Hillebrand G G, Winslow M S, Benzinger M J, Heitmeyer D A, Bissett D L
Procter & Gamble Company, Miami Valley Laboratories, Cincinnati, Ohio 45239-8707.
Cancer Res. 1990 Mar 1;50(5):1580-4.
The effects of acute, multiple, and chronic exposure of hairless mice to ultraviolet radiation (UVR) on induction of epidermal ornithine decarboxylase (ODC) (EC 4.1.1.17) activity were investigated. Acute UVR exposure results in a biphasic time course of induction of epidermal ODC activity. Enzyme activity maxima occur at 3 and 24 h postirradiation. The biphasic time course is observed in two different strains of hairless mice (Skh:HR-1 and Jackson HRS/J) when the UVR source is either UBV fluorescent tubes or a solar simulator. The ratio of 24-h/3-h postirradiation ODC activity increases with increasing UVR dose. UVR induction of ODC activity was not significant below the mouse minimum erythemal dose (MED). The 3- and 24-h ODC activities have similar apparent Kms for ornithine (34 and 50 microM, respectively), and thermal stabilities at 52 degrees C (t1/2 = 23 and 18 min, respectively), and exhibit similar half-lives in vivo (t1/2 = 15 and 18 min, respectively). Multiple UVR exposure experiments showed 24-h ODC activity is sensitive to the preexposure history of the mouse, while 3-h ODC is not. Preexposure of hairless mice to several sub-MED levels of simulated solar radiation (SSR) specifically suppresses induction of 24-h ODC by a follow-up 2 x MED of SSR. Preexposure to a single 2 x MED of SSR specifically enhances induction of 24-h ODC induced by a second 2 x MED of SSR administered 48 h after the first. The 3-h ODC was not significantly affected by either preexposure regimen. Preexposure to a single high or low dose of UVA radiation did not affect epidermal ODC activity nor had an effect on ODC induction by UVB radiation. Several weeks of chronic exposure to UVB radiation elevated basal levels of epidermal ODC substantially (up to 350-fold). In these chronically irradiated mice, exposure to 2 x MED SSR resulted in a further 3.5-fold increase in ODC activity over the elevated basal level. These data reveal novel properties of epidermal cell expression of ODC activity in response to acute and chronic UVR insult. The results provide additional insight into the use of ODC as a marker for skin photodamage.
研究了无毛小鼠急性、多次和慢性暴露于紫外线辐射(UVR)对表皮鸟氨酸脱羧酶(ODC,EC 4.1.1.17)活性诱导的影响。急性UVR暴露导致表皮ODC活性诱导呈现双相时间进程。酶活性最大值在照射后3小时和24小时出现。当UVR源为UVB荧光灯管或太阳模拟器时,在两种不同品系的无毛小鼠(Skh:HR-1和Jackson HRS/J)中均观察到双相时间进程。照射后24小时/3小时的ODC活性比值随UVR剂量增加而升高。低于小鼠最小红斑剂量(MED)时,UVR对ODC活性的诱导不显著。3小时和24小时的ODC活性对鸟氨酸具有相似的表观Km值(分别为34和50 microM),在52℃时具有相似的热稳定性(t1/2分别为23和18分钟),并且在体内具有相似的半衰期(t1/2分别为15和18分钟)。多次UVR暴露实验表明,24小时的ODC活性对小鼠的预先暴露历史敏感,而3小时的ODC则不敏感。无毛小鼠预先暴露于几个低于MED水平的模拟太阳辐射(SSR)会特异性抑制后续2倍MED的SSR诱导的24小时ODC。预先暴露于单次2倍MED的SSR会特异性增强在第一次48小时后给予的第二次2倍MED的SSR诱导的24小时ODC。3小时的ODC不受任何一种预先暴露方案的显著影响。预先暴露于单次高剂量或低剂量的UVA辐射既不影响表皮ODC活性,也不影响UVB辐射对ODC的诱导。几周的慢性UVB辐射显著提高了表皮ODC的基础水平(高达350倍)。在这些慢性照射的小鼠中,暴露于2倍MED的SSR导致ODC活性在升高的基础水平上进一步增加3.5倍。这些数据揭示了表皮细胞在响应急性和慢性UVR损伤时ODC活性表达的新特性。结果为将ODC用作皮肤光损伤标志物提供了更多见解。