[紫外线照射对六氯苯所致卟啉症影响的动物实验模型]。

P Lehmann, T Schäfer, K Bolsen, G Goerz
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引用次数: 0

摘要

紫外光照射对六氯苯致动物模型卟啉症的影响六氯苯可致人类及不同动物肝性卟啉症,与迟发性皮肤卟啉症相当。我们研究了六氯苯喂养是否也可以在无毛大鼠(Rowett-Nude)中诱导这种卟啉症,因为它们适合于光生物学研究。在肝性卟啉症发生后,用UV-A或UV-B光照射大鼠。研究了对卟啉代谢的生化影响以及临床和组织学皮肤变化。在卟啉大鼠的肝脏中,UV-A和UV-B照射引起氨基乙酰丙酸合成酶活性升高,并伴有肝卟啉含量的增加。与未受照射的动物相比,UV-A或UV-B照射也导致卟啉类动物皮肤中总卟啉含量增加。然而,在临床和组织学上,只有UV-A照射引起病变,这与迟发性皮肤卟啉症的皮肤表现相当。
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[Animal experiment model of the effect of ultraviolet irradiation on hexachlorobenzene-induced porphyria].

The Effect of UV-Irradiation on the Hexachlorobenzene-induced Porphyria in an Experimental Animal Model Hexachlorobenzene is able to induce in humans and different animal species a hepatic porphyria, which is comparable to porphyria cutanea tarda. We studied whether hexachlorobenzene feeding could induce this porphyria also in hairless rats (Rowett-Nude), as these are suitable for photobiologic studies. After development of hepatic porphyria the rats were irradiated either with UV-A or UV-B light. Biochemical effects on the porphyrin metabolism and clinical as well as histologic skin changes were examined. In the liver of the porphyric rats, UV-A and UV-B irradiation induced increased aminolevulinic acid synthase activity accompanied with augmentation of hepatic porphyrin content. UV-A or UV-B irradiation also lead to increased total porphyrin contents in the skin of porphyric compared to non-irradiated animals. Clinically and histologically, however, only UV-A irradiation induced lesions, which were comparable to skin manifestations of porphyria cutanea tarda.

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