Mak K M, Leo M A, Lieber C S
Alcohol Research and Treatment Center, VA Medical Center, Bronx, NY 10468.
J Natl Cancer Inst. 1987 Nov;79(5):1001-10.
The effect of ethanol (CAS: 64-17-5) consumption on the development of squamous metaplasia of the trachea caused by vitamin A deficiency was assessed in rats. To that effect, weanling male Sprague-Dawley rats were fed for 8-12 weeks either a nutritionally adequate liquid diet containing a standard amount of vitamin A or a diet lacking vitamin A. Littermates were pair-fed the same diets with ethanol (36% of total calories) isocalorically replacing part of the carbohydrates. In rats fed the vitamin A-deficient diets with or without ethanol, plasma vitamin A was very low (5.3 +/- 0.9 and 5.9 +/- 1.5 micrograms/dl; n = 20 pairs), while liver and tracheal vitamin A was unmeasurable. Squamous metaplasia was noted in 9 of 20 rats fed the vitamin A-deficient diet and in 13 of 20 rats fed the same diet plus ethanol. Severe lesions (those showing keratinization) were present in 42% of the tracheal sections from rats fed the vitamin A-deficient diet plus ethanol compared to 6% of the sections from rats fed the diet without ethanol (P less than .001). In the ethanol-fed group, 37% of all the sections showed metaplasia occupying more than 50% of the tracheal epithelium, whereas in the absence of ethanol, 14% of the sections had lesions occupying more than 50% of the epithelium (P less than .001). When the histologic grade and extent of the lesions were expressed as the percentage of rats affected, the differences between the 2 groups of animals were not statistically significant. Ethanol feeding resulted in a 70% increase in the labeling index of basal cells in squamous metaplasia (30.7 +/- 3.5 vs. 17.3 +/- 1.5%; P less than .02). The number of [3H]thymidine-labeled suprabasal cells was not altered after ethanol feeding. In ciliated cells of the tracheal epithelium that were not as yet involved in the formation of metaplasia, ciliary abnormalities and an increased number of lysosomes were observed in rats that had consumed ethanol.(ABSTRACT TRUNCATED AT 400 WORDS)
在大鼠中评估了摄入乙醇(CAS:64 - 17 - 5)对维生素A缺乏所致气管鳞状化生发展的影响。为此,将断乳雄性斯普拉格 - 道利大鼠用含标准量维生素A的营养充足的液体饲料或缺乏维生素A的饲料喂养8 - 12周。同窝出生的大鼠成对喂养相同的饲料,用乙醇(占总热量的36%)等热量替代部分碳水化合物。在喂食含或不含乙醇的维生素A缺乏饲料的大鼠中,血浆维生素A非常低(分别为5.3±0.9和5.9±1.5微克/分升;n = 20对),而肝脏和气管中的维生素A无法检测到。在喂食维生素A缺乏饲料的20只大鼠中有9只出现鳞状化生,在喂食相同饲料加乙醇的20只大鼠中有13只出现鳞状化生。喂食维生素A缺乏饲料加乙醇的大鼠气管切片中有42%出现严重病变(显示角化),而喂食不含乙醇饲料的大鼠切片中这一比例为6%(P<0.001)。在喂食乙醇的组中,所有切片中有37%显示化生占据气管上皮超过50%,而在未喂食乙醇的情况下,14%的切片有病变占据上皮超过50%(P<0.001)。当将病变的组织学分级和范围表示为受影响大鼠的百分比时,两组动物之间的差异无统计学意义。喂食乙醇导致鳞状化生中基底细胞的标记指数增加70%(30.7±3.5对17.3±1.5%;P<0.02)。喂食乙醇后,[3H]胸腺嘧啶标记的基底上层细胞数量未改变。在尚未参与化生形成的气管上皮纤毛细胞中,在摄入乙醇的大鼠中观察到纤毛异常和溶酶体数量增加。(摘要截短于400字)