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首页> 外文期刊>Zeitschrift fur Naturforschung, C. A Journal of Biosciences >The role of lipid peroxidation in aluminium toxicity in soybean cell suspension cultures
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The role of lipid peroxidation in aluminium toxicity in soybean cell suspension cultures

机译:脂质过氧化在大豆细胞悬浮培养物中铝毒性中的作用

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The primary reactions leading to Al toxicity in plant cells have not yet been elucidated. We used soybean (Glycine max [L.] Merr.) cell suspension cultures to address the question whether lipid peroxidation plays an important role in Al toxicity. Upon transfer to an Al-containing culture medium with a calculated Al3+ activity of 15 muM soybean cells showed a distinct and longtime increase in lipid peroxidation within 4h. At the same time a drastic loss of cell viability was observed. Butylated hydroxyanisole (BHA) and N,N'-diphmyl-p-phenylenediamine (DPPD), two lipophilic antioxidants, were able to almost completely suppress lipid peroxidation in Al-treated cells at a concentration of 20 muM. This effect was close-dependent for DPPD and was observed at minimum concentrations of 1-2 muM. When lipid peroxidation was suppressed by DPPD or BHA cell viability remained high even in the presence of toxic Al concentrations. These results suggest that Al-induced enhancement of lipid peroxidation is a decisive factor for Al toxicity in suspension cultured soybean cells. [References: 34]
机译:尚未阐明导致植物细胞中铝毒性的主要反应。我们使用大豆(Glycine max [L.] Merr。)细胞悬浮培养物来解决脂质过氧化是否在Al毒性中起重要作用的问题。转移至具有Al3 +活性计算为15μM的含Al培养基后,大豆细胞在4小时内显示出脂质过氧化的明显且长期的增加。同时观察到细胞活力的急剧丧失。两种亲脂性抗氧化剂丁基化羟基茴香醚(BHA)和N,N'-二苯甲基对苯二胺(DPPD)能够以20μM的浓度几乎完全抑制Al处理的细胞中的脂质过氧化。该效应对DPPD密切相关,在最小浓度为1-2μM时观察到。当脂质过氧化被DPPD或BHA抑制时,即使在有毒的Al浓度下,细胞活力仍保持高水平。这些结果表明,铝诱导的脂质过氧化作用的增强是悬浮培养的大豆细胞中铝毒性的决定性因素。 [参考:34]

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