Objectives: We investigated the mutual effects of overt hypothyroidism and prolonged sunlight exposure on free radical accumulation and oxidative skin damage.

Methods: Free radical accumulation was evaluated by monitoring the transformation of 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide (MTT) into MTT-formazan. The pro-oxidant enzymes xanthine oxidase (XO) and NADPH-diaphorase were measured in the skin. XO activity was estimated based on the yield of uric acid, while NADPH-diaphorase reactivity was monitored histochemically as an indirect marker of nitric oxide synthase and nitric oxide activity. Cellular damage was determined by malondialdehyde formation, a marker for lipid peroxidation.

Results: In the skin of both euthyroid and hypothyroid animals, solar simulated ultraviolet irradiance increased the activity of XO and the NADPHdiaphorase reactivity as a protective response to formation of free radicals, such as reactive oxygen or nitrogen species. These pro-oxidant enzymes diminished in hypothyroid rats. Accumulation of the same amount of free radicals led to similar peroxidation in both hypothyroid and irradiated euthyroid rats. Hypothyroid skin after UV-exposure showed even greater lipid peroxidation.

Discussion: The hypothyroid state could be a risk factor for enhanced oxidative skin damage in chronic photo-exposed skin due to oxidative stress. The lipid peroxidation is one of the major pathways by which photo-oxidative stress promotes photocarcinogenesis and photo-aging.

目的：我们调查了明显的甲状腺功能减退症和长时间的阳光照射对自由基积累和氧化性皮肤损伤的相互影响。

方法：通过监测3-（4,5-二甲基噻唑-2-基）-2,5-二苯基四唑溴化物（MTT）向MTT-甲酰胺的转化来评估自由基的积累。在皮肤中测量了促氧化酶黄嘌呤氧化酶（XO）和NADPH-心肌黄递酶。XO活性是根据尿酸的收率估算的，而NADPH-黄递酶的反应性是通过化学方法监测的，作为一氧化氮合酶和一氧化氮活性的间接标记。细胞损伤通过丙二醛形成来确定，丙二醛是脂质过氧化的标志。

结果：在正常甲状腺和甲状腺功能低下的动物的皮肤中，日光模拟的紫外线辐照增加了XO的活性和NADPH心肌黄递酶的反应性，作为对自由基（例如活性氧或氮物质）形成的保护性反应。这些促氧化酶在甲状腺功能减退的大鼠中减少。在甲状腺功能减退和正常辐射的甲状腺大鼠中，积累相同量的自由基会导致相似的过氧化。紫外线照射后的甲状腺功能减退的皮肤表现出更大的脂质过氧化作用。

讨论：甲状腺功能减退状态可能是慢性氧化暴露的皮肤由于氧化应激而增加氧化皮肤损伤的危险因素。脂质过氧化是光氧化应激促进光致癌作用和光老化的主要途径之一。