Factors Influencing the Toxicity, Detoxification and Biotransformation of Paralytic Shellfish Toxins - Reviews of Environmental Contamination and Toxicology - page 3

from respiratory failure (Baden and Trainer 1993 ). To date, there is no antidote for
PSP. However, the symptomatic treatments for PSP that are commonly used include
the following: fl uid therapy, blood pH monitoring, and artifi cial respiration with ben-
zedrine administration, and gastric lavage with dilute bicarbonate solution (Kao
1993 ). Su et al. ( 2004 ) discovered that PSTs also bind to the human potassium chan-
nel. However, the toxins modify the potassium channel, rather than blocking it as
occurs in sodium channels. To date, four or more PST molecules are known to bind
to extracellular sites of the potassium channel and to produce strong transmembrane
depolarization (Wang et al. 2003 ). Depolarization causes the channel to open and to
reduce potassium conductance. PSTs also act on voltage-gated calcium channels, by
incompletely blocking them at extracellular sites (Su et al. 2004 ).
In general, saxitoxin and its derivatives are grouped into three categories; carba-
mate toxins, decarbamoyl toxins, and N -sulfocarbamoyl toxins. The most potent
carbamate toxins include saxitoxin (STX), neosaxitoxin (neoSTX) and gonyautox-
ins (GTX1-4). The decarbamoyl analogues (viz., dcSTX, dcNEO, dcGTX1-4) are
reported to have intermediate toxicity, whereas the least toxic derivatives are the
N -sulfocarbamoyl toxins (B1 (GTX5), B2 (GTX6) and C1-C4) (Llewellyn 2006 ;
Lassus et al. 2000 ). The basic structure of the PSTs comprises a trialkyl tetrahydro-
purine skeleton, with positions 2 and 8 of the purine ring containing NH 2 groups
(Schantz et al. 1975 ). The 1,2,3-guanidine moiety carries a positive charge, whereas
the 7,8,9-guanidine group is partially deprotonated. In Table 1 , we present the
molecular structures of the PSTs, and provide information on their relative toxicity.
There are four functional groups (R1-4) clustered around the PST ring (Table 1 ).
These functional groups determine the toxic potency of STX.
PSTs are found in both marine and freshwater environments and are produced by
organisms inhabiting two taxonomic kingdoms: the prokaryotic cyanobacteria and
eukaryotic dinofl agellates. In marine habitats, the PSTs are produced by bloom-
forming dinofl agellates such as: Gymnodinium catenatum (Oshima et al. 1993 ),
Pyrodinium bahamense Va r. compressum (Usup et al. 1994 , 2002 ) and Alexandrium
spp. (Lim et al. 2005 ; Lefebvre et al. 2008 ). In Table 2 , we present a grid that shows
what PSTs are produced by different dinofl agellate organisms. As shown in Table 1 ,
the different PSTs possess different levels of toxicity. Gymnodinium catenatum is
widely distributed in the Gulfs of California and Mexico, Argentina, Japan, the
Philippines, Palau, Tasmania, the Mediterranean, the Atlantic coast of Morocco,
Portugal, and Spain (Hallegraeff 1993 ). Pyrodinium bahamense Va r. compressum is
largely responsible for PSP outbreaks in tropical waters of the Indo-West Pacifi c
(Sabah, Brunei, Philippines and Papua-New Guinea) (Usup et al. 1994 ) and East
Pacifi c (off the coast of Guatemala and Mexico) (Hallegraeff 1993 ). Alexandrium spp.
is widely distributed in both temperate and tropical waters of the Pacifi c coast, from
Alaska to southern California (Taylor 1984 ), Argentine Sea (Carreto et al. 1986 ),
Magallanes Strait (Benavides et al. 1995 ), Arabian Sea (Sharma et al. 2011 ), peninsular
Malaysia (Lim et al. 2001 ), Northeastern Canada (Parkhill and Cembella 1999 ),
Gulf of Thailand (Kodama 1990 ), Japan (Ogata et al. 1989 ), southern Australia, and
New Zealand (Bricelj and Shumway 1998 ).