Experimental uptake and depuration of paralytic shellfish toxins in Southern Rock Lobster, Jasus edwardsii

Abstract

In October 2012, paralytic shellfish toxins (PST) were detected in the hepatopancreas of Southern Rock Lobsters (Jasus edwardsii) collected from the east coast of Tasmania, Australia. This resulted in the first commercial closure in Australia for this species. Questions were raised on how the toxins were transferred to the lobsters, how long the toxins would persist, whether PST-contaminated hepatopancreas posed a risk to human health, and what management strategies could be applied. The aim of this study was to investigate whether PST-contaminated mussels are a potential vector enabling toxin accumulation in J. edwardsii and to collect information on toxin uptake, distribution and depuration rates and toxin profiles under controlled experimental settings. Lobsters were fed mussels naturally contaminated with PST for a period of 28 days in an experimental setting; following this, lobsters were allocated to either fed or starved treatment groups. PST were not detected in the tail tissue of lobsters at any stage of the experiment. Lobster hepatopancreas contained mean levels of 2.4 mg STX.2HCl eq/kg after 28 days of uptake, although substantial variability in total toxicity was observed. The PST profile of the hepatopancreas was similar to that of the contaminated mussels used as feed. Significant differences were noted in the PST depuration rates between fed and starved treatment groups. The daily depuration rate for total PST was estimated to be 0.019 and 0.013 mg STX.2HCl eq/kg for the fed and starved treatment groups respectively using a constant-rate decay model. After 42 days of depuration, total PST (STX equivalents) levels in the hepatopancreas of all lobsters were below 0.8 mg STX.2HCl eq/kg, which represents the regulatory level applied to bivalves. This result indicates that long-term holding to depurate PST may potentially be used as a risk management tool.

Field Validation of the Southern Rock Lobster Paralytic Shellfish Toxin Monitoring Program in Tasmania, Australia

“…The PST analogues present in J. edwardsii hepatopancreas were the same as those seen in experimental studies using mussels from Tasmanian east coast events as the prey source [4,8]. In the Maria zone in 2019, the proportion of C1&2 and C3&4 were higher than seen in the experimental studies, likely due to the prey sources available in the field.…”

“…Mussels were first investigated as a sentinel species for lobster risk management by Madigan et al in the initial research project following the 2012 bloom [ 26 ]. Mussels make ideal sentinels as their high feeding filtration rates result in rapid toxin accumulation, they provide an integrated toxicity estimate (compared to a single point in time as offered by a phytoplankton sample), analytical methods are well developed for this matrix, and they are easy to collect off existing marine infrastructure, or lines are easy to deploy where no infrastructure exists.…”

“…A significant body of research has occurred to underpin the Tasmanian rock lobster risk management program. Toxins were confirmed to accumulate to levels of concern only in the lobster hepatopancreas [ 4 ]. Cooking studies demonstrated that the toxicity of the hepatopancreas remained the same during steaming and boiling, with no change in the toxin profile but a reduction in the amount of hepatopancreas present for consumption [ 5 ].…”

Lobster Supply Chains Are Not at Risk from Paralytic Shellfish Toxin Accumulation during Wet Storage

“…The causative alga in Tasmania is Alexandrium catenella (Whedon and Kofoid) Balech, whilst New Zealand blooms may be A. minutum Halim, A. pacificum Litaker (previously identified as A. catenella) and Gymnodinium catenatum Graham [5,6]. The toxins accumulate in the lobster hepatopancreas via the consumption of contaminated prey but are not found in the tail meat [7,8].…”

Effects of paralytic shellfish toxins on the middle intestine of Oncorhynchus mykiss: Glutathione metabolism, oxidative status, lysosomal function and ATP-binding cassette class C (ABCC) proteins activity

“…These compounds are produced by marine dinoflagellates and freshwater cyanobacteria (Lagos, 2003, for a review; Kellmann et al, 2013), and can reach high levels in blooms or surface scums, which can particularly affect the use of water for tap water production, aquaculture and recreational activities (Testai et al, 2016a, for a review). PST may be accumulated in aquatic organisms and incorporated into the trophic chain (Ferrão-Filho and Kozlowsky-Suzuki, 2011;Lopes et al, 2014;Madigan et al, 2018;Su� arez-Isla, 2016). In fish, besides neuromotor effects (Bakke and Horsberg, 2007;Lefebvre et al, 2004), PST can produce oxidative stress (Clemente et al, 2010;da Silva et al, 2011) and lethal effects (Montoya et al, 1997;White, 1980).…”