Wang et al. indicated that mitochondrial vacuolation and swelling were caused by a high level of mutant SOD accumulation. Distinct ultrastructural changes supported the result of the histopathological assessment, and there was different extent of LY2109761 morphological damages in different germ cells, which may be dependent on the rate of Cd absorption and its distribution in the testes. In addition to a series of morphological changes, the apoptosis program is concurrent with some changes in biochemistry. Several studies suggest that Cd induces apoptosis, as indicated by the derivatives of Cd to stimulate DNA fragmentation. In our study, testis exposure to Cd resulted in a DNA ladder confirming the induction of apoptosis, and this feature was clearly observed when crabs were treated with 58.00 and 116.00 mg?L21 Cd. This result was similar to that of Lohmann et al., reporting that Cd was able to stimulate calcium-dependent endonuclease in the Ca2+ -free system, and the activation of the endonuclease responsible for apoptosis cuts the DNA into oligonucleotides in vitro in thymus cell nuclear. Apoptosis is a tightly regulated physiological process, although many potential stimuli can initiate apoptosis, it appears that these signals converge on the caspase pathway to execute the final phases of the apoptotic process. In the present study, we found that caspase-3 and caspase-9 activities were both increased in a concentration-dependent manner after Cd treatment, suggesting that caspase-3 and caspase-9 were required for apoptosis induced by Cd in testes of crabs. The activities of caspase-3 were observed significant increased in testes of crabs exposed to 116.00 mg?L21 Cd compared to the control group, and these results were in agreement with Ye et al., indicating that apoptosis is characterized by a significant enhancement of caspase-3 activity. Caspase-9 located at the peak of caspase cascade activation, which is tarnally important for the activation of mitochondria-dependent apoptosis pathway. In our study, we found a significant increase of caspase-9 activities in 58 and 116.00 mg?L21 Cd compared to the control group, suggesting that mitochondriadependent pathway was probably one of Cd-induced apoptotic mechanisms in testes of crabs. In summary, the present study clearly demonstrated that acute exposure to Cd led to apoptosis in the testis cells of freshwater crab, which may lend strong support to the conclusion that acute exposure to Cd results in a cumulative and/or progressive testis injury. The possible mechanism of apoptosis induced by Cd in the testis of freshwater crab was mitochondria-dependent apoptosis pathway through activating caspase-9. Nasopharyngeal carcinoma is a malignant tumor arising from the epithelial cells that line the nasopharynx.