In vivo normobaric oxygen exposure depresses spleen cell in vitro Con A response. Effects of 2-mercaptoethanol and peritoneal cells.
Normobaric O2 exposure decreased spleen cell (SC) response to T cell mitogen Con A. 3H-TdR incorporation of SC from O2 exposed mice (O2SC) compared to those of control mice (Air SC) decreased significantly after 72 and 87 h O2 exposure. The dose response kinetics to Con A were identical in O2SC or Air SC. Increasing SC number did not restore the response to Con A and the depressed hyperoxic effect was not related to suppressor cells in the spleen of O2 exposed mice. Response of O2SC to Con A was restored by the thiol compound 2-mercaptoethanol (2-ME), and the degree of restoration by 2-ME, was inversely proportional to the depressed response. Addition of intact peritoneal cells (PC) induced restoration within the same range as 2-ME. Restoration of the mitogenic response by 2-ME involved antioxidant properties and suggested that macrophages were functionally injured by O2 exposure. In cases where mitogen response was highly depressed, restoration was only partial; in these conditions in vivo O2 injury probably involved both macrophages and splenic T cells. The mechanisms of O2 toxicity have been discussed in terms of free radical generation under hyperoxic conditions.
D000818:Animals; D002452:Cell Count; D003208:Concanavalin A / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D005260:Female; D008264:Macrophages / Q000276:immunology*; D008623:Mercaptoethanol / Q000494:pharmacology*; D051379:Mice; D008810:Mice, Inbred C57BL; D008938:Mitosis / Q000187:drug effects; D010100:Oxygen; D010529:Peritoneal Cavity / Q000166:cytology; D013154:Spleen / Q000187:drug effects / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology
D003208:Concanavalin A; D008623:Mercaptoethanol; D010100:Oxygen