Our research is consistent representing the typically apoptotic characteristics lend further support to the earlier which demonstrated

One of the most damaging effects of these free radicals and their products in vivo was the peroxidation of membrane lipids. It is known that a loss in antioxidant capacities results in an intrinsic accumulation of MDA, which would be a reliable marker of free radical generation that indicates the risk of membrane damage. The degree of cell damage under heavy metal stress depends on the rate of ROS formation and on the efficiency and capacity of detoxification and repair mechanisms. The cellular defense system against toxicity from ROS includes superoxide dismutase, catalase and glutathion peroxidases. In present study, our results showed that low-concentration Cd stimulated the antioxidant activities probably due to the induction of an adaptive response, in the way of maintenance and/or increase of physiological activities under low concentration of Cd. However, exposure to the high concentration of Cd was apparently linked to a significant reduction of antioxidant activities compared to the control groups, indicating that the scavenging function of antioxidant activities were impaired under high concentration of Cd. Oxidative injury also results in multiple physiological and pathological changes. In the present study, our investigation demonstrated that exposure to Cd induced histopathological changes of testis in a concentration-dependent manner. Our findings were consistent with the results of El-Ashmawy, Youssef and Blanco et al., which demonstrated that Cd induced disordered arrangement of germ cells, sloughing and a decreased spermatogenic cell layer in the seminiferous tubules, destruction of basement membranes, disintegration of spermatocytes, and complete absence of the sperms. Several studies implicated that Cd-related histopathological changes resulted from testis blood vessel damage, considered as the main cause of Cd toxicity, as well as the mediator of the impaired testosterone secretion in mammalian testis. The exact mechanism of Cd-induced histopathological changes in crustacean testis is unclear. However, this does not exclude the possibility of direct toxicity of Cd to germ cells. Our findings support the results from other studies which indicated that Cd altered testis histology resulting in structural defects in germ cells. Microscopic examination of AO/EB stained cells can be recommended as the most reliable method to distinguish viable, early or late apoptotic and necrotic cells. In this study, three types of cells stained by AO/EB wererecognized under fluorescence Staurosporine microscope: live cells, live apoptotic cells, and dead cells by necrosis, indicating that the effect of Cd was related to the induction of apoptosis and/or necrosis of germ cells. The numbers of apoptotic and/or necrotic cells were increased with increasing Cd concentrations, in line with the results of histopathological changes in the present study. Another reliable method of detecting apoptosis is TEM, a powerful method to observe ultrastructural aspects.

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