title: Effects of hepatitis B virus S protein exposure on sperm membrane integrity and functions.
abstract: BACKGROUND
  Hepatitis B is a public health problem worldwide. Viral infection can affect a man's fertility, but only scant information about the influence of hepatitis B virus (HBV) infection on sperm quality is available. The purpose of this study was to investigate the effect of hepatitis B virus S protein (HBs) on human sperm membrane integrity and functions.
  
  
  RESULTS
  Reactive oxygen species (ROS), lipid peroxidation (LP), total antioxidant capacity (TAC) and phosphatidylserine (PS) externalization were determined. The terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assays and flow cytometric analyses were performed. (1) After 3 h incubation with 25 µg/ml of HBs, the average rates of ROS positive cells, annexin V-positive/propidium iodide (PI)-negative cells, Caspases-3,-8,-9 positive cells and TUNEL-positive cells were significantly increased in the test groups as compared to those in the control groups, while TAC level was decreased when compared with the control. The level of malondialdehyde (MDA) in the sperm cells exposed to 50 µg/ml of HBs for 3 h was significantly higher than that in the control (P<0.05-0.01). (2) HBs increased the MDA levels and the numbers of ROS positive cells, annexin V-positive/PI-negative cells, caspases-3, -8, -9 positive cells and TUNEL-positive cells in a dose-dependent manner. (3) HBs monoclonal antibody (MAb) and N-Acetylcysteine (NAC) reduced the number of ROS-positive sperm cells. (4) HBs decreased the TAC levels in sperm cells in a dose-dependent manner.
  
  
  CONCLUSIONS
  HBs exposure could lead to ROS generation, lipid peroxidation, TAC reduction, PS externalization, activation of caspases, and DNA fragmentation, resulting in increased apoptosis of sperm cells and loss of sperm membrane integrity and causing sperm dysfunctions.
authors.affiliation: Research Center for Reproductive Medicine, Shantou University Medical College, Shantou, China.
authors.forename: XiangJin
authors.initials: X
authors.lastname: Kang
authors.forename: QingDong
authors.initials: Q
authors.lastname: Xie
authors.forename: XiaoLing
authors.initials: X
authors.lastname: Zhou
authors.forename: FangZheng
authors.initials: F
authors.lastname: Li
authors.forename: JiHua
authors.initials: J
authors.lastname: Huang
authors.forename: DongLing
authors.initials: D
authors.lastname: Liu
authors.forename: TianHua
authors.initials: T
authors.lastname: Huang
mesh_terms: D000111:Acetylcysteine / Q000494:pharmacology; D017304:Annexin A5 / Q000378:metabolism; D000911:Antibodies, Monoclonal / Q000276:immunology / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects; D053148:Caspase 3 / Q000378:metabolism; D053181:Caspase 8 / Q000378:metabolism; D053453:Caspase 9 / Q000378:metabolism; D002462:Cell Membrane / Q000187:drug effects; D002875:Chromosomes / Q000378:metabolism; D004249:DNA Damage / Q000187:drug effects; D006514:Hepatitis B Surface Antigens / Q000276:immunology / Q000494:pharmacology*; D006515:Hepatitis B virus / Q000378:metabolism; D006801:Humans; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D010718:Phosphatidylserines / Q000378:metabolism; D011419:Propidium / Q000494:pharmacology; D017382:Reactive Oxygen Species / Q000378:metabolism; D013094:Spermatozoa / Q000187:drug effects* / Q000378:metabolism
chemical_list: D017304:Annexin A5; D000911:Antibodies, Monoclonal; D006514:Hepatitis B Surface Antigens; D010718:Phosphatidylserines; D017382:Reactive Oxygen Species; D011419:Propidium; D008315:Malondialdehyde; D053148:Caspase 3; D053181:Caspase 8; D053453:Caspase 9; D000111:Acetylcysteine