Russo I H, Koszalka M, Russo J
Department of Pathology, Michigan Cancer Foundation, Detroit 48201.
Br J Cancer. 1991 Sep;64(3):481-4. doi: 10.1038/bjc.1991.335.
Since it has been shown that pregnancy protects the mammary gland from chemically induced carcinogenesis, this study was designed with the dual purpose of determining whether treatment of young virgin rats with the placental hormone chorionic gonadotropin (hCG) mimics pregnancy-induced changes in the tumourigenic response of the mammary gland and also whether the effect induced by both pregnancy and hormonal treatments was transitory, or a more permanent one, exerting the same effect when the period of time between delivery or termination of treatment and exposure to the carcinogen is lengthened. Virgin Sprague-Dawley rats were utilised in two experimental protocols. For protocol I, 50 day-old rats were either mated (Group II), or started receiving a daily intraperitoneal injection of 100 IU hCG (Group III) at age 50. Age-matched untreated virgin rats were used as controls (Group I). Twenty-one days after either delivery or termination of treatment all the animals received an intragastric dose of 8 mg DMBA/100 gbw. For the second protocol, 50 day-old virgin rats were also mated (Group V) or were treated with hCG for 21 days (Group VI); the resting period between delivery or termination of treatment was lengthened to 63 days, at which time they received a dose of DMBA. Age-matched controls (Group IV) received DMBA only. Tumourigenesis was evaluated 24 weeks post-carcinogen administration in all the groups. Pregnancy and hCG followed by the 21-day resting period significantly depressed mammary carcinogenesis to 11% and 6% respectively, compared with 63% in control animals. When the resting period was prolonged to 63 days there was also a significant depression in adenocarcinoma incidence to 9% in pregnancy (Group IV) in which it was observed that tumour incidence was also reduced as a consequence of aging at the time of exposure to the carcinogen. These results clearly indicate that hCG is as efficient as pregnancy and significantly reduces mammary carcinogenesis, and that the protective effect of both pregnancy and hCG treatment is long-lasting and both are more efficient than aging in reducing mammary carcinogenesis.
由于已有研究表明怀孕可保护乳腺免受化学诱导的致癌作用,本研究旨在实现双重目的:确定用胎盘激素绒毛膜促性腺激素(hCG)处理年轻未孕大鼠是否能模拟怀孕诱导的乳腺肿瘤发生反应变化,以及怀孕和激素处理所诱导的效应是短暂的还是更持久的,即在分娩或终止治疗与接触致癌物之间的时间延长时是否仍发挥相同作用。在两个实验方案中使用了未孕的斯普拉格 - 道利大鼠。对于方案I,50日龄的大鼠要么交配(II组),要么在50日龄时开始每天腹腔注射100 IU hCG(III组)。年龄匹配的未处理未孕大鼠用作对照(I组)。在分娩或终止治疗21天后,所有动物接受8 mg DMBA/100 g体重的胃内给药。对于第二个方案,50日龄的未孕大鼠同样进行交配(V组)或用hCG处理21天(VI组);分娩或终止治疗后的休息期延长至63天,此时它们接受DMBA剂量。年龄匹配的对照(IV组)仅接受DMBA。在所有组中,致癌物给药后24周评估肿瘤发生情况。与对照动物的63%相比,怀孕和hCG处理后经过21天休息期,乳腺致癌作用分别显著降低至11%和6%。当休息期延长至63天时,怀孕组(IV组)腺癌发病率也显著降低至9%,在此观察到由于接触致癌物时的衰老,肿瘤发病率也降低。这些结果清楚地表明,hCG与怀孕一样有效,能显著降低乳腺致癌作用,并且怀孕和hCG处理的保护作用是持久的,两者在降低乳腺致癌作用方面都比衰老更有效。