facilitate cyanobacteria by grazing on their eukaryotic phototrophic competitors [51,
52]. Direct ingestion of cyanobacteria by zooplankters has been shown, and interactions between Daphnia and cyanobacteria have been investigated extensively.
Generally, cyanobacteria have toxic effects on Daphnia [53]. Rohrlack et al. [54]
found that metabolites from Microcystis sp. caused a lethal molting disruption in
Daphnia spp. The toxin microcin SF608 proved to inhibit the detoxification enzyme
glutathione S-transferase (sGST) of Daphnia [55]. However, Daphnia was able to
increase its tolerance if continuously exposed to cyanobacteria [56].
2.2.4 Higher Tropic Levels
Cyanobacterial toxins have also been found to target different aquatic vertebrates
and amphibians that may indirectly affect phytoplankton succession by top-down
control of zooplankton or their predators. Cyanobacterial exudates have teratogenic
effects on amphibians and interference with their embryo growth, and these effects
are similar to those caused by the famous teratogen retinoid [57]. Fish are often
strongly affected by cyanobacterial toxins, especially during their early development. Zi et al. [58] found that cell-free filtrates of M. aeruginosa posed a malformation of the heart at the embryo stage of an endangered Chinese fish species
(Sinocyclocheilus grahami). On the other hand, cyanobacteria decreased the mortality rates of fish by their antimicrobial properties against pathogen microbes [59].
Retinoid-like activities of cyanobacterial exudates caused diverse teratogenic effects
and interference with the growth of zebrafish embryos, but microcystins were not
responsible for any of the observed effects [60, 61]. Chronic toxicity on zebrafish
larvae by exudates of the bloom-forming cyanobacterium Cylindrospermopsis was
manifested by Zagatto et al. [62].
3
Cyanobacterial Secondary Metabolites and Their Mode of
Action
3.1
Secondary Metabolites
Cyanobacteria produce a wide range of toxins including hepatotoxins, cytotoxins,
neurotoxins, and dermatotoxins [10, 63]. The most famous toxins include microcystins, cylindrospermopsins, nodularins, anatoxins-a, and saxitoxins [63] which
were intensely studied due to their potential effects on human health and commercial
use. Each of them has a main structure core with diverse moieties to variants, and the
metabolic pathways of their synthesis have been elucidated [63–65].
Microcystins (MCs) are the most well-known and widespread cyanobacterial
toxins around the world. Their functions as feeding deterrent, metal-chelating
agent, and signaling molecule have been described, but the role of microcystins as
allelopathic compounds is still under discussion [66, 67]. From an evolutionary
perspective, the development of microcystins has been long before the occurrence of
eukaryotic phototrophs, and their initial role may not be related to allelopathic effects
[66]. However, several studies clearly indicate that microcystins can affect
328
Y. Pei et al.
52]. Direct ingestion of cyanobacteria by zooplankters has been shown, and interactions between Daphnia and cyanobacteria have been investigated extensively.
Generally, cyanobacteria have toxic effects on Daphnia [53]. Rohrlack et al. [54]
found that metabolites from Microcystis sp. caused a lethal molting disruption in
Daphnia spp. The toxin microcin SF608 proved to inhibit the detoxification enzyme
glutathione S-transferase (sGST) of Daphnia [55]. However, Daphnia was able to
increase its tolerance if continuously exposed to cyanobacteria [56].
2.2.4 Higher Tropic Levels
Cyanobacterial toxins have also been found to target different aquatic vertebrates
and amphibians that may indirectly affect phytoplankton succession by top-down
control of zooplankton or their predators. Cyanobacterial exudates have teratogenic
effects on amphibians and interference with their embryo growth, and these effects
are similar to those caused by the famous teratogen retinoid [57]. Fish are often
strongly affected by cyanobacterial toxins, especially during their early development. Zi et al. [58] found that cell-free filtrates of M. aeruginosa posed a malformation of the heart at the embryo stage of an endangered Chinese fish species
(Sinocyclocheilus grahami). On the other hand, cyanobacteria decreased the mortality rates of fish by their antimicrobial properties against pathogen microbes [59].
Retinoid-like activities of cyanobacterial exudates caused diverse teratogenic effects
and interference with the growth of zebrafish embryos, but microcystins were not
responsible for any of the observed effects [60, 61]. Chronic toxicity on zebrafish
larvae by exudates of the bloom-forming cyanobacterium Cylindrospermopsis was
manifested by Zagatto et al. [62].
3
Cyanobacterial Secondary Metabolites and Their Mode of
Action
3.1
Secondary Metabolites
Cyanobacteria produce a wide range of toxins including hepatotoxins, cytotoxins,
neurotoxins, and dermatotoxins [10, 63]. The most famous toxins include microcystins, cylindrospermopsins, nodularins, anatoxins-a, and saxitoxins [63] which
were intensely studied due to their potential effects on human health and commercial
use. Each of them has a main structure core with diverse moieties to variants, and the
metabolic pathways of their synthesis have been elucidated [63–65].
Microcystins (MCs) are the most well-known and widespread cyanobacterial
toxins around the world. Their functions as feeding deterrent, metal-chelating
agent, and signaling molecule have been described, but the role of microcystins as
allelopathic compounds is still under discussion [66, 67]. From an evolutionary
perspective, the development of microcystins has been long before the occurrence of
eukaryotic phototrophs, and their initial role may not be related to allelopathic effects
[66]. However, several studies clearly indicate that microcystins can affect
328
Y. Pei et al.