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Paralytic shellfish poisoning (PSP) toxin monitoring in shellfish is currently performed using the internationally accredited AOAC mouse bioassay. Due to ethical and performance-related issues associated with this bioassay, the European Commission has recently published directives extending procedures that may be used for official PSP control. The feasibility of using a surface plasmon resonance optical biosensor to detect PSP toxins in shellfish tissue below regulatory levels was examined. Three different PSP toxin protein binders were investigated: a sodium channel receptor (SCR) preparation derived from rat brains, a monoclonal antibody (GT13-A) raised to gonyautoxin 2/3, and a rabbit polyclonal antibody (R895) raised to saxitoxin (STX). Inhibition assay formats were used throughout. Immobilization of STX to the biosensor chip surface was achieved via aminocoupling. Specific binding and inhibition of binding to this surface was achieved using all proteins tested. For STX calibration curves, 0-1000 ng/mL, I[C.sub.50] values for each binder were as follows: SCR 8.11 ng/mL; GT13-A 5.77 ng/mL; and R895 1.56 ng/mL. Each binder demonstrated a different cross-reactivity profile against a range of STX analogues. R895 delivered a profile that was most likely to detect the widest range of PSP toxins at or below the internationally adopted regulatory limits.

Phenylbutazone, a non-steroidal anti-inflammatory drug commonly used to treat horses for musculoskeletal disorders, can cause adverse effects in humans and is therefore not permitted for use in food-producing animals in the EU. In recent years some equine and bovine samples have been found to be non-compliant. While physicochemical methods of analysis exist there is a need for less-expensive, rapid screening methods such as immunoassays. This study describes the production of antisera to detect phenylbutazone and its main metabolite, oxyphenylbutazone. Four haptens were chosen for immunogen preparation and two of these, suxibuzone and γ-hydroxyphenylbutazone, produced antisera with 50% of maximal inhibitory concentration (IC50s) of <5 ng mL−1for phenylbutazone. Antisera with IC50s of 5.5 ng mL−1for phenylbutazone and 5.6 ng mL−1for oxyphenylbutazone were produced by their respective haptens. The figures suggest that the antisera could deliver detection capabilities below the concentration that is recommended by the Community Reference Laboratory (5 ng mL−1). [ABSTRACT FROM PUBLISHER]