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OCR for page 304
Mercury
Mercury (Hg), a heavy silver-white element also caned quicksilver, was
named for Mercury, the Roman god of commerce and gain. It is the
only rnetaBic element found in the liquid phase at norms room tem-
perature. Cinnabar and calomel, the principal ores of mercury, have
been mined for 2,300 yews (D'Itri, 1971~. The most important industnal
uses for the metal involve electrical apparatus, chioralkali production,
water-base paint, and agriculture fungicides.
Mercury toxicosis has received considerable attention recently be-
cause of poisonings that have occurred in the human population (Curley
et al., 1971; Won, 1973; CIarksonet all, 19761. Animals can tee exposed
to mercury contamination from air, soil, and water, as well as from that
which may be ingested with feed. The concentration of mercury in the
environment is, in part, the result of waste products from manufactur-
ing processes that utilize mercury or of the disposal of products con-
tain~ng mercury. Fossil fuel combustion (Billings and Matson, 1972),
smelting of commercial ores, and agricultural fungicides also contribute
mercury to the environmental burden (D'1tri, l971~. Recent reviews on
mercury include Underwood (1977), D'Itn (1971), and Nelson et al.
(1971~.
ESSENTIALITY
Based on present evidence, mercury is not considered an essential
element for living organisms (Underwood, 1977~.
304
OCR for page 305
Mercury
METABOLISM
305
Metabolism of mercury has been reviewed by MacGregor and CIarkson
(19741. Living organisms can concentrate mercury when an excess is
available but the level of concentration depends on the type of organism
and the form of mercury contamination (D'Itri, 19711. Inorganic mer-
cury can be biomethylated before or after ingestion (Gage, 19751; con-
sequently, it is necessary to discuss metabolism of the element in both
forms. The radical, in which mercury is attached directly to a carbon
atom, is the organic form (MacGregor and CIarkson, 1974~. The mer-
curic ion (Hg2+) is a potential in viva metabolite of any of the major
mercurials (Hammond, 19731.
The short-chain alky~mercurials are more readily absorbed and thus
more toxic than other mercurial compounds when ingested. Degree of
toxicity decreases with increased length of the carbon chain. Alky~mer-
curtals are more toxic to living organisms because they are more stable
biologically than other forms of mercury (Monday biological half-time)
and resist degradation to inorganic mercury, which can be eliminated
from the body. Also, the alky~mercurials can readily cross the blood-
brain barrier and attack the central nervous system (D'Itri, 19711. In-
organ~c mercury follows metabolic pathways similar to those of zinc
and cadmium, but interrelationships between the mercuric ion and
other trace elements have not been investigated to any extent. Ele-
mental mercury vapor is more likely to cross the blood-bra~n barrier
than inorganic mercury salts (Magos, 1968), but only traces (30 ppb) of
either appear in the fetus, milk, or eggs (Clarkson et al., 1973~.
Since organic mercunals are more highly lipid-soluble, the organic
mercury salts are absorbed more completely than inorganic mercury
salts. Methy~mercury is lipid-soluble, and absorption is 60 to 100 per-
cent of intake for all species studied. CIarkson (1970) reported that only
2 percent of ingested inorganic mercuric compounds was absorbed,
while, in contrast, Fitzhugh et al. (1950) found that rats can absorb 50
percent of oral mercuric acetate. The mercuric ion was absorbed at 15
percent or less of intake with highest tissue accumulation occurring in
the liver and kidney (Ellis and Fang, 19671. Methy~mercury was ab-
sorbed' more readily (15 to 35 times) than inorganic mercury from
ligated segments of rat gut. The relative order of methylmercury ab-
sorption was as follows: duodenum > stomach = ileum > jejunum.
