Biology Reference
In-Depth Information
Figure 19:
Organization of the PST biosynthesis cluster in
Lyngbya wollei
, scale indicates gene size in base pairs, direction of
arrowed boxes indicates direction of transcription. With the kind permission of B. A. Neilan, Cyanobacteria and Astrobiology
Research Laboratory, School of Biotechnology and Biomolecular Sciences, The University of New South Wales, Sydney
2052, NSW, Australia [Mihali
et al
. (2011)
PLoS ONE
6(2):
e14657. doi:10.1371/journal.pone.0014657] doi:10.1371/journal.
pone.0014657.g002.
and reported the presence of 14 strains of
Aph
.
gracile
. These strains produced STX, dcSTX, neoSTX
and GTX5. Another study pertained to the monitoring of STX-producing cyanobacteria from the
lakes, dams and rivers of Australia. Al-Tebrineh
et al
. (2010) presented a quantitative estimation of
cell numbers of
A
.
circinalis
versus STX concentration and this correlated very well with the amplicon
numbers of
sxtA
gene.
ii) Toxicity studies with STXs
:
Of all the PSTs, toxicity studies only on STXs are available due to
availability of this toxin in suffi cient quantities when compared to the rest. The LD
50
of STX for male
mouse through different routes was 3.4 µg kg
-1
body weight (i.v.), 10.0 µg kg
-1
body weight (i.p.) and
263 µg kg
-1
body weight (oral) whereas for female mouse LD
50
of STX was 8.0 µg kg
-1
body weight
i.p. (Wiberg and Stephenson, 1960; Kupier-Goodman
et al
., 1999). The LD
50
of STX is 64 µg kg
-1
body
weight for 24 h old rats through oral ingestion while it is 5.5 µg kg
-1
body weight through i.p. route.
Wealings (rats of 21 days old) and adults (60-70 days) required LD
50
of 270 and 531 µg kg
-1
body
weight through oral ingestion, respectively whereas through i.p. LD
50
was 8.3 and 10 µg kg
-1
body
weight (Watts
et al
., 1966; Kupier-Goodman
et al
., 1999). The lethal dose of STX in human beings is
1-4 mg equivalents (Evans
et al
., 1978). Clinical symptoms of PSP in human beings appear when
0.72 mg of STX is ingested whereas acute toxicity symptoms appear when 0.9 to 3.6 mg of STX is
consumed (Levin, 1992).
Their toxicity is due to the presence of carbamoyl and hydroxyl groups in the molecule. These
inhibit nerve conduction by blocking sodium channels causing a disturbance in the propagation of
action potential to muscle cells. Sodium channels consist of a pore-forming α-subunit (of 260 kDa)
associated with auxiliary β-subunit (of 33-36 kDa). There are six distinct receptor sites on sodium
channel α-subunit and a number of neurotoxins such as tetrodotoxin, conotoxins, sea anemone
toxins, brevetoxins and ciguatoxin all bind with high affi nity and specifi city to these six receptor
sites. Characteristic alterations in the permeation and gating of sodium channels are brought out
by these toxins. These have been helpful in understanding the structure and function of voltage-
