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霉菌毒素展青霉素在哺乳动物细胞中诱导微核和染色体畸变:抗坏血酸作为展青霉素致断裂性调节剂的作用

Induction of micronuclei and chromosomal aberrations by the mycotoxin patulin in mammalian cells: role of ascorbic acid as a modulator of patulin clastogenicity.

作者信息

Alves I, Oliveira N G, Laires A, Rodrigues A S, Rueff J

机构信息

Department of Genetics, Faculty of Medical Sciences, New University of Lisbon, R. da Junqueira 96, P-1349-008 Lisbon, Portugal.

出版信息

Mutagenesis. 2000 May;15(3):229-34. doi: 10.1093/mutage/15.3.229.

DOI:10.1093/mutage/15.3.229
PMID:10792015
Abstract

Patulin is a mycotoxin produced by several species of Penicillium, Aspergillus and BYSSOCHLAMYS: Patulin is a common contaminant of ripe apples used for the production of apple juice concentrates and is also present in other fruits, vegetables and food products. Patulin has been reported to have mutagenic, carcinogenic and teratogenic properties. Nevertheless, these properties are still a matter of debate. In this report, we further investigated the genotoxicity of patulin in mammalian cells by two different approaches. Firstly, we evaluated the induction of micronuclei in cytokinesis-blocked human lymphocytes. This approach is important because available data concerning the genetic toxicity of patulin in human cells is sparse. Secondly, we chose an established model for patulin genotoxicity, i.e. the chromosomal aberration assay in V79 Chinese hamster cells, to clarify whether concomitant exposure to ascorbic acid with the mycotoxin modulates or not the clastogenicity of patulin. The results unequivocally show induction of DNA-damaged cells by patulin as assessed by both cytogenetic assays. In addition, an almost complete abolition of patulin (0.8 microM) clastogenicity was observed in the presence of 80 microM ascorbic acid (P < 0.05), showing that although a genetic risk is present, ascorbic acid could somehow partially modulate this problem.

摘要

展青霉素是由几种青霉菌、曲霉菌和丝衣霉菌产生的一种霉菌毒素:展青霉素是用于生产浓缩苹果汁的成熟苹果的常见污染物,也存在于其他水果、蔬菜和食品中。据报道,展青霉素具有致突变、致癌和致畸特性。然而,这些特性仍存在争议。在本报告中,我们通过两种不同方法进一步研究了展青霉素在哺乳动物细胞中的遗传毒性。首先,我们评估了胞质分裂阻滞的人淋巴细胞中微核的诱导情况。这种方法很重要,因为关于展青霉素在人类细胞中遗传毒性的现有数据很少。其次,我们选择了一种已确立的展青霉素遗传毒性模型,即V79中国仓鼠细胞中的染色体畸变试验,以阐明霉菌毒素与抗坏血酸同时暴露是否会调节展青霉素的断裂作用。两种细胞遗传学试验评估结果均明确显示展青霉素可诱导DNA损伤细胞。此外,在存在80微摩尔抗坏血酸的情况下,观察到展青霉素(0.8微摩尔)的断裂作用几乎完全消除(P < 0.05),表明尽管存在遗传风险,但抗坏血酸可能在某种程度上部分调节了这个问题。

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