erdogan University, Rize, Turkey
Suleyman Yuce
Internal Medicine, Kumru State Hospital, Ordu, Turkey
Erkan Cure
Department of Internal Medicine, Faculty of Medicine, RecepTayyip Erdogan University, Rize, Turkey

SINOPSIS

Introduction: Zoledronic acid (ZA), a bisphosphonate, increases the levels of cytokines, such as interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α), and reactive oxygen species (ROS) in subjects without cancer. Increased production of ROS, TNF-α, and IL-6 during ischemia and reperfusion (I/R) injury stimulates apoptosis that leads to renal injury. We aimed to investigate whether ZA treatment has a protective effect on renal tissues during I/R. Materials and Methods: Twenty-four Sprague-Dawley rats were used in this study, and they were subdivided randomly into three groups, each containing eight rats. Infrarenal abdominal aortic cross ligation was performed on the I/R group. After 2 h of ischemia, 2 h of reperfusion was applied. A single dose of 100 µg/kg ZA was administered intraperitoneally to the ZA group. I/R was performed after 48 h. Results: Whereas TNF-α, IL-6, and nitric oxide (NO) levels of the I/R group were higher than those of the control group, TNF-α, IL-6, and NO levels of the ZA group were higher than those of the I/R group [TNF-α (p=0.038), IL-6 (p=0.012), NO (p=0.002), and caspase-3 (p=0.037)] and the control group [TNF-α (p<0.001), IL-6 (p<0.001), NO (p<0.001), and caspase-3 (p<0.001)]. Whereas the carbonic anhydrase II (CA-II) level of the ZA group was lower than that of the control group (p=0.040), the CA-II level of the I/R group was higher than that of the control group (p=0.020). Conclusion: ZA may aggravate renal injury during I/R by increasing cytokine production and apoptosis. It may also increase renal injury and metabolic acidosis during I/R by suppressing CA-II enzyme activities.


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