Dinoflagellates and Toxin Production 219
Complex circadian systems control the behavior of dinoflagellates in vivo—as daylight and changes
in nutrient levels condition vertical migration (Doblin et al. 2006). Cell growth has to be coordinated
with cell division, not only to produce a homeostasis of cell size but also to allow cells respond properly
to nutrient availability. The cell size may affect buoyancy and sinking rates, and hence the period in
the photic zone (Wong and Kwok 2005). Phototactic vertical migrations of dinoflagellates, in response
to changing light intensity, are quite common and referred to as positive photoaxis (Erga et al. 2015).
Depending on the species, one may find aggregates of dinoflagellates in the upper layer of the ocean
during daylight (where they photosynthesize), which at night tent to move or sink as a response to gravity
(or positive geotaxis)—to deeper layers, where nutrient concentrations are higher (García-Camacho et al.
2007; Erga et al. 2015). It is presumed that their alternative modes of coupling cell cycle progression with
cell growth may play a role upon such slow growth (Wong and Kwok 2005).
HABs and toxin-related issues
Dinoflagellates are one of the major responsible for the so-called harmful algal blooms (HABs)—which
have implications upon aquatic faunal mortalities, marine food web chains, and ultimately, human health.
These high densities of dinoflagellates apparently kill fish and/or shellfish—either indirectly, because of
cell accumulation in animal gills and depletion of oxygen, or directly by toxin production (Hallegraeff
1993; Smayda 1997). Such toxins can be readily transferred into higher trophic levels through the food
chain (Wang 2008); and episodic mortalities of other animals, such as birds and other marine mammals,
are not uncommon (Scholin et al. 2000; Flewelling et al. 2005; Landsberg et al. 2009). How and why
these natural phenomena occur is not fully understood, but hydrographic and weather conditions have
been implicated (Wells et al. 2015). The proliferation of toxic species in non-endemic areas can be a
consequence of dragging of water currents, or even interaction with bivalves that can harbor viable cells
and cysts—thus aiding in their marine dispersion (Matsuoka et al. 2003). Furthermore, the high densities
of dinoflagellates in water environments near coastal areas also seems to be influenced by anthropogenic
action (i.e., discharges of industrial, domestic, and agriculture wastes), as crucial nutrient ratios (i.e.,
nitrogen:phosphorous) are essential for their metabolism (Hodgkiss and Ho 1997; Gobler and SañudoWilhelmy 2001; Hallegraeff 2003).
Depending on the period and extent of the occurrence, HABs economic impact may be more or less
severe. Those events are continuously monitored by several countries, which usually prohibit shellfish
harvesting and restrict human consumption thereof. Several local activities may be constrained: from
seafood distributors to restaurants and supermarkets, or even fish farms that can be forced to discontinue
production. In addition, HABs may cause discoloration (usually red, and less frequently yellow or brown)
in seaside water, and affect other tourism attractions in coastal areas. Poor advertisement of the affected
area may case deep negative impacts on tourism and associated activities (Steidinger and Baden 1984).
The consumption of contaminated shellfish (i.e., soft shell clams, mussels, oysters, scallops, hard
clams), crustaceans (i.e., shrimps, crabs, lobsters) or fish can be potentially lethal to humans. There are
six major toxic poisoning syndromes reported in the literature in regard to humans: paralytic shellfish
poisoning (PSP) (i.e., saxitoxin), neurologic shellfish poisoning (NSP) (i.e., brevetoxin), diarrheic
shellfish poisoning (DSP) (i.e., okadaic acid, pectenotoxin), ciguatera fish poisoning (CFP) (i.e.,
ciguatoxin, maitotoxin), azaspiracid shellfish poisoning (azaspiracid), and amnesic shellfish poisoning
(ASP) (i.e., domoic acid)—the latter not directly due to dinoflagellates, but to diatoms (Hackett et al. 2004;
Wong and Kwok 2005; Wang 2008; Lin 2011). In general, such intoxications can lead to neurological
and gastrointestinal illness. Some of them are so potent that affect normal nerve function, can act as
modulators of higher neurological processes (i.e., saxitoxin, domoic acid), and can ultimately lead to
death (Wang 2008). The symptoms associated to such type of intoxications are diverse and nonspecific
(i.e., headache, dizziness, nausea, vomiting, abdominal cramps)—which many times leads to misleading
symptoms and thus inaccurate medical diagnosis.
Due to the impacts on both public health and economy, extensive studies have been devoted to
HABs and environmental outcomes of dinoflagellate toxins in the latests decades (Hallegraeff 1993).