There was no difference in absorption of inorganic mercury among
sections of the intestinal tract (Sasser et al., 197X). Studies by Ruben-
stein and Soares (1979) based on intestinal wall mercury concentration
indicated that the upper small intestine appeared to be the site of pref-
OCR for page 306
306 MINERAL TOLERANCE OF DOMESTIC ANIMALS
erentia] absorption of CH3Hg+, while Hg2+ was absorbed in the ileum
and lower intestine in broiler chicks.
Following ingestion, methylmercury was distributed widely in all
tissues, including muscle, fetus, milk, eggs, hair, and feathers, but the
concentrations were all below those of the target organs, brain, liver,
and kidney. More than 9? percent of the total 203Hg in egg white from
chickens fed 20 ppm mercury as CH3HgC1 was associated with oval-
bumin (Magat and Sell, 1979~. PhenyI- and ethylmercuric salts tend to
dissociate more rapidly than methy~mercuric salts in viva (Clarkson et
al., 19731. When methy~mercuric chloride was double-labeled and fed
to rats, the 203Hg-~4C bond was cleaved in vivo, 8 percent in kidney and
6 percent in liver and brain (Garcia et al., 1974b).
Ingested labeled 203Hg2+ accumulated in the rumen wall of calves
(Ansari et al., 1973), suggesting a rapid attachment of Hg2+ to tissue
protein of the gastrointestinal tract. Labeled CH3Hg+ did not exhibit
this property (Neathery and Miller, 1975~. Apparent absorption of
either form appears to be lower in ruminants than in nonruminants, but
the biological half-time retentions for the ruminant (7X to 88 and 22
days, respectively, for HgCI2 and CH3HgCI) were similar to those esti-
mated for some other species (Norseth and Clarkson, 1970; Skerfving,
1972, 1974; Khan, 1974; Hollins et al., 1975; Sell and Davidson, 1975~.
Effects of mercury on ruminal microflora or epithelium appear not to
have been investigated.
Mercuric ions initially enter the serum fraction of blood and organic
mercury enters the erythrocytes (Alberg et al., 1969), but with time the
distribution becomes similar. The major mercury excretion route is
fecal, regardless of mercurial form. With repeated exposure even to low
mercury levels, the rate of mercury accretion may exceed the rate of
excretion, resulting in tissue accumulation of the metal and eventual
impairment of physiological function. Methylmercury is not contin-
uously accumulated if given over a long period of time. A steady state
is reached where excretion equals intake. Time required to reach the
steady state depends on the half-time and species involved. In rats, all
tissues except hair showed saturation kinetics with repeated intake of
methylmercury (Salvaterra et al., 1975~. Thiol groups in tissue pro-
teins have a high affinity for mercurials, and a major excretory mech-
anism appears to be via extrusion of intestinal epithelial cells (Norseth
and Clarkson, 19711.
Calves were given a single intravenous dose of mercury as
CH32°3HgC1 or 2°3HgCl2 (Stake e! al., 1975~. Mercury excretion in total
feces and urine was higher for HgCI2 (28.3 versus 8.1 percent of the
OCR for page 307
Mercury
307
dose) than for CH32°3HgCI. Retention of 203Hg from Hack was 2~
times greater in kidney, liver, spleen, lung, bone, serum, and intestine
but lower in brain, muscle, heart, and red blood cells than that from
CH3HgCl. Biliary excretion of mercury as 2°3HgCl2 or CH32°3HgC!
