Miguel Nadia Campos de Oliveira, Wajsenzon Inês Júlia R, Takiya Christina Maeda, de Andrade Leonardo Rodrigues, Tortelote Giovane G, Einicker-Lamas Marcelo, Allodi Silvana
Departamento de Histologia e Embriologia, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Ilha do Fundão, 21941-590 Rio de Janeiro, RJ, Brazil.
Cell Tissue Res. 2007 Jul;329(1):159-68. doi: 10.1007/s00441-007-0410-x. Epub 2007 Apr 4.
In invertebrates, a few studies have suggested apoptosis as the mechanism of choice to protect the retina after exposure to ultraviolet (UV) radiation. We demonstrated previously, by electron microscopy, that the retina and lamina ganglionaris (or lamina) cells of the crab Ucides cordatus displayed subcellular signs of apoptosis after exposure to UVB and UVC. Here, we first ascertained, by the TdT-mediated dUTP-biotin nick end-labeling (TUNEL) technique, that UV irradiation indeed produced the previously reported results. We next tested, in the visual system of U. cordatus, whether the expression (as analyzed by immunohistochemistry and observed with laser scanning microscopy) and levels (as examined by Western blotting) of catalase, Bax, and p53 were affected by the same dose of UV radiation as that used previously. Our data revealed that the intensity of catalase, Bax, and p53 labeling was stronger in irradiated retina and lamina cells than in non-irradiated retina and lamina. However, no significant difference was observed in the concentrations of these proteins isolated from the whole optic lobe. The results thus suggest that UVB and UVC induce apoptosis in the crustacean retina and lamina by increasing catalase expression and activating the Bax- and p53-mediated apoptosis pathways.
在无脊椎动物中,一些研究表明,细胞凋亡是暴露于紫外线(UV)辐射后保护视网膜的首选机制。我们之前通过电子显微镜证明,蟹类Ucides cordatus的视网膜和神经节层(或神经层)细胞在暴露于UVB和UVC后显示出细胞凋亡的亚细胞特征。在这里,我们首先通过TdT介导的dUTP生物素缺口末端标记(TUNEL)技术确定,紫外线照射确实产生了先前报道的结果。接下来,我们在U. cordatus的视觉系统中测试,过氧化氢酶、Bax和p53的表达(通过免疫组织化学分析并用激光扫描显微镜观察)和水平(通过蛋白质印迹法检测)是否受到与之前相同剂量紫外线辐射的影响。我们的数据显示,在受照射的视网膜和神经层细胞中,过氧化氢酶、Bax和p53标记的强度比未受照射的视网膜和神经层更强。然而,从整个视叶分离出的这些蛋白质的浓度没有观察到显著差异。因此,结果表明UVB和UVC通过增加过氧化氢酶表达并激活Bax和p53介导的凋亡途径,诱导甲壳类动物视网膜和神经层细胞凋亡。