Iversen O H
Institute of Pathology, University of Oslo, Norway.
Carcinogenesis. 1988 May;9(5):803-9. doi: 10.1093/carcin/9.5.803.
In a previous paper it was demonstrated on hairless mouse skin that 5% benzoyl peroxide (BP) in a gel (Panoxyl), or gel alone, applied just before UV radiation had a protective effect against UV-induced tumorigenesis, but both enhanced 7,12-dimethylbenz[a]anthracene (DMBA)-induced tumorigenesis. Groups of hairless (hr/hr) mice were therefore given ultraviolet (UV) irradiation with or without additional treatment with Panoxyl or gel in order to see whether Panoxyl or the gel given long time before, or after, irradiation influenced UV-induced tumorigenesis. Consequently, in some animals Panoxyl or gel was applied in the evening and the mice were irradiated the next day; in others, Panoxyl or gel was applied 5-30 min after UV irradiation. Enhancement of DMBA-induced carcinogenesis in hr/hr mice by the gel alone (assumed to be inert) was unexpected, and hence one group of hr/hr mice was first given 51.2 micrograms DMBA in acetone and thereafter treated twice a week with gel alone. All mice were tested and observed for skin tumors and other lesions for 52 weeks. Neither Panoxyl nor gel influenced UV tumorigenesis or carcinogenesis under these experimental conditions. In hr/hr mice there was this time no enhancement of DMBA-induced tumorigenesis by the gel, and a slight reduction of carcinogenesis. In addition, several groups of SENCAR mice (which have been bred for high sensitivity to skin carcinogenesis) were also treated, with acetone alone, with a single application of DMBA alone, with Panoxyl alone, or with DMBA followed by treatment with the ointment gel or with Panoxyl twice a week throughout the experiment. In SENCAR mice there was no difference between the results of treatment with DMBA followed by Panoxyl, or DMBA followed by gel, and both substances tended to reduce the tumorigenicity of DMBA alone, and Panoxyl or gel showed no tumorigenicity of their own. The total dose of UV used in this study was lower than that used in the first study. This reduction in dose significantly increased the tumorigenic effect of UV.
在之前的一篇论文中，在无毛小鼠皮肤上证实，在紫外线辐射前涂抹凝胶（泛酰醇）中的5%过氧化苯甲酰（BP）或单独的凝胶，对紫外线诱导的肿瘤发生有保护作用，但两者都会增强7,12-二甲基苯并[a]蒽（DMBA）诱导的肿瘤发生。因此，将无毛（hr/hr）小鼠分组，给予紫外线（UV）照射，同时或不给予泛酰醇或凝胶的额外处理，以观察在照射前或照射后长时间给予泛酰醇或凝胶是否会影响紫外线诱导的肿瘤发生。因此，在一些动物中，晚上涂抹泛酰醇或凝胶，第二天对小鼠进行照射；在其他动物中，在紫外线照射后5 - 30分钟涂抹泛酰醇或凝胶。仅凝胶（假定为惰性）增强hr/hr小鼠中DMBA诱导的致癌作用是出乎意料的，因此一组hr/hr小鼠首先在丙酮中给予51.2微克DMBA，然后每周用单独的凝胶处理两次。对所有小鼠进行52周的皮肤肿瘤和其他病变检测与观察。在这些实验条件下，泛酰醇和凝胶均未影响紫外线肿瘤发生或致癌作用。这次在hr/hr小鼠中，凝胶没有增强DMBA诱导的肿瘤发生，致癌作用略有降低。此外，还对几组SENCAR小鼠（已培育成对皮肤致癌高度敏感）进行了处理，分别单独用丙酮、单独单次应用DMBA、单独用泛酰醇，或在整个实验过程中先用DMBA然后每周两次用软膏凝胶或泛酰醇处理。在SENCAR小鼠中，先用DMBA然后用泛酰醇处理的结果与先用DMBA然后用凝胶处理的结果之间没有差异，两种物质都倾向于降低单独使用DMBA的致瘤性，并且泛酰醇或凝胶自身没有致瘤性。本研究中使用的紫外线总剂量低于第一项研究中使用的剂量。这种剂量的降低显著增加了紫外线的致瘤作用。
