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Blocking 1800 MHz mobile phone radiation-induced reactive oxygen species production and DNA damage in lens epithelial cells by noise magnetic fields / 浙江大学学报·医学版
Journal of Zhejiang University. Medical sciences ; (6): 34-38, 2008.
Artículo en Chino | WPRIM | ID: wpr-344380
ABSTRACT
<p><b>OBJECTIVE</b>To investigate whether the exposure to the electromagnetic noise can block reactive oxygen species (ROS) production and DNA damage of lens epithelial cells induced by 1800 MHz mobile phone radiation.</p><p><b>METHODS</b>The DCFH-DA method and comet assay were used respectively to detect the intracellular ROS and DNA damage of cultured human lens epithelial cells induced by 4 W/kg 1800 MHz mobile phone radiation or/and 2 muT electromagnetic noise for 24 h intermittently.</p><p><b>RESULT</b>1800 MHz mobile phone radiation at 4 W/kg for 24 h increased intracellular ROS and DNA damage significantly (P<0.05). However, the ROS level and DNA damage of mobile phone radiation plus noise group were not significant enhanced (P>0.05) as compared to sham exposure group.</p><p><b>CONCLUSION</b>Electromagnetic noise can block intracellular ROS production and DNA damage of human lens epithelial cells induced by 1800 MHz mobile phone radiation.</p>
Asunto(s)
Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Radiación / Efectos de la Radiación / Daño del ADN / ADN / Células Cultivadas / Especies Reactivas de Oxígeno / Biología Celular / Teléfono Celular / Campos Electromagnéticos / Células Epiteliales Límite: Humanos Idioma: Chino Revista: Journal of Zhejiang University. Medical sciences Año: 2008 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Radiación / Efectos de la Radiación / Daño del ADN / ADN / Células Cultivadas / Especies Reactivas de Oxígeno / Biología Celular / Teléfono Celular / Campos Electromagnéticos / Células Epiteliales Límite: Humanos Idioma: Chino Revista: Journal of Zhejiang University. Medical sciences Año: 2008 Tipo del documento: Artículo