Premium
Modulation of the Oxidative Burst in Trout Myeloid Cells by Adrenocorticotropic Hormone and Catecholamines: Mechanisms of Action
Author(s) -
Bayne Christopher J.,
Levy Sharon
Publication year - 1991
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.50.6.554
Subject(s) - respiratory burst , superoxide , superoxide dismutase , endocrinology , medicine , adrenocorticotropic hormone , agonist , biology , receptor , oxidative stress , chemistry , biochemistry , hormone , enzyme
The oxidative burst of rainbow trout (Oncorhynchus mykiss) phagocytes was previously found to be differentially modulated by adrenocorticotropic hormone (ACTH) and the catecholamine receptor agonists phenylephrine and isoproterenol. From data obtained using both luminol‐enhanced chemiluminescence (LECL) and ferricytochrome C (cyt C) reduction to measure oxidative burst kinetics, we postulated that the observed modulation was mediated by affects on enzymes responsible for the production and metabolism of superoxide anion. Using exogenous superoxide dismutase (SOD) and catalase as scavengers, nitroprusside to poison endogenous SOD, and an assay for hydrogen peroxide, we have tested our postulates by exploiting the differences with which various reactive oxygen intermediates influence LECL and cyt C reduction. The ability of ACTH to potentiate both assays of the oxidative burst appears due to its enhancing influence on the production of superoxide. Phenylephrine, an α‐adrenergic receptor agonist, appears to enhance the activity of endogenous SOD, whereas isoproterenol, a β‐adrenergic receptor agonist, may suppress SOD activity. This work reveals how components of the natural immune system may be regulated by products of the neuroendocrine system. Also, lymphocyte‐derived ACTH may provide a novel pathway for lymphoid regulation of inflammation.