RESUMO
Exposure to loud noise levels represents a problem in all regions of the world. Noise exposure is known to affect auditory structures in living organisms. However, it should not be ignored that many of the effects of noise are extra-auditory. In particular, it has been proposed that noise could affect immune system similarly to other stressors. Nevertheless, only a few studies so far have investigated the effects of noise on the immune function. The aim of the present work was to investigate the effect of chronic (2 weeks) noise (95-97 dBA) exposure on immune responses in BALB/c and C57 mice. To ascertain if the effect of noise is similar to other psychological stressors, the effect of chronic restraint--applied for the same time--on immune response was also analyzed. It was found that chronic noise impaired immune-related end-points in vivo and ex vivo depending on the strain used. Noise, but not restraint, affected C57Bl/6 mouse T-cell-dependent antibody production and ex vivo stimulated T-cell proliferation, but had no effect on these parameters in BALB/c mice or their cells. In fact, none of the stressors altered T-cell responses associated with the BALB/c mice. Further, noise exposure induced a decrease in corticosterone and catecholamines levels in BALB/c mice. In contrast, no differences were seen in these parameters for those BALB/c mice under restraint or for that matter C57Bl/6 mice exposed to restraint or noise. The results of these studies indicate that noise could seriously affect immune responses in susceptible individuals. In addition, it may also be concluded that noise possibility should not be considered a classic stressor.
Assuntos
Exposição Ambiental , Ruído , Restrição Física , Linfócitos T/imunologia , Animais , Formação de Anticorpos , Catecolaminas/metabolismo , Proliferação de Células , Células Cultivadas , Corticosterona/metabolismo , Exposição Ambiental/efeitos adversos , Feminino , Predisposição Genética para Doença , Sistema Imunitário/metabolismo , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C57BL , Ruído/efeitos adversos , Restrição Física/efeitos adversos , Estresse PsicológicoRESUMO
Ionizing radiations can induce oxidative stress on target tissues, acting mainly through reactive oxygen species (ROS). The aim of this work was to investigate if 17-ß-estradiol (ßE) was able to prevent hippocampal-related behavioral and biochemical changes induced by neonatal ionizing radiation exposure and to elucidate a potential neuroprotective mechanism. Male Wistar rats were irradiated with 5 Gy of X-rays between 24 and 48 h after birth. A subset of rats was subcutaneously administered with successive injections of ßE or 17-α-estradiol (αE), prior and after irradiation. Rats were subjected to different behavioral tasks to evaluate habituation and associative memory as well as anxiety levels. Hippocampal ROS levels and protein kinase C (PKC) activity were also assessed. Results show that although ßE was unable to prevent radiation-induced hippocampal PKC activity changes, most behavioral abnormalities were reversed. Moreover, hippocampal ROS levels in ßE-treated irradiated rats approached control values. In addition, αE administered to irradiated animals was effective in preventing radiation-induced alterations. In conclusion, ßE was able to counteract behavioral and biochemical changes induced in irradiated animals, probably acting through an antioxidant mechanism.