Oxidative stress precedes circulatory failure induced by 35-GHz microwave heating

Sustained whole-body exposure of anesthetized rats to 35-GHz radio frequenc y radiation produces localized hyperthermia and hypotension, leading to cir culatory failure and death. The physiological mechanism underlying the indu ction of circulatory failure by 35-GHz microwave (MW) heating is currently unknown. We hypothesized that oxidative stress may play a role in the patho physiology of MW-induced circulatory failure and examined this question by probing organs for 3-nitrotyrosine (3-NT), a marker of oxidative stress. An imals exposed to low durations of MW that increased colonic temperature but were insufficient to produce hypotension showed a 5- to 12-fold increase i n 3-NT accumulation in lung, liver, and plasma proteins relative to the lev els observed in control rats that were not exposed to MW. 3-NT accumulation in rats exposed to MW of sufficient duration to induce circulatory shock r eturned to low, baseline levels. Leukocytes obtained from peripheral blood showed significant accumulation of 3-NT only at exposure levels associated with circulatory shock. 3-NT was also found in the villus tips and vasculat ure of intestine and within the distal tubule of the kidney but not in the irradiated skin of rats with MW-induced circulatory failure. The relationsh ip between accumulation in liver, lung, and plasma proteins and exposure du ration suggests either that nitro adducts are formed in the first 20 min of exposure and are then cleared or that synthesis of nitro adducts decreases after the first 20 min of exposure. Taken together, these findings suggest that oxidative stress occurs in many organs during MW heating. Because nit ration occurs after microwave exposures that are not associated with circul atory collapse, systemic oxidative stress, as evidenced by tissue accumulat ion of 3-NT, is not correlated with circulatory failure in this model of sh ock.