Nitric oxide-mediated augmentation of polymorphonuclear free radical generation after hypoxia-reoxygenation

Sethi, Sonia ; Singh, Mahendra Pratap ; Dikshit, Madhu (1999) Nitric oxide-mediated augmentation of polymorphonuclear free radical generation after hypoxia-reoxygenation Blood, 93 (1). pp. 333-340. ISSN 0006-4971

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Abstract

Polymorphonuclear leukocytes (PMNLs), nitric oxide (NO), calcium, and free radicals play an important role in hypoxia/ischemia and reoxygenation injury. In the present study, NO donors, sodium nitroprusside (SNP), and diethylamine-NO (DEA-NO) at low concentrations (10 and 100 nmol/L) potentiated, while higher (10 μ mol/L to 10 mmol/L) concentrations inhibited free radical generation response in the rat PMNLs. Free radical generation response was found to be significantly augmented when hypoxic PMNLs were reoxygenated (hypoxia-reoxygenation [H-R]). This increase in free radical generation after reoxygenation or SNP (10 nmol/L) was blocked in the absence of extracellular calcium. SNP (10 nmol/L) or H-R-mediated increases in the free radical generation were prevented by the pretreatment of PMNLs with NO scavenger (hemoglobin), the polyadenine diphosphate (ADP)-ribosylation synthase inhibitor (benzamide) or the calcium channel antagonist (felodipine). A significant augmentation in the nitrite and intracellular calcium levels was observed during hypoxia. Hemoglobin pretreatment also blocked the increase in intracellular calcium levels due to SNP (10 nmol/L) or hypoxia. Thus, increased availability of NO during SNP treatment or H-R, may have led to an ADP-ribosylation-mediated increase in intracellular calcium, thereby increasing the free radical generation from the rat PMNLs.

Item Type:Article
Source:Copyright of this article belongs to American Society of Hematology.
ID Code:9637
Deposited On:02 Nov 2010 11:36
Last Modified:16 May 2016 19:25

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