Rath I, Barz W
Institut für Biochemie und Biotechnologie der Pflanzen, Westfälische Wilhelms-Universität Münster, Germany.
Z Naturforsch C J Biosci. 2000 Nov-Dec;55(11-12):957-64. doi: 10.1515/znc-2000-11-1218.
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 microM soybean cells showed a distinct and longtime increase in lipid peroxidation within 4 h. At the same time a drastic loss of cell viability was observed. Butylated hydroxyanisole (BHA) and N,N'-diphenyl-p-phenylenediamine (DPPD), two lipophilic antioxidants, were able to almost completely suppress lipid peroxidation in Al-treated cells at a concentration of 20 microM. This effect was dose-dependent for DPPD and was observed at minimum concentrations of 1-2 microM. 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.
导致植物细胞铝毒性的主要反应尚未阐明。我们使用大豆（Glycine max [L.] Merr.）细胞悬浮培养物来研究脂质过氧化是否在铝毒性中起重要作用这一问题。转移到计算出的Al3+活性为15微摩尔的含铝培养基中后，大豆细胞在4小时内脂质过氧化显著且长时间增加。与此同时，观察到细胞活力急剧丧失。两种亲脂性抗氧化剂丁基羟基茴香醚（BHA）和N，N'-二苯基对苯二胺（DPPD），在浓度为20微摩尔时能够几乎完全抑制铝处理细胞中的脂质过氧化。这种效应对于DPPD是剂量依赖性的，并且在最低浓度1-2微摩尔时就可观察到。当脂质过氧化被DPPD或BHA抑制时，即使存在有毒的铝浓度，细胞活力仍保持较高水平。这些结果表明，铝诱导的脂质过氧化增强是悬浮培养大豆细胞铝毒性的决定性因素。
