Abstract
Context: One of the main events associated with ischemia/reperfusion injury (IRI) is excessive production of reactive oxygen species (ROS). Zinc (Zn) and estradiol are considered as antioxidants that scavenge free radicals. Objectives: The aim of this study was to compare the protective effect of Zn and estradiol against renal IRI in ovariectomized rats. Materials and Methods: Ovariectomized Wistar rats were randomly divided into five experimental groups including control (sham operated), IRI, estradiol treated +IRI, estradiol and Zn treated +IRI, Zn treated +IRI groups. The IRI was induced by clamping renal vessels for 45 minutes followed by 24 hours reperfusion. During the last 6 hours of reperfusion, urine output was collected and the measurements were performed. Results: IRI caused an increase in kidney tissue damage score (KTDS) significantly (P<0.05). The serum levels of blood urea nitrogen (BUN) and the creatinine (Cr) also elevated by IRI, but theses parameters attenuated by Zn treatment significantly (P<0.05). Cr-clearance and urine flow were increased by Zn, and the percent of sodium excretion was increased by estradiol significantly (P<0.05). The kidney tissue level of malondialdehyde was decreased by co-treatment of Zn and estradiol statistically (P<0.05). Conclusions: Zn protected the kidney against IRI with an evident improvements of serum BUN and Cr levels, Cr clearance and tissue damage.
Highlights
One of the main events associated with ischemia/reperfusion injury (IRI) is excessive production of reactive oxygen species (ROS)
The serum levels of blood urea nitrogen (BUN) and the creatinine (Cr) elevated by IRI, but theses parameters attenuated by Zn treatment significantly (P < 0.05)
Implication for health policy/practice/research/medical education: Administration of zinc (Zn) as an antioxidant agent demonstrated an efficient role in preventing renal dysfunction induced by renal ischemia/reperfusion injury (IRI) in female rats
Summary
One of the main events associated with ischemia/reperfusion injury (IRI) is excessive production of reactive oxygen species (ROS). The pathogenesis of IRI induced AKI may aggravate by many factors such as reactive oxygen species (ROS), neutrophil infiltration, vasoactive peptides and ATP depletion [2]. IRI can lead to an imbalance between the productions of oxygen free radicals (ROS) and antioxidant [3], and produce kidney inflammation [4]. Pretreatment with antioxidants almost protects kidneys against IRI [5], and it may reduce apoptosis and lipid peroxidation by pre-ischemic activation of adenosine receptors [6]. Zinc (Zn) as an antioxidant is one of the most important elements in physiological processes while it is reported that Zn deficient diet enhances antioxidant capacity and decreases lipid peroxidation in rats damaged tissues [7,8]
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