ENVIRONMENTAL UV EFFECT ON MAMMALIAN SKIN

环境紫外线对哺乳动物皮肤的影响

• 批准号: 2156399
• 负责人: JULIAN M MENTER
• 金额: $ 16.77万
• 依托单位: MOREHOUSE SCHOOL OF MEDICINE
• 依托单位国家: 美国
• 财政年份: 1994
• 资助国家: 美国
• 起止时间: 1994-09-30 至 1997-09-29
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2156399
• 关键词: albino mouse; collagen; electronic spectra; hairless mouse; light adverse effect; mucopolysaccharides; photobiology; protein structure; pyrimidine dimers; radiation dosage; skin disorder; skin hyperplasia; ultraviolet radiation

The overall objective of this work is to understand the photobiological mechanisms involved in chronic environmental UV damage to mammalian skin in a manner sufficient to accurately explain and predict the photobiological consequences of on-going ozone depletion on chronic epidermal and dermal damage, including photocarcinogenesis and "photoaging." Observed action spectra are dose- and time-dependent ("dynamic"), mainly due to UV-induced hyperplasia. Correction for this effect allows construction of "intrinsic" action spectra that can be convoluted with various solar spectral distributions (including those which simulate changes due to stratospheric ozone depletion) to afford "biologically effective doses" under the various atmospheric conditions. Specifically, we wish to (l) expand ongoing photobiological studies in Sk-1 hairless mice to include clinical, histological, and biochemical responses as a function of total dose, wavelength, and dose delivery. We will monitor UV-induced increases in pyrimidine dimers, acid glycosminoglycans (GAG), and changes in collagen structure and fluorescence properties. (2) Construct action spectra for UV-induced DNA and dermal damages. These will be "corrected" for non-uniform absorption of incident radiation by inert stratum corneum-epidermis, to afford "intrinsic" action spectra. (3) Compare the effect of broad- vs. narrow band radiation on the dose-response and action spectra obtained above (test for UVA/UVB waveband interactions). In addition to providing fundamental photochemical and biochemical information, the mechanistic insight provided by these studies should enable more accurate explanation and prediction of photobiological consequences of ozone depletion or other atmospheric changes which would alter the amount of solar UV in the environment.

这项工作的总体目标是了解光生物学 环境紫外线对哺乳动物皮肤慢性损伤的机制 以一种足以准确解释和预测 持续臭氧消耗对慢性 表皮和真皮损伤，包括光致癌作用， “光老化。and the effect of dose-dependent and time-dependent （“动态”），主要是由于UV诱导的增生。更正一下 效应允许构建“内在”作用光谱， 与各种太阳光谱分布（包括那些 模拟平流层臭氧消耗造成的变化）， 在各种大气条件下的“生物有效剂量”。 具体来说，我们希望（l）扩大正在进行的光生物学研究， Sk-1无毛小鼠，包括临床，组织学和生化 响应作为总剂量、波长和剂量递送的函数。我们 将监测紫外线诱导的嘧啶二聚体，酸 糖胺聚糖（GAG）和胶原蛋白结构的变化， 荧光性质(2)紫外诱导DNA作用光谱的构建 和皮肤损伤。这些将被“校正”为非均匀吸收 入射辐射的惰性层皮质-表皮，以提供 “内在”作用光谱。(3)比较宽与窄的效果 带辐射的剂量反应和行动的光谱获得以上 (test用于UVA/UVB波段相互作用）。除了提供 基本的光化学和生物化学信息， 这些研究提供的见解应该能够更准确地解释 和预测臭氧消耗或其他 大气层的变化，这将改变太阳紫外线的数量， 环境