Effects of Local Hyperthermia Treatment on Skin SOD Activity in Mice

Abstract

SummaryThe effect of local hyperthermia treatment (43°C, 45 min) on normal mouse skin was studied by examining superoxide dismutase (SOD) activity and histology of the skin. SOD activity of the skin decreased significantly 1, 4, 7, and 14 days after the treatment. The decrease reached a peak 4 days after the treatment and recovered to some extent by 14 days after the treatment. The decrease in SOD activity may be due to consumption of SOD by inflammation as well as to the destruction of SOD by hyperthermia. Histological examination of hyperthermia-treated skin showed edema, bleeding, and inflammatory cell infiltration in the dermis, and individual cell keratinization and acanthosis in the epidermis. It is important to estimate the decrease in SOD activity and tissue injury of the skin by hyperthermia in order to use hyperthermia more effectively with fewer side effects. Hyperthermia has been successfully used in the treatment of cancer [1,2], and the importance of hyperthermia treatment has been increasing with the improvement of apparatus as well as the elucidation of the mechanisms of hyperthermia treatment. Hyperthermia has been also used in the treatment of dermatological diseases such as psoriasis vulgaris [3] and sporotrichosis [4]. However, skin damage induced by hyperthermia treatment has not been studied extensively.Recently it was reported that reactive oxygen species (ROS) may be involved in the cytotoxic mechanism of hyperthermia [5], and that the lipid peroxide level was demonstrated to increase after thermal injury in rats [6]. These reports suggest that ROS and lipid peroxides play roles in skin damage induced by hyperthermia treatment.In this study, we examined superoxide dismutase (SOD) activity of the skin of

Hyperthermia mediated by dextran-coated La0.7Sr0.3MnO3 nanoparticles: in vivo studies

“…In agreement with our results, Arnaud et al 35 reported that a 15-minute heat stress at 42°C did not modify SOD activities of the myocardium in Wistar rats. Yoshioka et al 36 reported unaltered activity of SOD after hyperthermia that could be attributed to degradation of SOD by heat. Induction of catalase in treated tumor observed in our study indicates attenuation of oxidative stress, and indirectly suggests elevation of reactive oxygen species in the tumor after hyperthermia.…”