Liver tumour promoting activity of 3,4,5,3′,4′-pentachlorobiphenyl and its interaction with 2,3,7,8-tetrachlorodibenzo-p-dioxin

Helena Hemming , Yvonne Bager , Sten Flodström , Ingrid Nordgren , Tony Kronevi , Ulf G. Ahlborg , Lars Wärngård
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引用次数: 32

Abstract

This study was undertaken to compare the tumour promoting effects induced by 3,4,5,3′,4′-pentachlorobiphenyl (PCB 126) and 2,3,7,8,-tetrachlorodibenzo-p-dioxin (TCDD). In addition, interactive effects in rats treated with combinations of PCB 126 and TCDD were studied. Partially hepatectomized female Sprague-Dawley rats were initiated with nitrosodiethylamin. After 5 weeks of recovery the promotion treatment started and continued for 20 weeks. The results from the present study demonstrate that PCB 126 elicit approximately 10% of TCDD's tumour promoting activity measured as enhancement of the development of γ-glutamyl-transpeptidase-positive altered heaptic foci in the liver. The factor required for the PCB to match the response of TCDD was adopted as a toxic equivalency factor and was in this case 0.1, which is the same as the factor suggested by Ahlborg et al. (1994).In the groups treated with a mixture of PCB 126 and TCDD the tumour promoting effect indicated an additive response. This result suggests that PCB 126 and TCDD act by the same mechanistical pathway, which in turn, supports that the toxic equivalency factor-concept can be used for TCDD-like tumour promoters.

3,4,5,3 ',4 ' -五氯联苯的促肝癌活性及其与2,3,7,8-四氯二苯并-对二恶英的相互作用
本研究比较了3,4,5,3 ',4 ' -五氯联苯(PCB 126)和2,3,7,8,-四氯二苯并-对二恶英(TCDD)对肿瘤的促进作用。此外,我们还研究了联用PCB 126和TCDD对大鼠的交互作用。雌性Sprague-Dawley大鼠部分肝切除后给予亚硝基二乙胺。恢复5周后开始促进治疗,持续治疗20周。本研究的结果表明,PCB 126可引起约10%的TCDD促肿瘤活性,通过增强肝脏中γ-谷氨酰转肽酶阳性改变的肝灶的发展来测量。将多氯联苯与TCDD反应相匹配所需的因子作为毒性等效因子,在本例中该因子为0.1,与Ahlborg等人(1994)建议的因子相同。在用PCB 126和TCDD混合处理的组中,肿瘤促进作用显示出加性反应。这一结果表明PCB 126和TCDD通过相同的机制途径起作用,这反过来支持毒性等效因子概念可用于TCDD样肿瘤启动子。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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