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近可见光-紫外线辐射可延缓紫外线B诱导的肿瘤发生。

Near-visible-UV radiation delays UVB tumorigenesis.

作者信息

Bech-Thomsen N, Poulsen T, Christensen F G, Lundgren K, Wulf H C

机构信息

Department of Dermatology, Copenhagen University Hospital, Denmark.

出版信息

J Photochem Photobiol B. 1994 Feb;22(2):119-23. doi: 10.1016/1011-1344(93)06956-4.

DOI:10.1016/1011-1344(93)06956-4
PMID:8176545
Abstract

The effect of UVA radiation (321-400 nm) on UVB photocarcinogenesis was examined in lightly pigmented hairless hr/hr C3H/Tif mice. Five groups of 22 mice were exposed to UVB radiation (281-320 nm) from one Philips 12 tube for 10 min per day and 4 days per week. Four of the groups were simultaneously exposed to UVA from two to six filtered Philips 09 tubes. The daily dose of UVB was 2.0 kJ m-2 in all five groups; the UVA2 (321-340 nm) dose varied from 0.7 to 4.5 kJ m-2 and the UVA1 (341-400 nm) dose from 0.3 to 45.6 kJ m-2. A sixth group was exclusively irradiated with the filtered UVA tubes and served as a control. Skin tumor development was not significantly different for the groups exposed to the UVB source alone or the UVB source in combination with the largest daily UVA dose (0.2 > p > 0.1). Skin tumor development was significantly delayed in the other groups irradiated with the UVB source and the lower doses of UVA (p < 0.001). No tumors were observed in the control group. This study suggests that UVA1 radiation delays UVB-induced skin tumor development. However, the delay cannot be expected to persist when UVA is administered in higher daily doses.

摘要

在浅色无毛hr/hr C3H/Tif小鼠中研究了UVA辐射(321 - 400纳米)对UVB光致癌作用的影响。将五组每组22只小鼠暴露于来自一根飞利浦12管的UVB辐射(281 - 320纳米)下,每天照射10分钟,每周照射4天。其中四组同时暴露于来自两到六根经过滤的飞利浦09管的UVA下。所有五组的UVB日剂量均为2.0 kJ m-2;UVA2(321 - 340纳米)剂量从0.7到4.5 kJ m-2不等,UVA1(341 - 400纳米)剂量从0.3到45.6 kJ m-2不等。第六组仅用经过滤的UVA管照射,作为对照组。单独暴露于UVB源或暴露于UVB源并结合最大日UVA剂量的组之间,皮肤肿瘤的发生没有显著差异(0.2 > p > 0.1)。在用UVB源和较低剂量UVA照射的其他组中,皮肤肿瘤的发生明显延迟(p < 0.001)。对照组未观察到肿瘤。这项研究表明,UVA1辐射会延迟UVB诱导的皮肤肿瘤发生。然而,当每天给予更高剂量的UVA时,这种延迟预计不会持续。

相似文献

1
Near-visible-UV radiation delays UVB tumorigenesis.近可见光-紫外线辐射可延缓紫外线B诱导的肿瘤发生。
J Photochem Photobiol B. 1994 Feb;22(2):119-23. doi: 10.1016/1011-1344(93)06956-4.
2
Carcinogenic and melanogenic effects of a filtered metal halide UVA source and a tubular fluorescent UVA tanning source with or without additional solar-simulated UV radiation in hairless mice.过滤后的金属卤化物UVA光源和管状荧光UVA晒黑光源在有无额外太阳模拟紫外线辐射情况下对无毛小鼠的致癌和致黑素生成作用。
Photochem Photobiol. 1995 Oct;62(4):773-9. doi: 10.1111/j.1751-1097.1995.tb08729.x.
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Carcinogenesis induced by UVA (365-nm) radiation: the dose-time dependence of tumor formation in hairless mice.UVA(365纳米)辐射诱导的致癌作用:无毛小鼠肿瘤形成的剂量-时间依赖性
Carcinogenesis. 1997 May;18(5):1013-20. doi: 10.1093/carcin/18.5.1013.
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UVA irradiation increases the incidence of epithelial tumors in UVB-irradiated hairless mice.紫外线A照射会增加经紫外线B照射的无毛小鼠上皮肿瘤的发生率。
Photodermatol Photoimmunol Photomed. 1990 Jun;7(3):109-15.
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UVA tanning devices interact with solar-simulated UV radiation in skin tumor development in hairless mice.紫外线A(UVA)晒黑设备在无毛小鼠皮肤肿瘤发展过程中与模拟太阳紫外线辐射相互作用。
Arch Dermatol Res. 1992;284(6):353-7. doi: 10.1007/BF00372039.
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The carcinogenic effect of UVA irradiation.紫外线A辐射的致癌作用。
J Invest Dermatol. 1983 Dec;81(6):517-9. doi: 10.1111/1523-1747.ep12522855.
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Photocarcinogenesis in hairless mice induced by ultraviolet A tanning devices with or without subsequent solar-simulated ultraviolet irradiation.使用或不使用随后的模拟太阳紫外线照射的紫外线A晒黑设备诱导无毛小鼠发生光致癌作用。
Photodermatol Photoimmunol Photomed. 1991 Aug;8(4):139-45.
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Carcinogenic potential of fluorescent UV tanning sources can be estimated using the CIE erythema action spectrum.可使用CIE红斑作用光谱来估计荧光紫外线晒黑光源的致癌潜力。
Int J Radiat Biol. 1993 Oct;64(4):445-50. doi: 10.1080/09553009314551631.
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Differences in narrow-band ultraviolet B and broad-spectrum ultraviolet photocarcinogenesis in lightly pigmented hairless mice.浅色素无毛小鼠中窄谱中波紫外线与广谱紫外线光致癌作用的差异。
Photodermatol Photoimmunol Photomed. 1994 Oct;10(5):192-7.
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The influence of ventral UVA exposure on subsequent tumorigenesis in mice by UVA or UVB irradiation.
Carcinogenesis. 1992 Nov;13(11):2169-74. doi: 10.1093/carcin/13.11.2169.

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Jpn J Cancer Res. 1996 Jul;87(7):685-90. doi: 10.1111/j.1349-7006.1996.tb00278.x.