title: Hydrogen-rich saline protects immunocytes from radiation-induced apoptosis.
abstract: BACKGROUND
  Radiation often causes depletion of immunocytes in tissues and blood, which results in immunosuppression. Molecular hydrogen (H2) has been shown in recent studies to have potential as a safe and effective radioprotective agent through scavenging free radicals. This study was designed to test the hypothesis that H2 could protect immunocytes from ionizing radiation (IR).
  
  
  METHODS
  H2 was dissolved in physiological saline or medium using an apparatus produced by our department. A 2-[6-(4'-hydroxy) phenoxy-3H-xanthen-3-on-9-yl] benzoate (HPF) probe was used to detect intracellular hydroxyl radicals (•OH). Cell apoptosis was evaluated by annexin V-FITC and Propidium iodide (PI) staining as well as the caspase 3 activity. Finally, we examined the hematological changes using an automatic Sysmex XE 2100 hematology analyzer.
  
  
  RESULTS
  We demonstrated H2-rich medium pretreatment reduced •OH level in AHH-1 cells. We also showed H2 reduced radiation-induced apoptosis in thymocytes and splenocytes in living mice. Radiation-induced caspase 3 activation was also attenuated by H2 treatment. Finally, we found that H2 rescued the radiation-caused depletion of white blood cells (WBC) and platelets (PLT).
  
  
  CONCLUSIONS
  This study suggests that H2 protected the immune system and alleviated the hematological injury induced by IR.
authors.affiliation: Department of Radiation Medicine, Faculty of Naval Medicine, 2nd Military Medical University, Shanghai, PR China.
authors.forename: Yanyong
authors.initials: Y
authors.lastname: Yang
authors.forename: Bailong
authors.initials: B
authors.lastname: Li
authors.forename: Cong
authors.initials: C
authors.lastname: Liu
authors.forename: Yunhai
authors.initials: Y
authors.lastname: Chuai
authors.forename: Jixiao
authors.initials: J
authors.lastname: Lei
authors.forename: Fu
authors.initials: F
authors.lastname: Gao
authors.forename: Jianguo
authors.initials: J
authors.lastname: Cui
authors.forename: Ding
authors.initials: D
authors.lastname: Sun
authors.forename: Ying
authors.initials: Y
authors.lastname: Cheng
authors.forename: Chuanfeng
authors.initials: C
authors.lastname: Zhou
authors.forename: Jianming
authors.initials: J
authors.lastname: Cai
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects* / Q000528:radiation effects; D053148:Caspase 3 / Q000378:metabolism; D002478:Cells, Cultured; D019610:Cytoprotection / Q000187:drug effects* / Q000528:radiation effects; D004789:Enzyme Activation / Q000187:drug effects / Q000528:radiation effects; D005720:Gamma Rays; D006801:Humans; D006859:Hydrogen / Q000494:pharmacology*; D017665:Hydroxyl Radical / Q000378:metabolism; D008214:Lymphocytes / Q000187:drug effects / Q000473:pathology* / Q000528:radiation effects; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D011837:Radiation-Protective Agents / Q000494:pharmacology*; D012965:Sodium Chloride / Q000494:pharmacology*; D013154:Spleen / Q000187:drug effects / Q000201:enzymology / Q000528:radiation effects
chemical_list: D011837:Radiation-Protective Agents; D017665:Hydroxyl Radical; D012965:Sodium Chloride; D006859:Hydrogen; D053148:Caspase 3