Purpose: The main acute and late effects of ionizing radiation on living organisms are the formation of reactive oxygen species (ROS), apoptosis and DNA damage. Since the Rac1 molecule is a subunit of the NADPH oxidase enzyme, it is known to participate in the generation of ROS. The aim of this study was to investigate the role of Rac1 molecule in testicular damage induced by low (0.02 Gy), medium (0.1 Gy) and high (5 Gy) dose irradiation.
Material and method: In this study, Wistar rats (except the control group) were received whole body X-ray irradiation. Testicular tissues were removed 2 hours, 24 hours and 7 days after radiation exposure. Testicular damage was examined by hematoxylin-eosin staining and Johnsen's score. Immunohistochemical staining and G-LISA method were used to determine Rac1 expression and activation. To evaluate the generation of ROS in the testicular tissues, intracellular ROS, superoxide dismutase (SOD) and malondialdehyde (MDA) levels were measured.
Results: Increases in testicular damage were detected in all radiation exposed groups in a dose- and time-dependent manner. Compared to the control group, Rac1 expression decreased in all irradiated groups, while Rac1 activation increased. In addition, intracellular ROS and MDA levels were increased and SOD activity levels decreased in the irradiated groups compared to the control group.
Conclusion: Our findings suggest that Rac1 has a role in the increase of intracellular ROS and lipid peroxidation which led to an increase in radiation- induced testicular damage.
Keywords: Ionizing radiation; Rac1; Reactive oxygen species (ROS); Testis; radiation damage.