Biology Reference
In-Depth Information
in CHO-K1 cells as well as in human lymphocytes. Another explanation given to the DNA strand
breaks is the probable role of MC-LR in inhibiting the DNA repair enzymes (Lankoff
et al
., 2004).
DNA-dependent protein kinase is the key enzyme identifi ed in the repair of radiation-induced DNA
breaks by mediating the non-homologous end joining (Douglas
et al
., 2001). Lankoff
et al
. (2006)
demonstrated that pre-treatment of human lymphocytes and human glioblastoma cell lines MO59J
and MO59K with MC-LR (0.5 mg ml
-1
) not only inhibited repair of radiation-induced damage but
also enhanced the frequencies of chromosomal aberrations including dicentric chromosomes.
viii) Protection against toxicity
:
The role of membrane bound vitamin E in protecting against
MC-LR toxicity was investigated in mice fed with lower or higher vitamin E supplements, 8.33
or 33.3 units mouse
-1
day
-1
for 4 weeks, respectively. The evaluation of vitamin E protection was
performed by determining the levels of LPO, alanine transaminase and glutathione S-transferase.
Some protection was noticed at lower vitamin E concentration by limiting toxin-induced leakage
of alanine transaminase and glutathione-S-transferase. A higher dose of vitamin E signifi cantly
increased the rate of mortality and percentage weight loss of liver of mice when challenged with
lethal dose of MC-LR (Gehringer
et al
., 2003b). BALB/c mice pre-treated with selenium (sodium
selenite administered at the rate of 1.5 µg mouse
-1
day
-1
for two weeks) reduced the liver damage
caused by MC-LR and decreased alanine trasaminase and LPO levels. However, the increase of liver
glutathione peroxidase activity indicated the possible route of selenium protection in mice (Gehringer
et al
., 2003a). In an attempt to fi nd out a suitable chemoprotectant against the toxicity of MC-LR, Rao
et al
. (2004) screened a variety of substances either by way of pre-treatment, co-treatment or post-
treatment against the lethal dose of MC-LR (100 µg kg
-1
body weight) in a mouse (Swiss albino female)
bioassay. Though some of them offered no protection (D-glucose, mannitol, L-cysteine, naringin
and amifostine) but extended the survival time. Some others like N-acetylcysteine, glutathione
and Trolox
®
partially protected on either pre- or co-treatment. On the other hand, pre-treatment
with rifampin (25 mg kg
-1
), cyclosporin (10 mg kg
-1
) and silymarin (400 mg kg
-1
) gave complete
protection. Of these three agents, the fi rst two gave complete protection when co-administered with
MC-LR. However, in post-treatment rifampin was effective when administered after 15 minutes.
Any chemoprotectant either should possess the ability to inhibit the interaction of MCs with PPs
or inhibit the uptake of the toxin into hepatocytes. It was further suggested that possibly rifampin,
cyclosporin and silymarin conferred protection by inhibiting intracellular transport of the toxin
into the liver (Rao
et al
., 2004). Oxidative damage caused by nodularin is alleviated in presence of
melatonin. The activities of SOD, catalase, glutathione peroxidase in mouse exhibited an increase
when co-treatment of nodularin (1, 5 µg kg
-1
body weight) was given along with melatonin (5, 10, 15
mg kg
-1
body weight) for seven days. A treatment with nodularin (5 µg kg
-1
body weight for seven
days) followed by a post-treatment with melatonin (5, 10, 15 mg kg
-1
body weight) also protected
from the oxidative damage when compared to nodularin treatment alone (Lankoff
et al
., 2002).
II. NEUROTOXINS
These are one of the most toxic compounds produced by cyanobacteria that interfere with the
functioning of neuromuscular system. Species of
Nostoc
(Davidson, 1959),
Anabaena
(Carmichael
et
al
., 1990),
A
.
planctonica
(Bruno
et al
., 1994),
A
.
fl os-aquae
(Devlin
et al
., 1977; Carmichael
et al
., 1975,
1979),
Oscillatoria
(Sivonen
et al
., 1989a; Edwards
et al
., 1992; Skulberg
et al
., 1992) are reported to
produce four neurotoxins, i.e. anatoxin-a, anatoxin-a(s), STX and neo-STX (Ressom
et al
., 1994;
