Environmental Engineering Reference
In-Depth Information
(Valavanidis et al., 2006), including that caused by MeHg.
For example, Berntssen et al. (2003) fed diets containing
0.03 (control), 4.35 (medium), or 8.48 (high) µg MeHg g
-1
dry weight to juvenile Atlantic salmon (
Salmo salar
) for
4 months. Dietary MeHg had no effect on growth, body
condition, or mortality of the salmon parr. However, induc-
tion of redox defense enzymes and lipid peroxidation of
tissues due to MeHg exposure was apparent. The activ-
ity of SOD increased twofold in the brains of fish fed the
medium-MeHg diet. In the brains of fish fed the high-MeHg
diet, levels of SOD and glutathione peroxidase (gSH-Px)
decreased significantly, which suggested failure of the redox
defense system, and there was a sevenfold increase in the
concentration of thiobarbituric acid reactive substances,
a product of lipid peroxidation. The high-MeHg diet also
significantly inhibited cerebral monoamine oxidase in the
brain, an observation that was associated with reduced
behavioral activity by the fish. Brains of fish exposed to the
medium- and high-MeHg diet had Hg concentrations of
1.16 and 0.68 µg g
-1
wet weight, respectively, and exhibited
severe vacuolization and cell necrosis. Increased activity of
SOD and gSH-Px was also measured in livers of fish receiv-
ing the high-MeHg diet. The apparent decline in brain Hg
accumulation at the high (10 µg g
-1
) compared with the
medium (5 µg g
-1
) MeHg diet was related to gross brain
edema in the highest-dose group, which decreased apparent
tissue Hg concentration on a wet weight basis. (Berntssen
et al., 2003).
Altered histology in liver and other internal organs of
fish may occur as a result of oxidative stress due to MeHg
exposure. Mela et al. (2007) fed adult
Hoplias malabaricus,
a
neotropical species, control or MeHg-contaminated diets at
a dosage equivalent to 0.075 µg MeHg g
-1
wet body weight
for 70 days; subsequent Hg concentrations in the muscle of
the fish were 0.67 (control diet) and 1.45 µg g
-1
wet weight
(treatment diet). An increased number of melano-macro-
phage centers were among the numerous cellular changes
observed in liver and head kidney of exposed fish. These
groups or aggregations of macrophages contain yellow or
black pigments and collect components of damaged cells,
including those damaged by oxidation and lipid peroxida-
tion (Wolke, 1992). Moreover, there were increased num-
bers of dead and abnormal cells and necrotic tissues in fish
receiving the MeHg-contaminated diet.
changes in biochemistry and tissue histology associated
with oxidative stress occur in wild populations of fish
subject to non-point source contamination by Hg. Larose
et al. (2008) reported altered glutathione metabolism among
yellow perch (
Perca flavescens)
) and walleye (
Sander vitreus
)
from four boreal lakes in canada. The activity of sele-
nium-dependent glutathione peroxidase and glutathione
S
-transferase (gST) were negatively related to MeHg in the
liver of yellow perch from the lake with the highest mean
Hg concentration in the fish. In the lake with the high-
est mean concentration of MeHg in the walleye, activity
of gST and glutathione reductase were related to liver size,
which, in turn, was negatively related to the concentration
of MeHg in the liver. A decrease in the size of the liver may
have been due, in part, to MeHg causing oxidative stress
and lipid peroxidation (Larose et al., 2008).
Drevnick et al. (2008) reported that liver damage due
to lipid peroxidation and poor body condition were cor-
related to Hg concentration in northern pike (
Esox lucius
)
from eight inland lakes of Isle Royale, a relatively pristine
and remote U.S. National Park in Lake Superior. Liver color
(absorbance of liver homogenate at 400 nm) and total Hg
(range 0.048-3.074 µg g
-1
wet weight) were positively cor-
related; concentration of total Hg in the liver was positively
related to that in the axial fillet (range, 0.069-0.622 µg g
-1
wet weight). Lipofuscin was subsequently identified as the
pigment responsible for altered liver color. An analysis of
covariance revealed that lipofuscin accumulation was pri-
marily associated with Hg exposure, and this association
was independent of any normal accumulation of lipofuscin
due to aging (Drevnick et al., 2008). Lipofuscin is formed as
a result of lipid peroxidation of membranous organelles and
is a pigment frequently found in melano-macrophage cen-
ters (Wolke, 1992). Raldúa et al. (2007) found higher con-
centrations of Hg and a greater prevalence of melano-mac-
rophage centers and lipofuscin in livers of fish downstream
from a chlor-alkali plant than in fish collected upstream
from the plant. Schwindt et al. (2008) examined the rela-
tionship between melano-macrophage centers and Hg con-
centrations in salmonids (lake trout,
Salvelinus namaycush;
brook trout
, S. fontinalis;
cutthroat trout,
Oncorhynchus
clarkii;
and rainbow trout,
O. mykiss
) obtained from 14 lakes
in eight U.S. national parks or preserves. Independent of
fish age, the number of melano-macrophage centers in the
kidney and spleen were positively related to whole-body
concentrations of MeHg. Although more than 90 pesticides
and other chemical compounds were measured in brook
trout, Hg alone explained more than one third of the vari-
ability in macrophage aggregates in the spleen.
Alterations in gene transcription can be used to detect
the induction of antioxidant defenses and other effects
following MeHg exposure, to provide additional insight
into MeHg's mode of toxicity. Moran et al. (2007) com-
pared levels of gene expression in livers of cutthroat trout
from high-altitude lakes of western Washington state that
had low (Skymo Lake) and high (Wilcox Lake) levels of
Hg contamination. Of the 147 genes evaluated in the fish,
the expression of 45 was significantly different between
the two lakes, including those associated with cell main-
tenance, immune function, stress response, metabolism
and growth, reproduction, and response to xenobiotics. For
example, expression of glutathione peroxidase in high-Hg
trout from Wilcox Lake was more than 1300% that in low-
Hg trout from Skymo Lake. Although low concentrations
of organic contaminants (e.g., dichlorodiphenyldichlo-
roethylene [DDE] and polychlorinated biphenyls [PcBs])
were also present in the trout, differences in transcrip-
tional responses of fish were attributed to differences in
