Algal toxins

Toxins of algal origin (also called phycotoxins) are most often produced by unicellular marine flagellates, particularly dinoflagellates, but also by members of other major flagellate algal groups, such as raphidophytes, haptophytes and pelagophytes. A few species of the diatom genus Pseudo-nitzschia synthesize a potent neurotoxin, domoic acid. In fresh and brackish waters, cyanobacteria (‘blue-green algae’) are often implicated as toxic algal contaminants in drinking-water supplies for humans and livestock. In the marine environment, cyanobacterial toxins are responsible for ‘netpen liver disease’ in caged salmonids. When present in high abundance or during periods of rapid growth (‘blooms’), algae can cause water discolorations known as ‘red tides’, usually in fresh or coastal waters – these phenomena are not always associated with toxicity. Toxic events associated with algae may be divided into two types: (i) those caused by the production of specific toxic metabolites; and (ii) those resulting from secondary effects, such as post-bloom hypoxia, ammonia release, or other artefacts of decomposition on marine flora and fauna. Phycotoxins and their causative organisms are globally distributed in marine coastal environments, from the tropics to polar latitudes, and few areas are exempt from their effects, which may be expanding in geographical extent, severity and frequency on a global basis. In a few cases, this may be linked to eutrophication, but there is no general hypothesis to explain all such events.

Among the thousands of extant species of marine microalgae, only several dozen produce highly potent biotoxins that profoundly affect the health of marine ecosystems, as well as human and other animal consumers of seafood products. As an operational category, certain toxic microalgae are often called ‘fishkillers’ because of their potent direct effects on fish, particularly in aquaculture systems. Such toxins are poorly characterized and the mechanism of action is often not well understood, although the toxic effects are typically mediated through the gills. In contrast, the toxins associated with human illnesses by consumption of contaminated finfish (e.g. ciguatera fish poisoning, clupeotoxicity) and paralytic, amnesic, neurotoxic and diarrhoeic shellfish poisoning (PSP, ASP, NSP and DSP, respectively) caused by ingestion of shellfish are much better known. The phycotoxins responsible for these syndromes constitute a heterogeneous group of compounds, affecting a variety of receptors and metabolic processes, acting as Na+-channel blockers, Ca2+-channel activators, glutamate agonists, phosphatase inhibitors etc. These pharmacologically active compounds also include the emerging problems associated with ‘fast-acting toxins’ of poorly defined human health significance, such as gymnodimine and spirolides. Many of the phycotoxins can be propagated within marine food webs from phytoplankton through zooplankton (copepods, krill), then from ichthyoplankton to large carnivorous fish, and even marine birds and mammals. Toxin accumulation within fish stocks (e.g. anchovies) harvested for fish-meal production may even be a risk for aquaculture of certain species. Except in bivalve shellfish, where oxidative and reductive transformations mediated by both enzymatic and non-enzymatic processes have been determined, and in the case of biotransformation within fish tissues of ciguatoxin precursors from dinoflagellates, metabolism of phycotoxins is poorly understood.