RESUMEN
Ionizing radiation causes its biological effects mainly through oxidative damage induced by reactive oxygen species. Previous studies showed that ozone oxidative preconditioning attenuated pathophysiological events mediated by reactive oxygen species. As inhalation of ozone induces lung injury, the aim of this study was to examine whether ozone oxidative preconditioning potentiates or attenuates the effects of irradiation on the lung. Rats were subjected to total body irradiation, with or without treatment with ozone oxidative preconditioning (0.72 mg/kg). Serum proinflammatory cytokine levels, oxidative damage markers, and histopathological analysis were compared at 6 and 72 h after total body irradiation. Irradiation significantly increased lung malondialdehyde levels as an end-product of lipoperoxidation. Irradiation also significantly decreased lung superoxide dismutase activity, which is an indicator of the generation of oxidative stress and an early protective response to oxidative damage. Ozone oxidative preconditioning plus irradiation significantly decreased malondialdehyde levels and increased the activity of superoxide dismutase, which might indicate protection of the lung from radiation-induced lung injury. Serum tumor necrosis factor alpha and interleukin-1 beta levels, which increased significantly following total body irradiation, were decreased with ozone oxidative preconditioning. Moreover, ozone oxidative preconditioning was able to ameliorate radiation-induced lung injury assessed by histopathological evaluation. In conclusion, ozone oxidative preconditioning, repeated low-dose intraperitoneal administration of ozone, did not exacerbate radiation-induced lung injury, and, on the contrary, it provided protection against radiation-induced lung damage.
Asunto(s)
Animales , Femenino , Lesión Pulmonar/prevención & control , Pulmón/efectos de la radiación , Estrés Oxidativo/fisiología , Ozono/uso terapéutico , Traumatismos Experimentales por Radiación/prevención & control , Cromatografía Líquida de Alta Presión , Ensayo de Inmunoadsorción Enzimática , Interleucina-1beta/sangre , Malondialdehído/sangre , Ratas Wistar , Protectores contra Radiación/uso terapéutico , Superóxido Dismutasa/metabolismo , Factor de Necrosis Tumoral alfa/sangreRESUMEN
Ionizing radiation causes its biological effects mainly through oxidative damage induced by reactive oxygen species. Previous studies showed that ozone oxidative preconditioning attenuated pathophysiological events mediated by reactive oxygen species. As inhalation of ozone induces lung injury, the aim of this study was to examine whether ozone oxidative preconditioning potentiates or attenuates the effects of irradiation on the lung. Rats were subjected to total body irradiation, with or without treatment with ozone oxidative preconditioning (0.72 mg/kg). Serum proinflammatory cytokine levels, oxidative damage markers, and histopathological analysis were compared at 6 and 72 h after total body irradiation. Irradiation significantly increased lung malondialdehyde levels as an end-product of lipoperoxidation. Irradiation also significantly decreased lung superoxide dismutase activity, which is an indicator of the generation of oxidative stress and an early protective response to oxidative damage. Ozone oxidative preconditioning plus irradiation significantly decreased malondialdehyde levels and increased the activity of superoxide dismutase, which might indicate protection of the lung from radiation-induced lung injury. Serum tumor necrosis factor alpha and interleukin-1 beta levels, which increased significantly following total body irradiation, were decreased with ozone oxidative preconditioning. Moreover, ozone oxidative preconditioning was able to ameliorate radiation-induced lung injury assessed by histopathological evaluation. In conclusion, ozone oxidative preconditioning, repeated low-dose intraperitoneal administration of ozone, did not exacerbate radiation-induced lung injury, and, on the contrary, it provided protection against radiation-induced lung damage.
Asunto(s)
Lesión Pulmonar/prevención & control , Pulmón/efectos de la radiación , Estrés Oxidativo/fisiología , Ozono/uso terapéutico , Traumatismos Experimentales por Radiación/prevención & control , Animales , Cromatografía Líquida de Alta Presión , Ensayo de Inmunoadsorción Enzimática , Femenino , Interleucina-1beta/sangre , Malondialdehído/sangre , Protectores contra Radiación/uso terapéutico , Ratas Wistar , Superóxido Dismutasa/metabolismo , Factor de Necrosis Tumoral alfa/sangreRESUMEN
Some cases of idiopathic pruritus anu may be refractory to treatment with dietary and hygienic instructions and short-term topical medications. In this study, we documented our technique and results with methylene blue injection in a large series of patients with intractable idiopathic pruritus ani. The results of 30 adult patients with well-documented intractable idiopathic pruritus ani who were treated with intradermal methylene blue injection are reported. No antibiotic prophylaxis, anesthesia or sedation was used. A total of 15 ml of a 1% methylene blue solution was injected intracutaneously and subcutaneously in the affected perianal area. A second injection (rescue treatment) was offered one month later to patients who declared partial response, and follow-up was restarted. One month after injection, 24 patients (80%) were symptom-free, 5 declared partial remissions, and one patient still had the same degree of pruritus ani. Five patients with partial remission underwent a second methylene blue injection, which provided complete relief in four. Therefore, the early response rate was 80% with single injection and 93.3% (28 of 30) with the rescue treatment. At six months, three recurrences were noted, indicating to a success rate of 83.3% (25 of 30). At 12 months after treatment, 23 patients (76.7%) were symptom free. This study has shown that intradermal methylene blue injection is a safe, simple, fast and efficient method of treating intractable idiopathic pruritus ani.