Pomati Francesco, Rossetti Carlo, Manarolla Gianluca, Burns Brendan P, Neilan Brett A
Cyanobacteria and Astrobiology Research Laboratory, School of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney 2052, NSW, Australia.
DBSF, University of Insubria, via J. H. Dunant 3, 21100 Varese, Italy.
Microbiology (Reading). 2004 Feb;150(Pt 2):455-461. doi: 10.1099/mic.0.26350-0.
Saxitoxin (STX) is the most potent representative among the paralytic shellfish poisoning (PSP) toxins, which are highly selective Na(+) channel-blocking alkaloids. This study investigated, in cultures of the cyanobacterium Cylindrospermopsis raciborskii T3, the effects of pH, salt, amiloride and lidocaine hydrochloride on total cellular levels of Na(+) and K(+) ions and STX accumulation. Both Na(+) levels and intracellular STX concentrations increased exponentially in response to rising alkalinity. NaCl inhibited cyanobacterial growth at a concentration of 10 mM. In comparison with osmotically stressed controls, however, NaCl promoted STX accumulation in a dose-dependent manner. A correlation was seen in the time-course of both total cellular Na(+) levels and intracellular STX for NaCl, amiloride and lidocaine exposure. The increase in cellular Na(+) induced by NaCl at 10 mM was coupled with a proportional accumulation of STX. The two Na(+) channel-blocking agents amiloride and lidocaine had opposing effects on both cellular Na(+) levels and STX accumulation. Amiloride at 1 mM reduced ion and toxin concentrations, while lidocaine at 1 micro M increased the total cellular Na(+) and STX levels. The effects of the channel-blockers were antagonistic and dependent on an alkaline pH. The results presented suggest that, in C. raciborskii T3, STX is responsive to cellular Na(+) levels. This may indicate that either STX metabolism or the toxin itself could be linked to the maintenance of cyanobacterial homeostasis. The results also enhance the understanding of STX production and the ecology of PSP toxin-producing cyanobacteria.
石房蛤毒素(STX)是麻痹性贝类中毒(PSP)毒素中最具毒性的代表物,这类毒素是高度选择性的钠通道阻断生物碱。本研究在蓝藻圆柱鞘丝藻T3的培养物中,调查了pH值、盐、氨氯吡脒和盐酸利多卡因对细胞内钠(Na⁺)和钾(K⁺)离子总量以及STX积累的影响。随着碱度升高,Na⁺水平和细胞内STX浓度均呈指数增加。10 mM浓度的NaCl抑制蓝藻生长。然而,与渗透胁迫对照组相比,NaCl以剂量依赖方式促进STX积累。在NaCl、氨氯吡脒和利多卡因暴露的过程中,细胞内总Na⁺水平和细胞内STX之间存在相关性。10 mM的NaCl诱导的细胞内Na⁺增加与STX的成比例积累相关。两种钠通道阻断剂氨氯吡脒和利多卡因对细胞内Na⁺水平和STX积累具有相反的作用。1 mM的氨氯吡脒降低离子和毒素浓度,而1 μM的利多卡因增加细胞内总Na⁺和STX水平。通道阻断剂的作用具有拮抗性且依赖于碱性pH值。所呈现的结果表明,在圆柱鞘丝藻T3中,STX对细胞内Na⁺水平有反应。这可能表明STX代谢或毒素本身可能与蓝藻内稳态的维持有关。这些结果也增进了对STX产生以及产生PSP毒素的蓝藻生态学的理解。