In contrast to mammalian cells, bacteria such as Escherichia coli have been shown to display tolerance towards the neurotoxin β-methylamino-l-alanine (BMAA) suggesting that these prokaryotes possess a way to metabolise BMAA or its products, resulting in their export, degradation, or detoxification. Single gene deletion mutants of E. coli K-12 with inactivated amino acid biosynthesis pathways were treated with 500 μg/ml BMAA and the resulting growth was monitored. Wild type E. coli and most of the gene deletion mutants displayed unaltered growth in the presence of BMAA over 12 h. Conversely, deletion of genes in the cysteine biosynthesis pathway, cysE, cysK or cysM resulted in a BMAA dose-dependent growth delay in minimal medium. Through further studies of the ΔcysE strain, we observed increased susceptibility to oxidative stress from H₂O₂ in minimal medium, and disruptions in glutathione levels and oxidation state. The cysteine biosynthesis pathway is therefore linked to the tolerance of BMAA and oxidative stress in E. coli, which potentially represents a mechanism of BMAA detoxification.

相比于哺乳动物细胞，细菌，如大肠杆菌已显示出对神经毒素β甲基氨基-显示公差升丙氨酸（BMAA）表明这些原核生物具有一种方式来代谢BMAA或它的产品，从而导致它们的出口，降解，或者排毒。具有灭活氨基酸生物合成途径的大肠杆菌K-12 的单基因缺失突变体用 500 μg/ml BMAA 处理，并监测所得生长。野生型大肠杆菌和大多数基因缺失突变体在 BMAA 存在下超过 12 小时显示出未改变的生长。相反，半胱氨酸生物合成途径cysE、cysK中基因的缺失或cysM在基本培养基中导致 BMAA 剂量依赖性生长延迟。通过对 Δ cysE菌株的进一步研究，我们观察到对基本培养基中H ₂ O ₂氧化应激的敏感性增加，以及谷胱甘肽水平和氧化态的破坏。因此，半胱氨酸生物合成途径与大肠杆菌中 BMAA 的耐受性和氧化应激有关，这可能代表了 BMAA 解毒的机制。