Factors Influencing the Toxicity, Detoxification and Biotransformation of Paralytic Shellfish Toxins - Reviews of Environmental Contamination and Toxicology - page 15

sensitivity for neoSTX and GTX1, 4 (Usleber et al. 2001 ). A general quantitative
immunoassay specifi c to all STX group toxins is not available (by using only
one type of antibody). Therefore, immunoassays were developed and are used for
pre-screening analyses, which reduces the requirement for mouse bioassays.
Fortunately, immunoassay provides qualitative (presence/absence) screening results
for saxitoxin in less than 20 min (Inami et al. 2004 ).
A range of immunoassays have been developed with poly- and mono-clonal anti-
bodies to analyze for saxitoxin and several of its derivatives. Commercially available
kits include the Ridascreen fast saxitoxin test (R-BioPharm), the Abraxis ELISA for
PSP (Abraxis) and the Maxsignal saxitoxin ELISA (Bio Scientifi c). The Ridascreen
assay, with monoclonal antibodies, has a much better (0.02 μg L

− 1 ) detection limit
than does the polyclonal antibody-based (Abraxis and MaxSignal) assays, the limit
of detection for which is 1.2 μg L

− 1 (Usleber et al. 2001 ). The immunoassay allows
rapid screening for detecting positive samples and is very helpful to regulatory agen-
cies, shellfi sh processing plants and the aquaculture industry. The positive samples
that are detected by using this assay can be subjected to further quantitative analysis
by using more defi nitive methods. One disadvantage of these immunoassays is the
differential affi nity of the antibody mixture for individual PSP toxins.

6 Biotransformation of PSTs

Most PSTs in marine bivalves are biotransformed in the digestive gland, indicating
the presence therein of toxin transforming enzymes or bacteria (Fast et al. 2006 ;
Lu and Hwang 2002 ). The concentration of toxins in bivalves is generally similar to
the concentration in the dinofl agellates on which they feed. Bivalves, however, usu-
ally contain higher amounts of the carbamate toxin (GTXs) form than do the dino-
fl agellates, and lower levels of the N-sulfocarbamoyl (C) toxins (Kwong et al. 2006 ;
Choi et al. 2003 ). This difference appears to result from the biotransformation of
these PSTs by the bivalves from the less stable ʲ -epimer (C2, GTX3, GTX4) form to
the more stable ʱ -epimer (C1, GTX1, GTX2) form, until these moieties reach an ʱ : ʲ
ratio of 1:3 (Bricelj and Shumway 1998 ; Oshima 1995 ). The transformation of the
C2 toxin to GTXs and dcGTX increases the net toxicity of the shellfi sh to consumers
by four to tenfold. This transformation process is accelerated at higher temperature
and pH (Oshima 1995 ). The biotransformation of toxins possibly involves both
enzymatic and non-enzymatic conversion reactions. The probable metabolic mecha-
nisms involved include desulfation, oxidation, reduction and epimerization. Such
transformation mechanisms are known to alter the overall toxicity of the PSTs.
Kotaki et al. ( 1985 ) were the fi rst to suggest that the PSTs are biotransformed by
the bacteria, Vibrio and Pseudomonas spp. Most of the early studies demonstrated
that bacteria transform less toxic PSTs to more toxic PSTs. Conversion of GTX5 to
STX was documented to occur in Blue mussels (Sullivan 1982 ). Moreover, bacterial
isolates from the viscera of marine crabs, snails and red algae have also been dem-
onstrated to transform GTX 1-4 to STX and neoSTX (Sugawara et al. 1997 ; Kotaki
1989 ; Kotaki et al. 1985 ). Transformation of these less toxic PSTs (e.g., GTX 1, 2