The production of toxins by different dinoflagellate is well documented, but the mechanisms regulating
Complex circadian systems control the behavior of dinoflagellates in vivo—as daylight and changes
in nutrient levels condition vertical migration (Doblin et al. 2006). Cell growth has to be coordinated
with cell division, not only to produce a homeostasis of cell size but also to allow cells respond properly
to nutrient availability. The cell size may affect buoyancy and sinking rates, and hence the period in
the photic zone (Wong and Kwok 2005). Phototactic vertical migrations of dinoflagellates, in response
to changing light intensity, are quite common and referred to as positive photoaxis (Erga et al. 2015).
Depending on the species, one may find aggregates of dinoflagellates in the upper layer of the ocean
during daylight (where they photosynthesize), which at night tent to move or sink as a response to gravity
(or positive geotaxis)—to deeper layers, where nutrient concentrations are higher (García-Camacho et al.
2007; Erga et al. 2015). It is presumed that their alternative modes of coupling cell cycle progression with
cell growth may play a role upon such slow growth (Wong and Kwok 2005).
HABs and toxin-related issues
Dinoflagellates are one of the major responsible for the so-called harmful algal blooms (HABs)—which
have implications upon aquatic faunal mortalities, marine food web chains, and ultimately, human health.
These high densities of dinoflagellates apparently kill fish and/or shellfish—either indirectly, because of
cell accumulation in animal gills and depletion of oxygen, or directly by toxin production (Hallegraeff
1993; Smayda 1997). Such toxins can be readily transferred into higher trophic levels through the food
chain (Wang 2008); and episodic mortalities of other animals, such as birds and other marine mammals,
are not uncommon (Scholin et al. 2000; Flewelling et al. 2005; Landsberg et al. 2009). How and why
these natural phenomena occur is not fully understood, but hydrographic and weather conditions have
been implicated (Wells et al. 2015). The proliferation of toxic species in non-endemic areas can be a
consequence of dragging of water currents, or even interaction with bivalves that can harbor viable cells
and cysts—thus aiding in their marine dispersion (Matsuoka et al. 2003). Furthermore, the high densities
of dinoflagellates in water environments near coastal areas also seems to be influenced by anthropogenic
action (i.e., discharges of industrial, domestic, and agriculture wastes), as crucial nutrient ratios (i.e.,
nitrogen:phosphorous) are essential for their metabolism (Hodgkiss and Ho 1997; Gobler and SañudoWilhelmy 2001; Hallegraeff 2003).
Depending on the period and extent of the occurrence, HABs economic impact may be more or less
severe. Those events are continuously monitored by several countries, which usually prohibit shellfish
harvesting and restrict human consumption thereof. Several local activities may be constrained: from
seafood distributors to restaurants and supermarkets, or even fish farms that can be forced to discontinue
production. In addition, HABs may cause discoloration (usually red, and less frequently yellow or brown)
in seaside water, and affect other tourism attractions in coastal areas. Poor advertisement of the affected
area may case deep negative impacts on tourism and associated activities (Steidinger and Baden 1984).
The consumption of contaminated shellfish (i.e., soft shell clams, mussels, oysters, scallops, hard
clams), crustaceans (i.e., shrimps, crabs, lobsters) or fish can be potentially lethal to humans. There are
six major toxic poisoning syndromes reported in the literature in regard to humans: paralytic shellfish
poisoning (PSP) (i.e., saxitoxin), neurologic shellfish poisoning (NSP) (i.e., brevetoxin), diarrheic
shellfish poisoning (DSP) (i.e., okadaic acid, pectenotoxin), ciguatera fish poisoning (CFP) (i.e.,
ciguatoxin, maitotoxin), azaspiracid shellfish poisoning (azaspiracid), and amnesic shellfish poisoning
(ASP) (i.e., domoic acid)—the latter not directly due to dinoflagellates, but to diatoms (Hackett et al. 2004;
Wong and Kwok 2005; Wang 2008; Lin 2011). In general, such intoxications can lead to neurological
and gastrointestinal illness. Some of them are so potent that affect normal nerve function, can act as
modulators of higher neurological processes (i.e., saxitoxin, domoic acid), and can ultimately lead to
death (Wang 2008). The symptoms associated to such type of intoxications are diverse and nonspecific
(i.e., headache, dizziness, nausea, vomiting, abdominal cramps)—which many times leads to misleading
symptoms and thus inaccurate medical diagnosis.
Due to the impacts on both public health and economy, extensive studies have been devoted to
HABs and environmental outcomes of dinoflagellate toxins in the latests decades (Hallegraeff 1993).
The production of toxins by different dinoflagellate is well documented, but the mechanisms regulating