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放线菌酮和丁硫氨酸亚砜亚胺可阻止镉盐对大麦胚性芽细胞中甲基汞氯化物诱导的遗传毒性适应。

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

作者信息

Patra J, Subhadra A V, Panda B B

机构信息

Department of Botany, Berhampur University, India.

出版信息

Mutat Res. 1995 Sep;348(1):13-8. doi: 10.1016/0165-7992(95)90015-2.

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 significant reduction (p < or = 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 < or = 0.05) the Cd-induced genotoxic adaptation. That underscores a possible involvement of proteins in addition to phytochelatins in the underlaying mechanisms.

摘要

用10⁻⁶ M放线菌酮(CH)或10⁻⁴ M丁硫氨酸亚砜胺(BSO)预处理过的大麦(Hordeum vulgare L.)预浸种子,暴露于10⁻⁴ M氯化甲基汞(MMCl)中,有无10⁻⁴ M硫酸镉(CdSO₄)预先处理。随后,随着种子发芽,在恢复40、44、48和52小时时固定胚胎芽细胞,测量的终点指标为有丝分裂指数、有丝分裂异常细胞和微核(MNC)。畸变或MNC细胞产量显著降低(p≤0.05)表明,结果证实CdSO₄预处理引发了对MMCl挑战的适应性反应。CH和BSO预处理虽然增强了MMCl的遗传毒性,但显著阻止了(p≤0.05)镉诱导的遗传毒性适应。这突出了除植物螯合肽外,蛋白质可能参与了潜在机制。

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