ed to determine the relationship between HBs exposure and lipid peroxidation, and total antioxidant 24020966 capacity in sperm 17328890 cells, respectively. As shown in Externalization of PS in sperm cells induced by HBs The apoptosis-inducing effects of HBs were assessed by flowcytomeric analysis using double staining with annexin V and PI. As seen in HBs induces the activation of caspases-3, -8,- 9 in sperm cells Apoptosis is dependent on the activation of a group of proteolytic enzymes called caspases. A possible link between HBs exposure and caspases-3, -8 and -9 activations in sperm cells was investigated to determine whether HBs exposure can cause apoptosis. The sperm cells in the test and control groups were labeled with 1 ml of FITC-DEVD-FMK, FITC-IETD-FMK and FITC-LEHD-FMK for 1 h, respectively followed by washing and analysis by flow cytometry. The results showed in Effects of HBs exposure on oxidative DNA damage in sperm cells The effects of HBs exposure on oxidative DNA damage in sperm cells in the control and the test groups were assessed by flow-cytomeric analysis using TUNEL assay. The results are shown in Discussion HBV DNA presented in sperm cells was first addressed by French scientists who proposed that HBV may be a cause of male infertility by damaging spermatozoa. Subsequently, it was reported that in the male genital tract, viral infections could lead to an oxidative stress by spermatozoa and leukocytes including neutrophils and macrophages and a lack of antioxidant 
protection. Although viral infection can affect a man’s fertility, however up to now, only scant information is available on the influence of HBV infection on the sperm function. Effects of HBs on Sperm Functions HBs exposure induced oxidative stress in sperm cell Successful fertilization requires a sperm plasma membrane with normal integrity and functions. The numerous functions of the membrane are related to cell metabolism, for maintaining sperm motility, capacitation, acrosome reaction and sperm-oocyte interactions. It has been documented that ROS plays a key role in inducing sperm damage. In the present study, a significant get BAY41-2272 increase in ROS positive cells was observed after 3 h exposure to 25 mg/ml of HBs when compared with control. Conversely, the average rates of ROS positive cells significantly reduced when sperm cells were pretreated with HBs monoclonal antibody or the ROS scavenger NAC, respectively. These data provided solid evidences that HBs exposure was able to increase ROS production in sperm cells. Furthermore, our results revealed that the exposure of sperm cells to HBs caused a dosedependent ROS generation. In the previous study, however, Zhou et al reported that the incubation of sperm with HBs plus HBs MAb apparently accelerated the sperm motility loss and showed a harmful effect on sperm functions. It seems to be conflicting with the results of the present study, in which HBs plus HBs MAb significantly decreased ROS generation in sperm cells and showed a beneficial effect on sperm functions. The reason for this discrepancy might be that HBs MAb played different roles. On one hand, HBs MAb can directly neutralize the biological activity of HBs to reduce ROS generation in sperm cells, and on the other hand, HBs MAb can bind to HBs to form HBsHBs MAb complex that accelerated the sperm motility loss. Some also reported the similar findings in which the neutralizing effect of induced anti-HBs immunoglobulins decreased the HBsAg in the serum but the induced