Cycloheximide and buthionine sulfoximine prevent induction of genotoxic adaptation by cadmium salt against methyl mercuric chloride in embryonic shoot cells of Hordium vulgare L

Jita Patra, A.V. Subhadra, Brahma B. Panda
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引用次数: 13

Abstract

Presoaked seeds of barley Hordeum vulgare L. pretreated with cycloheximide (CH), 10−6 M or bythionine sulfoximine (BSO), 10−4 M, were exposed to methyl mercuric chloride (MMCl), 10−4 M, with or without prior conditioning with cadmium sulfate (CdSO4), 10−4 M. Subsequently as the seeds germinated the endpoints measured were mitotic index, cells with mitotic aberrations and micronuclei (MNC) in embryonic shoot cells fixed at 40, 44, 48 and 52 h of recovery. Indicated by the significance reduction (p ≤ 0.05) of the yield of cells with aberrations or MNC, the results confirmed that CdSO4-conditioning triggered an adaptive response to MMCl-challenge. Pretreatments of CH and BSO, whereas they potentiated the genotoxicity of MMCl, significantly prevented (p ≤ 0.05) the Cd-induced genotoxic adaptation. That underscores a possible involvement of proteins in addition to phytochelatins in the underlaying mechanisms.

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氯己胺和丁硫醚磺酰亚胺对镉盐诱导大麦胚芽细胞对甲基汞基因毒性适应性的影响
用10−6M的环己酰亚胺(CH)或10−4M的二硫腙磺酰亚胺(BSO)预处理的大麦Hordeum vulgare L.的预浸种种子暴露于10−3M的甲基氯化汞(MMCl)中,无论是否事先用10−4MM的硫酸镉(CdSO4)预处理。随后,当种子发芽时,测量的终点为有丝分裂指数,在恢复的40、44、48和52小时固定的胚胎芽细胞中具有有丝分裂畸变和微核(MNC)的细胞。通过具有畸变或MNC的细胞产量的显著降低(p≤0.05)表明,结果证实CdSO4处理触发了对MMCl攻击的适应性反应。CH和BSO的预处理虽然增强了MMCl的遗传毒性,但显著阻止了(p≤0.05)Cd诱导的遗传毒性适应。这强调了除植物螯合素外,蛋白质可能参与底层机制。
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