ABSTRACT
In an experiment (N = 206) using skin cancer prevention messages and a 2 (mortality: salient, control) × 2 (freedom-limiting language: freedom-limiting, autonomy-supportive) independent-group design, we tested the terror management health model and integrated its predictions with the theory of psychological reactance. We used a sample of young adults because they are most at risk for excessive tanning. Consistent with the study predictions about proximal defenses, mortality salience significantly increased intentions to wear sunscreen all year around, relative to the control condition. A significant interaction between freedom-limiting language and mortality salience on behavioral intention to purchase high-SPF lotion revealed that, when a freedom-limiting message was paired with mortality salience, intentions to purchase high-SPF lotion were significantly greater as compared to autonomy-supportive language, indicating that mortality salience mitigated the maladaptive effects of reactance. These results add to a growing body of research identifying boundary conditions for reactance effects and, further, point to the utility of directive (albeit freedom-limiting language) in health-prevention messages attempting to communicate deadly health risks.
ABSTRACT
UNLABELLED: The aim of this study was to examine the induction of oxidative stress and apoptosis-associated gene expression profiles in retina after proton irradiation exposure at 0.5 to 4 Gy. MATERIALS AND METHODS: One eye of each Sprague-Dawley rat (6 per group) was irradiated with a conformal proton beam to total doses of 0, 0.5, 1 and 4 Gy. Retinal tissues were isolated for characterization of gene expression profiles 6 hours after proton radiation. RESULTS: For oxidative stress, many genes responsible for regulating the production of reactive oxygen species (ROS) were significantly up-regulated (Fmo2, Gpx2, Noxa1 and Sod3) compared to controls. Several important genes involved in the initiation or activation of apoptotic signaling pathways were significantly up-regulated following irradiation (Fas, Faslg, Trp63 and Trp73). TUNEL assay and caspase-3 immunocytochemical analysis revealed increased apoptotic immunoreactivity following irradiation. CONCLUSION: The data revealed that exposure to proton radiation induced oxidative stress-associated apoptosis. In response to ionizing radiation, the expression of genes involved in pathways mediating apoptosis may be differentially regulated in different dose regimens.
