RT Journal Article
ID 355028b31a5df801
A1 Sehitoglu, Ibrahim
A1 Tumkaya, Levent 
A1 Bedir, Recep 
A1 Kalkan, Yildiray 
A1 Cure, Medine Cumhur 
A1 Yucel, Ahmet Fikret
A1 Zorba, Orhan Unal 
A1 Yuce, Suleyman 
A1 Cure, Erkan
T1 Zoledronic Acid Aggravates Kidney Damage During Ischemia Reperfusion Injury in Rat
JF Journal of Environmental Pathology, Toxicology and Oncology
JO JEP(T)
YR 2015
FD 2015-02-27
VO 34
IS 1
SP 53
OP 61
K1 zoledronic acid
K1 ischemia/reperfusion
K1 kidney
K1 interleukin-6
K1 carbonic anhydrase II
AB 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.
PB Begell House
LK https://www.dl.begellhouse.com/journals/0ff459a57a4c08d0,455443d31df03fbb,355028b31a5df801.html