联苯胺衍生染料直接黑38大鼠活体致癌作用的代谢干预试验

STUDIES ON THE INTERVENTION OF CARCINOGENESIS IN- DUCED BY BEZIDINE BASED DB38 IN INTACT RATS

本实验包括①Ｆ３４４大鼠直接黑３８（ＤＢ３８）２００ｐｐｍ食粉饲养４ｗｋ②ＳＤ大鼠ＤＢ３８１５００ｐｐｍ食粉饲养３２ｗｋ，③同②组，但以３７５ｍｇ每ｗｋｌ次灌胃试验。各组均平行作抗菌素肠道细菌干预和单纯抗菌素而不施用ＤＢ３８的对照组，试验结束后全部内脏作组织病理学检查。４ｗｋＦ３４４大鼠ＤＢ３８饲养组显示肝内卵圆细胞和胶原纤维增生较抗菌素干扰组为严重，统计学差异极显著ｘ２＝３６．２９，Ｐ＜０．０００１），单纯抗菌素组皆正常。ＳＤ大鼠灌胃组第２４ｗｋ发生１例、第３２ｗｋ发生３例、共４例淋巴细胞样白血病。而饲养组在第２４ｗｋ、３２ｗｋ各发生１例。与单纯抗菌素对照组比较，前者有显著差异（Ｐ＜０．０５）后者差异不显著，两个相应的抗菌素干扰组皆在第３２ｗｋ各发生１例同样病变。显示抑制肠道菌可以延迟和降低ＤＢ３８导致的白血病。

Intervention with antibiotics(perOS)to suppress the biotransformation by nor-mal intestinal flora on the carcinogenesis by benzidine derived dyl DB38 was studied in vivo. The studies consisted of a)4 wk test of feeding DB38 to 27 F344 rats,with/without antibioticintervention;b)32 wk feeding DB38 to l00 SD rats,with intervention to 50;c)32 wk test ofgavaging DB38 to l00 SD rats,with intervention to 50;The latter two groups shared a com-mon control group of 50 SD rats receiving antibiotics only. Results indicated that the proliferation of oval cells was significantly reduced by antibi-otic intervention in feeding tests(x2=36.29,P=0.0001).The attenuation of proliferative le- sions in liver by intervention was significant in the 32 wk test(4/43 versus l2/35,x2=5.93,P=0.014).Acute lymphoid leukemias ocurred in DB38 groups were 6/83 versus 2/90 in theintervention group.The difference did not reach significance level(X2=1.28,P=0.257). However,there was a significant difference between DB38 gavaging group and antibioticstreated control group(4/39 versus 0/50,P<0.05),those in the intervention group werepostponed(delayed to 32wk from 24wk).It suggested that the suppression of bioactivation ofthe carcinogen through inhibition of intestinal flora might delay and attenuate the ocurrenceof malignancy induced by aromatic amines.