Cells and tissues can be protected against a potentially lethal stress by f
irst exposing them to a brief dose of the same or different stress. This "p
re-conditioning" phenomenon has been documented in many models of protectio
n against oxidative stress, including ischemia/reperfusion and ultraviolet
(UV) light exposure. Stimuli which induce this protective response include
heat, chemicals, brief ischemia, and electromagnetic (EM) field exposures.
We report here that constant mechanical vibration pre-conditions chick embr
yos, protecting them during subsequent stress from hypoxia or UV light expo
sure. Continuously mechanically vibrated embryos (60 Hz, 1 g (32 ft/s(2)),
20 min) exhibited nearly double the survival (67.5%, P < 0.001) after subse
quent hypoxia as compared to non-vibrated controls (37.6%), As a second set
of experiments, embryos were vibrated and then exposed to UV light stress.
Those embryos that were vibrated prior to UV had nearly double the surviva
l 3 h after UV exposure (66%, P < 0.001) as compared to controls (35%). The
degree of protection, however, was dependent on the constancy of the vibra
tion amplitude. When vibration was turned on and off at 1-s intervals throu
ghout exposure, no increase in hypoxia protection was noted. For 50 s on/of
f vibration intervals, however, hypoxia protection comparable to continuous
vibration was obtained. In contrast, random, inconstant mechanical vibrati
on did not induce protection against subsequent UV exposure. These data sug
gest that to be an effective pre-conditioning agent, mechanical vibration m
ust have a degree of temporally constancy (on/off intervals of greater than
1 s). Further experiments in both models (hypoxia and UV) indicated an int
eraction between vibration and EM field-induced protection. Vibration-induc
ed hypoxia protection was inhibited by superposition of a random EM noise f
ield (previously shown to inhibit EM field-induced protection). In addition
, EM field-induced UV protection was inhibited by the superposition of rand
om mechanical vibration. Thus, the superposition of either vibrational or E
M noise during pre-conditioning virtually eliminated protection against hyp
oxia and UV. This link between EM field exposures and mechanical vibration
is consistent with the hypothesis that cells sense these stimuli via a simi
lar mechanism involving counter ion displacement. (C) 2000 Elsevier Science
S.A. All rights reserved.