[Nitric oxide (NO) inactivation by polymorphonuclear leukocytes as a mechanism for the development of periodontal lesions].
To investigate the mechanism by which polymorphonuclear leukocytes (PMNLs) contribute to tissue injury in periodontitis, NO-activity was bioassayed by measuring its ability to increase cGMP accumulation in cultured fibroblasts in the absence or presence of PMNLs isolated from blood and gingival fluid in healthy volunteers and patients with periodontitis. Non-activated PMNLs do not NO-induced stimulation of cGMP accumulation in the detector cells. However, activated PMNLs inhibited NO-induced cGMP accumulation whereas the effects of sodium nitroprusside was unaffected. Peripheral PMNLs periodontitis impaired NO-dependent cGMP accumulation more markedly than from healthy volunteers. PMNLs from periodontal pockets in periodontal patients destroyed NO significantly higher than in venous blood of the same patients without additional activation. It is assumed that the deactivation of NO by activated PMNLs is a one of the pathomechanisms of disorders in periodontitis.
Akopov
S E
SE
Kankanian
A P
AP
D000328:Adult; D002460:Cell Line; D002478:Cells, Cultured; D002908:Chronic Disease; D006152:Cyclic GMP / Q000378:metabolism; D005347:Fibroblasts / Q000378:metabolism; D005883:Gingival Crevicular Fluid / Q000166:cytology; D006801:Humans; D008875:Middle Aged; D009504:Neutrophils / Q000378:metabolism*; D009569:Nitric Oxide / Q000037:antagonists & inhibitors* / Q000378:metabolism; D010518:Periodontitis / Q000209:etiology* / Q000378:metabolism
D009569:Nitric Oxide; D006152:Cyclic GMP
Inaktivatsiia oksida azota (NO) polimorfnoiadernymi leikotsitami kak mekhanizm razvitiia porazheniĭ parodonta.