- 期刊
- OpenAccess
The Inhibitory Effect of Four Chemicals on Experimental Carcinogenesis
四種化學物對誘導生癌之抑制效能
摘要
本實驗研究二種PAH致癌物（BP及MC）及二種非PAH之疑似致癌物（NTP及MNAB）對用DMBA誘導生癌作用之抑制效能，用金黃色倉鼠七十隻分為四個實驗組（用每種化學物塗一組倉鼠之頰囊，三至十週，休息八至十週，再塗DMBA十週）及四個對照組（分別塗以①每種化學物②溶劑或礦物油③DMBA④不塗任何物品，紀錄各組倉鼠頰囊中之腫瘤數目大小，及其粘膜上血管之數目與大小等變化。至塗DMBA後第二十週，犧牲動物，將腫瘤切片以觀察腫瘤之性質，並將頰粘膜作DNA合成作用與GGTase染色反應等試驗。將諸結果用以評估各化學物品之抑癌效能，結果發現四種化學物均有抑制DMBA致癌作用之能力，其作用機轉曾予討論。化學物品與細胞中的DNA先結合，致DMBA不能再與DNA結合而導致癌症，應為其抑癌作用之主要機轉，此種作用且可產生記憶現象而傳至其後代細胞。其他如各化學物品能使頰囊粘膜局部之血流減少，使DNA合成變慢，並使GGTase之活動降低等，亦可能與其抑癌效能有關。
並列摘要
The inhibitory effect of two PAH carcinogens, benz(a)pyrene (BP), 20-methylcholanthrene (MC), and two non-PAH suspected carcinogens, N(N'-methyl-N'-nitroso-aminomethyl)-benzamide(MNAB) and 5-nitroso-2,4,6-triaminopyrimidine (NTP) on experimental carcinogenesis induced by 9,10-dimethyl-1,2-benzanthracene(DMBA) was studied on 70 Syrian hamsters. Four experimental groups (BP, MC, NTP or MNAB + DMBA) and four control groups including chemical controls(BP, MC, NTP and MNAB), normal conrtrol vehicle or mineral oil control and DMBA control were designed. In the experimental groups, the painting of different chemicals on the mucous membrane of the animal's buccal pouches was followed by DMBA application. In the control groups, no DMBA or DMBA only was applied to the buccal pouches of the animals. The architecture of blood vessels of the buccal pouches, in both number and diameter, and tumor formation were observed. Animals were sacrificed after 20 weeks of DMBA painting. After sacrifice, the tumors and the pouch mucosa were dissected to study the tumor nature and the biochemical reactions of DNA synthesis and GGTase activity. The inhibitory effect of each chemical was evaluated according to the results of these examinations. All four chemicals possessed similar inhibitory efficacy on experimental carcinogenesis. The mechanism of the inhibition was discussed. Competitive binding of the chemicals with the guanine base of DNA to prevent the binding of DMBA and the initiation of carcinogenesis was probably the main mechanism of this cancer inhibition effect. The effect may also relate to a memory phenomenon on cellular DNA. Other related factors included insufficient local blood flow, slow DNA synthesis and low GGTase activity.