@article{mbs:/content/journal/micro/10.1099/mic.0.26350-0, author = "Pomati, Francesco and Rossetti, Carlo and Manarolla, Gianluca and Burns, Brendan P. and Neilan, Brett A.", title = "Interactions between intracellular Na+ levels and saxitoxin production in Cylindrospermopsis raciborskii T3", journal= "Microbiology", year = "2004", volume = "150", number = "2", pages = "455-461", doi = "https://doi.org/10.1099/mic.0.26350-0", url = "https://www.microbiologyresearch.org/content/journal/micro/10.1099/mic.0.26350-0", publisher = "Microbiology Society", issn = "1465-2080", type = "Journal Article", keywords = "PSP, paralytic shellfish poisoning", keywords = "STX, saxitoxin", abstract = "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 μM 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.", }