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YALÇIN, AHMET SUHA

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AHMET SUHA

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Author: HAKLAR, GONCAGÜL × Start date: 2002 ×

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    The role of reactive oxygen species and apoptosis in the pathogenesis of varicocele in a rat model and efficiency of vitamin E treatment
    (WILEY, 2004) YALÇIN, AHMET SUHA; Cam, K; Simsek, F; Yuksel, M; Turker, L; Haklar, G; Yalcin, S; Akdas, A
    We investigated role of reactive oxygen species (ROS) and apoptosis in the pathogenesis of infertility in experimental model of varicocele. The protective effect of vitamin E was also examined. Three groups of rats were constructed as the first group had sham operation, experimental varicoceles were established by partial ligation of the left renal vein in later two groups. Third group had received vitamin E. Production of ROS was determined by chemiluminescence assay (CL). The in situ end labelling technique was utilized to investigate apoptosis. Tissue vitamin E levels were measured by high performance liquid chromatography. The differences between luminol enhanced CL levels of groups were not statistically significant. However, the difference between CL levels of lucigenin probe in left testicles of sham and varicocele groups were statistically significant (p = 0.0007). Similarly, the results of the third group receiving vitamin E significantly differed from the varicocele group (p = 0.0025). The difference of apoptotic index was also statistically significant between sham and varicocele groups (p = 0.0038). Although the values of apoptotic index detected in the vitamin E group were lower compared with the varicocele group, the difference was not significant. This study proposes that ROS production and apoptosis in the testicles were induced with experimental varicocele. Vitamin E had a protective role. An increased rate of apoptosis with experimental varicocele suggests a molecular alteration, which may involve ROS overproduction as the triggering mechanism. Consequently, this study indicates an association between varicocele and infertility at molecular level through stimulation of ROS and apoptosis.
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    Thyroxine prevents reoxygenation injury in isolated proximal tubule cells
    (SPRINGER, 2003) YALÇIN, AHMET SUHA; Erkan, E; Sakarcan, A; Haklar, G; Yalcin, S
    Ischemia is characterized by cessation of blood flow and oxygen delivery to tissues that results in disruption of cellular structure and organelles. However, restoration of blood flow following ischemia causes reperfusion injury, characterized by further damage in the tissues mediated by reactive oxygen species. In the kidney, reactive oxygen molecules have been implicated in ischemic, toxic and immunological glomerular damage. Thyroxine has been shown to be cytoprotective in toxic and ischemic injury. Thyroxine's cytoprotective effect is postulated to be secondary to stimulation of intracellular ATP synthesis. However, the underlying mechanism of that beneficial effect remains to be investigated. In this study we investigated the effect of thyroxine (T4) on free oxygen radical production in an in vitro model of reperfusion injury. Free oxygen radical (FOR) levels were determined by a chemiluminescence method after freshly isolated rabbit proximal tubule cells were subjected to 15 min of anoxia followed by 45 min of reoxygenation. Reoxygenation injury resulted in a significant increase in FOR levels (P<0.0001). FOR levels were significantly lower in the group treated with thyroxine (P=0.01) and cells treated with thyroxine displayed better preservation of cellular structure. We conclude that thyroxine's cytoprotective effect might be via decreased synthesis of FOR, and thyroxine treatment may confer cytoprotection in renal conditions characterized by FOR-mediated injury.