CYANOBACTERIAL TOXINS - Cyanobacteria - page 522

The accumulation of MCs in freshwater mussel ( Hyridella menziesi ) and rainbow trout in lakes of
Rotoiti and Rotoehu (New Zealand) has been investigated along with variations in concentrations
of MCs in the bloom algae. Phytoplankton samples revealed 760 µg L -1 in Lake Rotoiti. Freshwater
mussels suspended in cages in lake waters revealed variants of MC-LR, MC-YR, MC-RR, MC-AR,
MC-FR, MC-LA and MC-WR but these were not detected in muscle or liver tissues of rainbow
trout (Wood et al ., 2006). During a bloom of No . spumigena in Gippsland Lakes of Southern Victoria,
nodularin concentration reached alarming levels in mussels and in prawn viscera at cell counts nearly
30,000 cells ml -1 (Van Buynder et al ., 2001). Freshwater mussel Anodonta cygnea accumulated CYN
up to 2.52 µg g -1 tissue dry weight after being exposed to C . raciborskii cultures for 16 days. At the
end of two-week period, CYN distribution in different parts of the body was 68.1% in haemolymph,
23.3% in viscera, 7.7% in foot and gonad and 0.9% in mantle (Saker et al ., 2004). A link in the food
web of Baltic Sea for biomagnifi cation of nodularin has been established. Eiders (a northern sea
duck; Somateria mollissima ) that fed on mussels in the Baltic Sea showed accumulation of nodularin
in their liver from 3 to 180 µg kg -1 body weight and 0.1 to 5.8 µg nodularin per liver (dry weight)
(Sipia et al ., 2005).
iii) Amphibians : Embryos of Xenopus laevis (African clawed frog) were exposed to biomass of M .
aeruginosa (with MC-LR) and M . wesenbergii (without MC-LR) and purifi ed MC-LR (0-250 µg L -1
and 500 µg L -1 ) in a 96 h teratogenesis assay (FETAX). MC-LR and biomass of M . aeruginosa caused
signifi cant lethality up to 30% and 50%, respectively. The LC 25 concentrations were 380 µg L -1 for
MC-LR and 300 mg L -1 (=250 µg L -1 MC-LR) for biomass of M . aeruginosa . At lower concentrations
of MC-LR (25 µg L -1 ) there was increase in number of malformations. However, surviving embryos
(53%) from among those treated with 250 µg L -1 of MC-LR and biomass of M . wesenbergii showed
malformations (Dvorakova et al ., 2002).
iv) Mammals : In mammals when administered intravenously (i.v.) or intraperitoneally (i.p.), MCs
get localized in the liver (Falconer et al ., 1986; Nishiwaki et al ., 1994). Extensive haemorrhage,
accumulation of yellow fl uid in body cavities and acute hepatic necrosis have been noted in sheep
dosed with water containing bloom of No . spumigena and guinea pigs developed periacinar liver
necrosis leading to death (Main et al ., 1977). Cows developed signs of anorexia, mental derangement,
dehydration, recumbency and ruminal atony upon ingestion of Microcystis bloom water. Increase
of liver associated enzyme activities (alkaline phosphatase, γ-glutamyltransferase, aspartate
transaminase and lactate dehydrogenase) was noted after a week of bloom ingestion. Hepatic
enlargement associated with hepatic dissociation, degeneration and necrosis was common in cows
administered with bloom alga intraruminally. When orally ingested, MC-LR is transported across
the ileum into blood stream via bile-acid transporter (also known as the multi-specifi c organic ion
transport system) present in the hepatocytes and cells lining the small intestines (Runnegar et al .,
1991; Falconer et al ., 1992). The other variants of MCs are more hydrophobic than MC-LR and may
cross cell membranes by other mechanisms including diffusion (Kuiper-Goodman et al ., 1999).
The localization of MCs in liver appears to be due to the specifi city in their binding to hepatocytes
(Dawson, 1998; Chorus and Bartram, 1999; Dow and Swoboda, 2000).
Isotopically labelled MCs when administered either i.v. or i.p. in mice or rats, the accumulation
of nearly 70% of the label was found in the liver (Falconer et al ., 1986; Runnegar et al ., 1986; Brooks
and Codd, 1987; Robinson et al ., 1989, 1991; Meriluto et al ., 1990; Lin and Chu, 1994a; Nishiwaki et
al ., 1994). Uptake studies on 3 H-dihydromicrocystin-LR by rat hepatocytes revealed that the uptake
is a specifi c feature of hepatocytes whereas uptake by other cell lines (human hepatocarcinoma cell
line HepG2 as well as mouse fi broblast cell line NIH-3T3 and human neuroblastoma cell line SH-