Abstract
To analyze the oxidative damage and histopathological alterations caused by ischemia-reperfusion (I/R) injury and ameliorative effects of carvedilol (CVD) in the rat testis. Twenty-one male rats were randomized into 3 groups as follows: Group I (n = 7); control (sham) group, Group II (n = 7); I/R group, in which I/R injury was performed by torsing the left testis 720 ° clockwise for 2 hours and detorsing for 2 hours. Group III (n = 7); CVD treatment group; in addition to I/R process, one-dose of CVD was administered (2mg/kg, i.p) 30 min. before detorsion. Levels of antioxidant enzymes, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and levels of malondialdehyde (MDA) and protein carbonyl (PC) were determined in testicular tissues and serum of rats. Testicular tissues were also examined histopathologically and Johnsen scores were determined. Activities of SOD and GSH-Px in serum and testicular tissues were increased by I/R, but administration of CVD decreased these levels (p < 0.001 and p = 0.001). Significantly increased MDA levels in serum and testicular tissues were decreased by CVD treatment (p < 0.001 and p = 0.001). Concerning PC levels in serum and testicular tissues, there was no statistically significant difference between the groups (p = 0.989 and p = 0.428). There was not a statistically significant difference in terms of mean Johnsen scores between the groups (p = 0.161). Administration of CVD decreased oxidative damage biochemically in the rat testis caused by I/R injury, but histopathologically no change was observed betwe¬en all of the groups.
Highlights
Ischemia-reperfusion (I/R) injury is a deleterious clinical entity in the organism that occurs when blood circulation is restored after an episode of acute ischemia
In addition to showing the activation of several antioxidant defense mechanisms to avoid the tisssue damage due to reactive oxygen species (ROS), which included the production of endogenous antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), the alterations in the serum and tissue levels of lipid peroxidation product malondialdehyde (MDA) and protein denaturation product protein carbonyl (PC) have been been analyzed in related studies to delineate the damaging effects of ROS [1,2,3,4,5]
The results of serum SOD, MDA, GSH-PX and PC values in all groups are presented in Table-2
Summary
Ischemia-reperfusion (I/R) injury is a deleterious clinical entity in the organism that occurs when blood circulation is restored after an episode of acute ischemia. In this type of injury the blood supply of the tissue is interrupted initially which leads to damage of metabolically active tissues, but the restoration of blood flow to the tissues, which initiates paradoxic cascade of events, leads to further cellular and tissue damage eventually [1]. The main pathological mechanism of the testicular injury following TT has not been completely understood, the I/R established during torsion and detorsion and OS generated by these events has been implicated as the main factors in cellular and tissue damage [4,5]. In addition to showing the activation of several antioxidant defense mechanisms to avoid the tisssue damage due to ROS, which included the production of endogenous antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), the alterations in the serum and tissue levels of lipid peroxidation product malondialdehyde (MDA) and protein denaturation product protein carbonyl (PC) have been been analyzed in related studies to delineate the damaging effects of ROS [1,2,3,4,5]
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