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Age‐related alterations in superoxide anion generation in mouse peritoneal macrophages studied by repeated stimulations and heat shock treatment
Author(s) -
Lavie Lena,
Weinreb Orly,
Gershon David
Publication year - 1992
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041520220
Subject(s) - zymosan , superoxide , stimulation , endocrinology , superoxide dismutase , nadph oxidase , chemistry , medicine , phorbol , heat shock protein , oxidative stress , andrology , immunology , protein kinase c , biochemistry , signal transduction , enzyme , in vitro , gene
The ability of thioglycollate‐elicited peritoneal macrophages (PM) from young and senescent mice to generate superoxide anions (O − 2 ) under repeated stimulation or thermal stress was studied using either zymosan, opsonized zymosan (OZ), or phorbol myristate acetate (PMA). A diminished capacity to recover from repeated stimulation was found with aging. When stimulated for a second time 24 hours after the primary stimulation, PM from young animals generated 80% of the initial O − 2 responses to either zymosan, or OZ. Under the same conditions, PM from senescent mice generated 62% of the initial O − 2 produced in response to zymosan, and 45% in response to OZ. In both age groups the response to a second PMA stimulation comprised only 10% of the primary response. A considerably diminished capacity to generate O − 2 was also demonstrated in PM from senescent mice after recovery from exposure to thermal stress. Exposure to 42.5°C for 20 minutes was found to be the threshold temperature for irreversible loss of activity in senescent PM, whereas at this temperature, PM from young animals recovered up to 70% of their O − 2 generating activity. Since NADPH oxidase and superoxide dismutase activities were only mildly affected by the hyperthermia in all age groups, they could not account for the age‐related decline in the recovery from stress. Age‐related alterations in signal transduction or receptor alterations could possibly play a primary role in this decline. © 1992 Wiley‐Liss, Inc.