Patra J, Subhadra A V, Panda B B
Department of Botany, Berhampur University, India.
Mutat Res. 1995 Sep;348(1):13-8. doi: 10.1016/0165-7992(95)90015-2.
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.
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。
