頁籤選單縮合
題 名 | 殺菌劑快得寧之致變異性與致癌可能性評估=Evaluation of Genotoxicity and Carcinogenicity on Fugicide, Copper 8-hydroxyquinolate, by Short-term Tests |
---|---|
作 者 | 游碧堉; 王雲鶴; 郭明良; | 書刊名 | 植物保護學會會刊 |
卷 期 | 41:2 1999.06[民88.06] |
頁 次 | 頁119-132 |
分類號 | 433.85 |
關鍵詞 | 快得寧; 沙門菌回復突變測試; 枯草菌重組檢定; 姊妹染色體交換測試; 細胞間隙傳遞; 二階段肝腫瘤促進試驗; Copper 8-hydroxyquinolate; Ames test; Rec assay; SCE assay; GJIC; Two-step hepatocarcinogenesis; |
語 文 | 中文(Chinese) |
中文摘要 | 殺菌劑快得寧(copper 8-hydroxyquinolate)的原料化合物8-hydroxyquinoline為致變異性物質並有致癌疑慮 ,為了確保快得寧農藥對人畜仍具有安全性,本文以沙門菌回復突變(Ames test)、枯草菌重組檢定(rec assay)以及倉鼠卵巢細胞(CHO)姊妹染色體交換(sister chromatid exchanges,SCE,assay)等基因毒性簡速偵測法(short-term tests)來綜合評估快得寧的致變異性,同時也以Wistar大鼠之二階段肝 腫瘤促進試驗(two-step hepatocarcinogenesis assay)及鼠肺細胞株(V79)之細胞間隙連繫(gap junctional intercellular communication, GJIC)影響等非基因毒性(epigenetic toxicity)試驗來評估快得 寧在促進腫瘤及轉化細胞方面的可能致癌影響。試驗結果顯示快得寧本身對供試之生物並無直接之基因毒 性,但經肝臟酵素活化後轉而具有致變異性,其顯著引起沙門菌之鹽基置換突變,增加對枯草菌的DNA危 害,同時也使CHO細胞之SCE呈劑量反應關係。而在非基因毒性方面﹕快得寧農藥不會抑制V79細胞的GJIC ,對於經誘變劑N-nitrosodiethylamine(DEN) 啟動變異的大鼠肝臟組織,也不會促成肝腫瘤的形成。因此快得寧農藥可歸屬為“具有致變異性的非致癌劑(mutagenic-noncarcinogen)”。此外,快得寧可使大鼠 肝細胞之γ-麩胺醯轉化��(γ-glutamyltranspeptidase,GGT)的活性增加並使肝細胞萎縮,其可能對肝臟有 其它潛在的慢性傷害,因此,有關快得寧農藥之毒性安全評估似有重新檢討的必要。 |
英文摘要 | Copper 8-hydroxyquinolate (oxine copper, Quinolate) is one of the most widely used fungicides in Taiwan. Recently,the parent compound of oxime copper,8-hydroxyquinoline, has been found to be a mutagen as well as a potent carcinogen. In this context,it seems necessary to re-evaluate the mutagenicity/carcinogenicity of oxine copper. To evaluate the genotoxicity of oxime copper, a battery of short-term tests, i.e. Salmonella/microsomal reversion assay (Ames test), rec assay and sister chromatid exchanges (SCEs) assay, were employed in this study. Fuethermore, the tumor promoting effests of oxine copper were also examined by using in vivo hepatocarcinogenesis as well as in vitro gap junctional intercellular communication assay. In the presence of rat liver S9 extract, oxine copper significantly induced base-pair substitution of his gene in S. typhimurium TA100, DNA damages in Bacillus sudtilis and SCEs in CHO cells. However, oxine copper did not induce genotoxic responses in these systems in the absence of rat liver S9 extract. In two-step hepatocarcinogenesis examination, oxine copper did not alter the morphologv of rat liver and the number of proliferating cells; yet, the relative liver weight was reduced. Oxine copper failed to inhibit the GJIC in V79 cells either in the presence or absence or absence of S9 bioactivation These results suggest that oxine copper did not promote hepatocarcinogenesis in Wistar rats However,r-glutamyltranspeptidase activity was increased in oxine copper-treated rats implying that a chronic toxic response occurred in treated liver. Toxicity of oxine copper in mammals should be evaluated further and more detailed echanisms should be studied to diminish the risk of oxine copper-induced mutagenicity and/or carcinogenicity. |
本系統中英文摘要資訊取自各篇刊載內容。