Pashko L L, Schwartz A G
J Gerontol. 1983 Jan;38(1):8-12. doi: 10.1093/geronj/38.1.8.
This study was undertaken to determine whether a reduction in body weight in laboratory mice by regimens that appear to delay the rate of aging (i.e., food restriction and chronic dehydroepiandrosterone (DHEA) treatment), or a production of obesity by the presence of the ob (obese) gene or by gold thioglucose-induced hyperphagia alter the rate of binding of 3H-7,12-dimethylbenz(a)anthracene (3H-DMBA) to mouse skin deoxyribonucleic acid (DNA). We have found that treating A/J mice with food containing .6% DHEA for 10 weeks or reducing the food intake of non-DHEA treated mice to 60% of ad libitum fed animals significantly reduces the amount of 3H-DMBA bound to mouse skin DNA 12 hours after a topical application of the carcinogen. Conversely, A/J mice made obese by a gold thioglucose-induced hyperphagia and C57BL/6J mice with the ob mutation bind significantly increased amounts of 3H-DMBA to skin DNA when compared to their nonobese counterparts.
本研究旨在确定通过似乎能延缓衰老速度的方案(即食物限制和慢性脱氢表雄酮(DHEA)治疗)使实验室小鼠体重减轻,或者因ob(肥胖)基因的存在或金硫葡萄糖诱导的摄食过量导致肥胖,是否会改变3H - 7,12 - 二甲基苯并(a)蒽(3H - DMBA)与小鼠皮肤脱氧核糖核酸(DNA)的结合速率。我们发现,用含0.6%DHEA的食物处理A/J小鼠10周,或将未用DHEA处理的小鼠食物摄入量减少至随意进食动物的60%,在局部涂抹致癌物12小时后,可显著降低与小鼠皮肤DNA结合的3H - DMBA量。相反,与非肥胖对照相比,金硫葡萄糖诱导摄食过量而致肥胖的A/J小鼠和带有ob突变的C57BL/6J小鼠,其皮肤DNA与3H - DMBA的结合量显著增加。