title: Hyperbaric oxygen enhances apoptosis in hematopoietic cells.
abstract: Hyperbaric oxygen (HBO) is 100% oxygen administered at elevated atmospheric pressure. In this study, we examined the effect of HBO on hematopoietic cell apoptosis. Cells exposed to HBO were incubated in a chamber containing 97.9% O(2) and 2.1% CO(2) at 2.4 atmospheres absolute (ATA). HBO enhanced spontaneous HL-60 cell apoptosis in a time-dependent manner; a 12 h exposure increased apoptosis by 42%. Exposing these cells to hyperoxia at standard atmospheric pressure (95% O(2), 5% CO(2) at 1 ATA) or increased pressure alone (8.75% O(2), 2.1% CO(2) at 2.4 ATA) had minimal effect on apoptosis. HBO also enhanced stimulus-induced apoptosis. HL-60 cells stimulated to die using gamma radiation underwent 33% more apoptosis than cells exposed to radiation alone. HBO enhanced melphalan, camptothecin, and chlorambucil-induced apoptosis by 22%, 13%, and 8%, respectively. Jurkat cells stimulated to die with anti-Fas antibody underwent 44% more apoptosis when exposed to HBO. Spontaneous apoptosis was increased by 15% in HBO-exposed murine thymocytes. HBO's effect on apoptosis did not require new protein synthesis. As expected, HBO exposure increased the intracellular concentration of H(2)O(2). Incubating HL-60 cells in the presence of dehydroascorbic acid partially abrogated HBO-induced increases in intracellular H(2)O(2) and apoptosis. In summary, HBO enhances spontaneous and stimulus-induced apoptosis in hematopoietic cells, at least in part, by enhancing the intracellular accumulation of H(2)O(2).
authors.affiliation: Department of Veterinary and Animal Sciences and Program in Molecular and Cellular Biology, University of Massachusetts, Amherst, Massachusetts 01003, USA.
authors.forename: B J
authors.initials: BJ
authors.lastname: Ganguly
authors.forename: N
authors.initials: N
authors.lastname: Tonomura
authors.forename: R M
authors.initials: RM
authors.lastname: Benson
authors.forename: B A
authors.initials: BA
authors.lastname: Osborne
authors.forename: E V
authors.initials: EV
authors.lastname: Granowitz
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects* / Q000502:physiology; D053148:Caspase 3; D020169:Caspases / Q000096:biosynthesis; D002374:Catalase / Q000378:metabolism; D003683:Dehydroascorbic Acid / Q000494:pharmacology; D005260:Female; D018922:HL-60 Cells; D006413:Hematopoietic System / Q000166:cytology* / Q000187:drug effects*; D006801:Humans; D006861:Hydrogen Peroxide / Q000378:metabolism; D006874:Hydrostatic Pressure; D006931:Hyperbaric Oxygenation; D018496:Hyperoxia; D066298:In Vitro Techniques; D019169:Jurkat Cells; D051379:Mice; D008807:Mice, Inbred BALB C; D019384:Nucleic Acid Synthesis Inhibitors / Q000494:pharmacology; D010100:Oxygen / Q000502:physiology; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology; D017382:Reactive Oxygen Species / Q000378:metabolism; D013601:T-Lymphocytes / Q000166:cytology / Q000187:drug effects
chemical_list: D019384:Nucleic Acid Synthesis Inhibitors; D011500:Protein Synthesis Inhibitors; D017382:Reactive Oxygen Species; D006861:Hydrogen Peroxide; D002374:Catalase; C505407:CASP3 protein, human; C505409:Casp3 protein, mouse; D053148:Caspase 3; D020169:Caspases; D010100:Oxygen; D003683:Dehydroascorbic Acid