Biologic effects of microwave exposure. II. Studies on the mechanisms controlling susceptibility to microwave-induced increases in complement receptor-positive spleen cells

• Published in: Bioelectromagnetics Vol. 1; no. 4; p. 405
• Main Authors: Schlagel, C J, Sulek, K, Ho, H S, Leach, W M, Ahmed, A, Woody, J N
• Format: Journal Article
• Language: English
• Published: United States 1980
• Subjects: Aging; Animals; Hydrocortisone - pharmacology; Lipopolysaccharides - pharmacology; Mice; Mice, Inbred Strains; Microwaves; Receptors, Complement - radiation effects; Species Specificity; Spleen - cytology; Spleen - radiation effects; T-Lymphocytes - radiation effects
• ISSN: 0197-8462
• DOI: 10.1002/bem.2250010407

In attempting to evaluate the mechanisms responsible for susceptibility to the inductive increase in splenic complement receptor-positive (CR+) cells following exposure to 2450-MHz microwaves, it was found that sensitivity to microwave-induced CR+ cell increases was under genetic control. In particular, evidence was accumulated suggesting that regulation was under the control of a gene or genes closely associated with but outside of the mouse major histocompatibility complex (H-2). All responsive strains of mice tested were of the H-2k haplotype, while mice of the H-2a, H-2b, H-2d and H-1i5 haplotypes were refractory to the microwave-induced increases in CR+ cells. By utilizing certain H-2k strains of mice that were genetically unable to respond to endotoxin, we were able to show that these strains of mice responded to microwaves, but not to endotoxin, by increasing CR+ cells. Microwave-induced increases in CR+ cells were not mimicked by the intraperitoneal injection of hydrocortisone. Athymic mice responded to microwave exposure, indicating that this event was not regulated by the T-cell population. Mice less than eight weeks old were found not to be susceptible to exposure to 2450-MHz microwaves. These studies indicate that microwaves do induce changes in the population of cells with specific cell-surface receptors, that susceptibility to these changes is under genetic control, and that it is unlikely that endotoxin, corticosteroids, or regulatory T cells play a significant role in the mechanisms regulating these increases.