It is possible to write whole books on the relationships between algae and the environment. In this chapter I have chosen a few subjects which have generated the most interest in the last decade.

Toxic algae

Algae can be harmful in two basic ways (Hallegraeff et al., 2003).

1Producing large populations in the aquatic environment Large growths of some algae (e.g., the diatom Chaetoceros (Figs. 17.44, 17.45) or the prymnesiophyte Chrysochromulina (Fig. 23.1(c))) can clog the gills of fish and can be particularly a problem in aquaculture systems. Anoxic conditions, resulting in fish kills, can occur at the end of blooms of other algae (e.g.,

green algae) as the algae die and decompose.

2Production of toxins Some algae produce toxins that sicken and kill other organisms that prey on these algae. Indeed, this probably was the reason that these algae were selected for in the evolutionary process since it reduced predation by grazers (Gilbert, 1996). Filter-feeding shellfish can accumulate large quantities of these toxins as they filter the algae out of the water. Consumption of the shellfish by man, birds, and animals results in sickness and death.

The algae that produce phycotoxins are:

Cyanophyceae (cyanobacteria)

•Neurotoxins anatoxin (Fig. 23.2(c)) and saxitoxin

(Fig. 23.2(c)) that block the transmission of

signal from neuron to neuron. These alkaloids (nitrogen containing compounds) bind to voltage-activated Na -channels and block influx of Na , thereby preventing the generation of an action potential (Shimizu, 2000).

•Hepatotoxins microcystin (Fig. 23.2(b)) and nodularin (Fig. 23.2(b)) that are inhibitors of protein phosphatases 1 and 2A.

Dinophyceae (dinoflagellates)

•Diarrhetic shellfish poisoning caused by okadaic acid (Fig. 23.3(e)), macrolide toxins, and yessotoxins (Fig. 23.4(f )). Okadaic acid and the related dinophysistoxins (Fig. 23.3(e)) are inhibitors of protein phosphatases, The free carboxyl groups bind to the catalytic site of the protein phosphatase. Yessotoxin may interfere with cyclic AMP in cells causing cytotoxicity (Cembella, 2003).

•Ciguatera fish poisoning caused by ciguatoxin

(Fig. 23.4(f )), maitotoxins (Fig. 23.4(f )), and brevetoxins (Fig. 23.4(f )). All of these compounds are ion-channel disrupters, increasing the permeability of the cell membrane to positive ions and causing membrane depolarization. Brevetoxins require a lactone ring for activity. Ciguatoxin and brevetoxin bind voltage-sensitive channels, increasing the permeability of the cell membrane and causing membrane depolarization (Cembella, 2003). Maitotoxin initiates Ca2 -channel activation, causing Ca2 -influx and activation of calmodulin (Igarashi et al., 1999). This is followed by

promotion of phospholipase A2 activity and ultimately cell membrane disruption.

•Paralytic shellfish poisoning caused by saxitoxin (Fig. 23.2(c)) and approximately two dozen naturally occurring analogues (Fig. 23.2(c)). The saxitonins bind to voltageactivated Na -channels, blocking influx of Na and preventing the generation of an action potential. Saxitoxins are retained primarily inside cells with very little excretion or leakage from cells. These highly water-soluble, but stable, compounds must be released during senescence or cell lysis, which coincides with the decline of a bloom (Cembella, 2003).

•Spirolide poisoning. This group of cyclic imines include the spirolides (Fig. 23.3(d )), gymnodimine (Fig. 23.3(d )), pteriatoxin and pinnatoxins. The imine ring gives the molecules their toxic properties. They are “fast-acting toxins”, causing death of mice within minutes after oral application.

Bacillariophyceae (diatoms)

•Amnesic shellfish poisoning caused by the neurotoxin domoic acid (Fig. 23.2(a)). Domoic acid is an amino acid that functions as a glutamate agonist (compound that has an affinity for a cell receptor), and in humans causes extensive depolarization in areas rich in glutamate receptors (e.g., the hippocampus). The biosynthesis of domoic acid is inducible and sustained only under stress conditions (Pan et al., 1998).

Raphidophyceae (chloromonads)

•“Red tide” poisoning. Members of the Raphidophyceae produce brevetoxins (Fig. 23.4 (f )), neurotoxins that bind to voltage-activated Na -channels causing rapid influx of Na -ions and membrane depolarization.

Prymnesiophyceae (haptophytes)

•The phycotoxin prymnesin (Fig. 23.3(e)) produces hemolysis of red blood cells by disrupting the pores in the cell membrane, causing influx of positive ions and membrane depolarization.

Another way of classifying phycotoxins is by their chemical structure (Cembella, 2003):

1Amino acid analogues. Domoic acid (Fig. 23.2(a)). This is a glutamate receptor agonist produced

by the diatom Pseudo-nitzchia spp. (Figs. 17.27, 17.29, 23.1(d )).

2Peptides. Microcystins (Figs. 23.2(b)) and nodularin (Fig. 23.2(b)). These phycotoxins are produced by cyanobacteria. Microcystin is formed by species of Microcystis (Figs. 2.48, 2.56(b)), Anabaena (Figs. 2.16, 2.18(d )), Nostoc (Figs. 2.46(b), (c), (d), 2.57(a)), Nodularia (Fig. 2.42(a)) and Oscillatoria (Figs. 2.19(a), (b), 2.34(a)), while nodularins are produced by species of

Nodularia (Fig. 2.42(a)).

3Purine derivatives. Saxitoxins (Fig. 23.2(c )), gonyautoxins (Fig. 23.2(c)), and anatoxin

(Fig. 23.2(c )). There are about two dozen analogues of these molecules with their potency varying over several orders of

magnitude. Saxitoxin has a LD50 of 10 g kg 1. The decarbamoyl derivates have intermediate

toxicity (decarbamoyl saxitoxin has a LD50 of 20 g kg 1) while the N-sulphocarbamoyl

forms have a low toxicity (N-sulphocarbamoyl

(B-toxin)) has a LD50 of 163 g kg 1). Saxitoxins are produced by some

cyanobacteria and by the dinoflagellates Alexandrium spp. (Figs. 7.35, 7.36, 23.1(f )),

Pyrodinium bahamense (Fig. 7.34), and Gymnodinium catenatum. Anatoxin is produced by the cyanobacteria Anabaena (Figs. 2.16, 2.18(d )), Aphanizomenon (Fig. 2.18(b)), Oscillatoria

(Figs. 2.19(a), (b), 2.34(a)), and Trichodesmium

(Fig. 2.56(g)).

4Cyclic imines. Spirolides (Fig. 23.3(d )) and gymnodimine (Fig. 23.3(d )). The spirolides are

produced by the marine dinoflagellate

Alexandrium ostenfeldii while gymnodimine is produced by the dinoflagellate Karenia selliformis.

5Non-nitrogen compounds containing linear and macrocyclic polyethers. Okadaic acid (Fig. 23.3(e)), dinophysistoxins (Fig. 23.3(e)), and prymnesium (Fig. 23.3(e)). Okadaic acid and the related dinophysistoxins are produced by the benthic dinoflagellate Prorocentrum (Figs. 7.30(c), 7.55) and the planktonic forms of Dinophysis (Figs. 7.30(a), (b)). Prymnesium is formed by species of the haptophyte Prymnesium (Fig. 22.7).