Seng W L, Glogowski J A, Wolf G, Berman M B, Kenyon K R, Kiorpes T C
Invest Ophthalmol Vis Sci. 1980 Dec;19(12):1461-70.
A mild trauma in the form of a thermal burn was applied to corneas of vitamin A--deficient rats and their pair-fed controls. The control corneas routinely showed rapid re-epithelialization without stromal changes. The corneas of deficient rats recovered more slowly, frequently exhibiting stromal edema, leukoma, and sometimes ulceration. Because collagenase is thought to initiate collagen destruction in corneal ulceration, the relationships among vitamin A status, severity of trauma, and collagenase levels were determine. Mild thermal burns were found to cause corneas from less severely deficient rats to ulcerate rarely but no release increased levels of collagenase, mainly on the first day of culture, as in the case of nonburned, severely deficient rats. Comparable burns of corneas of pair-fed control rats resulted in no ulceration and in very little collagenase release. Severe burns of either pair-fed control or normal rat corneas caused ulceration and collagenase release, but collagenase activity was maximal on the second and third days of culture. Differences in vitamin A status at time of burning gave rise to different patterns of collagenase. By following the development of the vitamin deficiency, it was determined that little active collagenase is released after mild burns of corneas in animals in the pre--weight plateau stage but that much more active enzyme is released when animals are in weight plateau or 5% weight loss stages. Studies of the effect of recovery from vitamin A deficiency on the response to mild thermal burn indicated that the longer the interval between feeding vitamin A and the burn, the lower the postburn level of collagenase in the day 1 medium. Thus it would appear that restitution of vitamin A status decreased the level of active collagenase after the mild thermal burn. The system developed here can be used to study the biochemical basis for ulceration in vitamin A deficiency, and the possibility exists that the ulceration characteristic of keratomalacia in people can be initiated by an environmental trauma.
对维生素A缺乏的大鼠及其配对喂养的对照大鼠的角膜施加轻度热烧伤形式的轻微创伤。对照角膜通常显示快速重新上皮化且无基质变化。缺乏维生素A的大鼠的角膜恢复较慢，经常出现基质水肿、角膜白斑，有时还会出现溃疡。由于胶原酶被认为在角膜溃疡中引发胶原蛋白破坏，因此确定了维生素A状态、创伤严重程度和胶原酶水平之间的关系。发现轻度热烧伤会使维生素A缺乏程度较轻的大鼠的角膜很少发生溃疡，但不会释放增加水平的胶原酶，主要是在培养的第一天，就像未烧伤、严重缺乏维生素A的大鼠一样。配对喂养的对照大鼠的角膜进行类似的烧伤不会导致溃疡，胶原酶释放也很少。配对喂养的对照大鼠或正常大鼠的角膜严重烧伤会导致溃疡和胶原酶释放，但胶原酶活性在培养的第二天和第三天最高。烧伤时维生素A状态的差异导致了胶原酶的不同模式。通过跟踪维生素缺乏的发展情况，确定在体重平稳前期的动物中，角膜轻度烧伤后很少释放活性胶原酶，但当动物处于体重平稳期或体重减轻5%阶段时，会释放更多活性酶。对从维生素A缺乏恢复后对轻度热烧伤反应的影响的研究表明，喂食维生素A和烧伤之间的间隔时间越长，第1天培养基中烧伤后胶原酶的水平越低。因此，似乎维生素A状态的恢复降低了轻度热烧伤后活性胶原酶的水平。这里开发的系统可用于研究维生素A缺乏时溃疡形成的生化基础，并且存在人类角膜软化症的溃疡特征可能由环境创伤引发的可能性。
