Schmitz S, Garbe C, Jimbow K, Wulff A, Daniels H, Eberle J, Orfanos C E
Department of Dermatology, Free University of Berlin, University Medical Center Steglitz, Germany.
Recent Results Cancer Res. 1995;139:43-55. doi: 10.1007/978-3-642-78771-3_4.
Long-wavelength ultraviolet radiation (UVA) can cause cancer. A carcinogenic mechanism involved may be the induction of harmful reactive oxygen species resulting from photodynamic effects. UVA is generally assumed to induce photodynamic effects, but evidence from experiments with viable biological materials has been indirect until present. Here we measured the induction of (lipid) hydroperoxides as direct indicators of photodynamic reactions. Cultured human fibroblasts were irradiated with 10J UVA/cm2. The induced hydroperoxides were measured by an enzymatic method using glutathione peroxidase and glutathione reductase (GR). Additionally, reduced glutathione (GSH) was determined as parameter for the constitutive antioxidant defense. UVA was found to increase lipid hydroperoxides in fibroblasts by 116% (p < 0.001), when compared to nonirradiated controls. Conversely GSH was decreased in the irradiated cells by 51% (p < 0.001). Because of the induced hydroperoxides, it is concluded that the UVA effects were mediated by a photodynamic mechanism. The photodynamic mechanism resulted in the formation of reactive oxygen species and the consumption of constitutive antioxidants. This suggests a role for antioxidants during the photodynamic mechanism. Photodynamic mechanisms may play a crucial role in carcinogenic events, especially after UVA.
长波紫外线辐射(UVA)可致癌。一种可能的致癌机制是光动力效应诱导产生有害的活性氧物种。一般认为UVA会诱导光动力效应,但直到目前,来自活体生物材料实验的证据一直是间接的。在此,我们测量了(脂质)氢过氧化物的诱导情况,将其作为光动力反应的直接指标。用10J UVA/cm²照射培养的人成纤维细胞。使用谷胱甘肽过氧化物酶和谷胱甘肽还原酶(GR)通过酶法测量诱导产生的氢过氧化物。此外,测定还原型谷胱甘肽(GSH)作为组成型抗氧化防御的参数。与未照射的对照组相比,发现UVA使成纤维细胞中的脂质氢过氧化物增加了116%(p < 0.001)。相反,照射细胞中的GSH减少了51%(p < 0.001)。由于诱导产生了氢过氧化物,得出结论:UVA的效应是由光动力机制介导的。光动力机制导致活性氧物种的形成和组成型抗氧化剂的消耗。这表明抗氧化剂在光动力机制中发挥作用。光动力机制可能在致癌事件中起关键作用,尤其是在UVA照射后。