Epstein J H
Department of Dermatology, University of California, San Francisco.
J Invest Dermatol. 1988 Aug;91(2):114-6. doi: 10.1111/1523-1747.ep12464129.
Previous studies demonstrated that BPO can promote chemically initiated tumor formation in SENCAR mice. In addition, a number of chemicals have been shown to promote and/or enhance UVR induced carcinogenesis. This study examined the effect of BPO on UVR initiated tumor formation. One hundred and forty-eight Uscd mice received 270 mJ/cm2 of UVB radiation to the posterior halves of their backs 3 times a week for 8 weeks. Four weeks later the mice were divided into 4 groups. Group I received croton oil in acetone applications to the back 5 times a week for the duration of the study. Group II received acetone, Group III received the BPO diluent, and Group IV received the BPO in an aqueous diluent applications as in Group I. One mouse in Group II (acetone) and one in Group IV (BPO) developed tumors in unirradiated skin. In the UVR initiated skin 38% of the survivors developed tumors in Group I (croton oil), whereas 5% did in Group II (acetone), 8% in Group III (BPO base), and 8% group IV (BPO). Thus under the circumstances of this study croton oil did promote UV initiated tumor formation but BPO did not. These results are consistent with those recently reported by Iversen.
先前的研究表明，过氧化苯甲酰（BPO）可促进SENCAR小鼠化学诱导的肿瘤形成。此外，已证实多种化学物质可促进和/或增强紫外线（UVR）诱导的致癌作用。本研究检测了BPO对UVR引发的肿瘤形成的影响。148只Uscd小鼠背部后半部接受270 mJ/cm2的UVB辐射，每周3次，共8周。4周后，将小鼠分为4组。在研究期间，第I组小鼠每周5次在背部涂抹巴豆油的丙酮溶液。第II组小鼠涂抹丙酮，第III组小鼠涂抹BPO稀释剂，第IV组小鼠涂抹与第I组相同的BPO水性稀释剂。第II组（丙酮组）和第IV组（BPO组）各有1只小鼠在未照射的皮肤上出现肿瘤。在UVR引发的皮肤肿瘤中，第I组（巴豆油组）38%的存活小鼠出现肿瘤，而第II组（丙酮组）为5%，第III组（BPO基质组）为8%，第IV组（BPO组）为8%。因此，在本研究条件下，巴豆油确实促进了UV引发的肿瘤形成，但BPO没有。这些结果与Iversen最近报道的结果一致。
