Okada K, Takahashi Y, Ohnishi K, Ishikawa O, Miyachi Y
Department of Dermatology, Gunma University School of Medicine, Japan.
J Dermatol Sci. 1994 Dec;8(3):183-6. doi: 10.1016/0923-1811(94)90052-3.
Reactive oxygen species are produced by ultraviolet (UV) exposure and cause oxidative damage. Enzymic antioxidants such as superoxide dismutase (SOD) and catalase (CAT) may play important defensive roles in vivo. The previous studies have focused on the acute effects after single UV irradiation on those enzyme activities. In this study, we investigated the chronic effects of ultraviolet-A (UVA) or ultraviolet-B (UVB) exposure on the skin SOD and CAT activities using hairless mice. Accumulated doses of UVA and UVB after 36-week irradiation conducted 3 times a week were 3240 J/cm2 and 4320 mJ/cm2, respectively. SOD activity was increased by UVB irradiation and gradually returned to control levels, but was unaffected by UVA irradiation. In contrast, CAT activity was suppressed by UVA irradiation, indicating that the skin SOD and CAT activities are not coordinately regulated by long-term UV irradiation. These findings suggest that SOD activity is induced by repeated exposures to UVB in response to chronic photooxidative stress. However, continual cumulative stress may overwhelm the capacity of this system. These time-dependent changes of the cutaneous antioxidant system by chronic UV irradiation should provide us with important information on photooxidative events in cutaneous photoaging.
活性氧由紫外线（UV）照射产生，并导致氧化损伤。超氧化物歧化酶（SOD）和过氧化氢酶（CAT）等酶性抗氧化剂可能在体内发挥重要的防御作用。先前的研究集中在单次紫外线照射后对这些酶活性的急性影响。在本研究中，我们使用无毛小鼠研究了紫外线A（UVA）或紫外线B（UVB）照射对皮肤SOD和CAT活性的慢性影响。每周进行3次，持续36周照射后的UVA和UVB累积剂量分别为3240 J/cm²和4320 mJ/cm²。UVB照射使SOD活性增加，并逐渐恢复到对照水平，但不受UVA照射的影响。相反，UVA照射抑制了CAT活性，表明皮肤SOD和CAT活性不受长期紫外线照射的协同调节。这些发现表明，SOD活性是由反复暴露于UVB诱导的，以应对慢性光氧化应激。然而，持续的累积应激可能会超过该系统的能力。慢性紫外线照射引起的皮肤抗氧化系统的这些时间依赖性变化应为我们提供有关皮肤光老化中光氧化事件的重要信息。
