Environmental Engineering Reference
In-Depth Information
Hg contamination between the two lakes. gonzalez et al.
(2005) found that expression of genes associated with oxi-
dative stress (including SOD), mitochondrial metabolism,
and apoptosis was up-regulated in the skeletal muscle and
liver of adult male zebrafish (
Danio rerio
) 21 to 63 days after
dietary exposure to 5 µg MeHg g
-1
dry weight. genes asso-
ciated with DNA repair were down-regulated in the skeletal
muscle. However, there was no change in gene expression
in the brains of the exposed fish, including those genes
associated with antioxidant defense, suggesting that a lack
of transcriptional response to MeHg in the brain may con-
tribute to its neurotoxic effects.
Oxidative stress due to MeHg may also affect gonadal
tissue and subsequently inhibit the production of sex
hormones and reproductive success of fish. Manipulative
laboratory experiments and mensurative field studies have
documented effects of MeHg on gonadal development
and histology, sex hormone production, and reproduction
in fish. Friedmann et al. (1996) fed juvenile walleye for
6 months with diets naturally contaminated with 0.04
(control), 0.137 (low-Hg diet) or 0.987 (high-Hg diet) µg
MeHg g
-1
wet weight. Mercury concentrations in the car-
cass of the walleye (whole body minus viscera) were 0.06
(control), 0.254 (low-Hg diet), and 2.37 (high-Hg diet) µg g
-1
wet weight. gonadal development of the male walleye was
suppressed and multifocal cell atrophy and hypertrophy of
cells adjacent to atrophied cells was evident in the gonads.
Hammerschmidt et al. (2002) reported that dietary MeHg
reduced gonad size, delayed spawning, and reduced repro-
ductive effort of female fathead minnows (
Pimephales
promelas
). Relative to control fish, there was a 39% reduction
in spawning success of fish fed diets with 0.88 µg Hg g
-1
dry weight. Mean carcass concentrations of the male and
female fish fed this diet were 0.71 and 0.86 µg Hg g
-1
wet
weight. In a similar study with fathead minnows, Drevnick
and Sandheinrich (2003) found that dietary MeHg sup-
pressed plasma testosterone and estradiol as well as reduced
reproduction. Male fathead minnows fed control diets had
plasma testosterone concentrations 20% and 106% greater
than those fed diets with 0.87 (low) and 3.93 µg (medium)
Hg g
-1
dry weight. control female fish had estradiol con-
centrations about 150% and 400% greater than those fed
low- and medium-MeHg diets, respectively. Klaper et al.
(2006) reported suppression of genes related to endocrine
function—up-regulation in vitellogenin mRNA in indi-
vidual Hg-exposed males and a significant decline in vitel-
logenin gene expression in female fish with increasing Hg
concentrations—as well as changes in expression of other
genes, including those associated with egg fertilization
and development, sugar metabolism, apoptosis, and elec-
tron transport. Altered reproductive behavior of male fat-
head minnows caused by suppressed levels of testosterone
(Sandheinrich and Miller, 2006) also occurred as a result of
MeHg exposure. The synthesis of sex steroid hormones in
fish occurs in the Leydig cells of testes and follicular cells
of the ovaries (Fostier et al., 1983). Drevnick et al. (2006)
found that dietary MeHg significantly increased the num-
ber of apoptotic cells in ovarian follicles of female fathead
minnows. The size of the ovaries and levels of plasma
estradiol were inversely related to the number of apoptotic
follicular cells. Oxidative stress from MeHg exposure was
proposed as the cause of follicular-cell apoptosis and subse-
quent suppression of estradiol and reproductive success in
these fish. crump and Trudeau (2009) thoroughly reviewed
Hg-induced reproductive impairment in fish.
Suppressed concentrations of sex hormones have also
been found in wild fish with elevated concentrations of
Hg. There was a significant negative correlation between
concentrations of Hg in the muscle of male white sturgeon
(
Acipenser transmontanus
) in the lower columbia River and
concentrations of plasma testosterone and 11-ketotestoster-
one (Webb et al., 2006). An inverse relationship between
the relative size of the testes and concentrations of Hg
suggested that MeHg may have been responsible for sup-
pression of sex-steroid production in immature male fish.
Similarly, there was a negative correlation between con-
centrations of Hg in the liver of female fish and plasma
estradiol. There was also a significant negative correla-
tion between concentrations of Hg in the gonad and liver
and the condition factor and relative weight of the fish.
conversely, a positive correlation between Hg in the axial
fillet and plasma 11-ketotestosterone in male largemouth
bass (
Micropterus salmoides
) from three lakes in New Jersey
was reported by Friedmann et al. (2002). However, there
was no significant relationship between Hg in the muscle
of the largemouth bass and plasma testosterone concentra-
tion. Tan et al. (2009) have reviewed the endocrine effects
of Hg in humans, fish, and wildlife.
In summary, environmentally relevant concentrations of
MeHg resulting from non-point source pollution are suffi-
cient to cause oxidative stress in fish. Evidence of oxidative
stress is manifested at the molecular, biochemical, cellular,
and organismal levels of biologic organization. Future stud-
ies should seek to determine specific links between bio-
markers of MeHg exposure and oxidative stress to effects
on reproduction and population change in wild fish popu-
lations and more clearly define the deleterious effects of
low-level Hg exposure.
Mercury in Amphibians and reptiles
Despite their overall biomass and importance to aquatic
and terrestrial ecosystems, Hg and MeHg bioaccumulation
dynamics and toxicity in amphibians and reptiles are not
well studied, especially as compared with other vertebrate
taxa such as birds, mammals, and fish. However, vari-
ous studies have reported Hg concentrations in tissues of
a number of amphibian and reptiles species. Population
declines in amphibians are well documented and are likely
caused by multiple stressors, including climate change,
exotic species introductions, fungal pathogens, habitat
loss and degradation, and exposure to toxic pollutants,