following intravenous injection is a minor route. Over a 2-hour period,
less than 0.5 percent of the amount administered (0.03, 0.1, 0.3, 1.0, and
3.0 mg mercury per kilogram of body weight), regardless of dose or
form of mercury, was excreted in the bile of rats. Pretreatment with
pregnenolone -16 a-sarbonitrile (PCN) doubled the amount of mercury
excreted in bile (Klassen, 1975a). With time or increased dosage, this
compound was reabsorbed completely within 1 hour in rats (Norseth
and Clarkson, 1970, 1971; Tichy et al., 1975) and resulted in redistr~bu-
tion of methylmercury in the animal. Only one-half the mercuric ion in
higher-molecular-weight biliary proteins was reabsorbed in rats 1 hour
after dosing. However, in studies with broiler chicks (Rubenstein and
Scares, 1979), bile served as an important route of mercury excretion
for HgCl2 but a less important route for CH3HgC12. These studies seem
to contradict those of Norseth (1974), in which the organomercurials
were more readily excreted into bile. The difference may be the mode
of administration. Methylmercury glutathione and methylmercury
cysteine are the major mercury components in bile following injection
of CH3HgCl (Norseth and Clarkson, 1971), but, when this mercury
source is given orally, Hg2+ appears as the major form in bile (Berlin et
al., 1975).
Formation of metallothioneins has been suggested as a means of
detoxification for inorganic cadmium and mercury (Shaikh et al., 1973;
MacGregor and CIarkson, 1974; Piotrowski et al., 1974a,b) but has not
appeared to affect detoxification of methy~mercury (Chen et al., 1973,
1975a). The metalloproteins appear to have a limit of elemental satur-
ability (Cousins, 1974; Colucci et al., 1975~. The amount of mercury
required to saturate the sites was 300 500 mg mercury and corre-
sponded to levels required to elicit frank nephrotoxicity (MacGregor
and Clarkson, 1974~. Although inorganic mercury is absorbed at 5 per-
cent or less of intake, it is sequestered preferentially in tissue proteins
in the kidney, liver, and gastrointestinal tissue. With repeated low
dosage, rate of absorption can exceed the excretory capacity, and, at
tissue elemental saturation, extrusion of damaged cell proteins bearing
the toxic element may occur. The potential capacity for biomethylation
or demethylation of inorganic microelements in viva appears to influ-
ence the degree and mode of toxicity.
Metallothioneins loaded with "abnormal'' metals apparently are in-
OCR for page 308
308 MINERAL TOLERANCE OF DOMESTIC ANIMALS
capable of significant turnover in tissue cytoplasm, and this fact sug-
gests that high concentrations of "abnormal" metals in association with
metallothionein in target tissues are due to the apparent absence of
turnover (Mills, 1974; Chen et al., 1974, 1975b) rather than to increased
de novo synthesis (Fowler and Nordberg, 1975; Nordberg and Nord-
berg, 1975; Shaikh and Smith, 1975; Webb, 1975~.
SOURCES
The more important sources of mercury under practical feeding condi-
tions would be fish protein concentrates and contaminated seed grain,
which may be used accidentally. Fish concentrate methylmercury by
ingestion of contaminated food, as well as by direct uptake from the
water. Johnels (1967) reported that the biological magnification of each
organism appears to be a function of its metabolic rate and that pike
have exhibited muscle mercury levels that were 3,000 times greater
than the level of the water from which they were taken. Rucker and
Amend (1969) found that rainbow trout exposed to water containing 60
ppb of methylmercury daily for 1 hour over 10 days had mercury levels
of 4,000 and 17,300 ppb (dry basis) in muscle and kidney, respectively.
Fish taken from Korean waters contained from 20 to 580 ppb (fresh
basis) (Won, 19?3), while walleye and pike from Ball Lake, Ontario,
contained 3.24 and 5.55 ppm mercury on a wet tissue basis (Annett et
al., 1975~.
There are several citations of poisoning in human populations from
treated seed grains (Hag, 1963; Ordonez et al., 1966; Curley et al.,
1971; Bakir et al., 1973; Clarkson et al., 19761.
The mercury content of cow's milk can range from 3 to 10 ppb
(Mullen et al., 1975; Rob et al., 19751. At 24 days following an 8-day
exposure, goats milk had 1.22 and 0.22 percent of total oral dosages,
respectively, of organic and inorganic mercury (Sell and Davidson,
19751. All mercury from either source was in milk proteins. Similar
results were reported for CH3Hg+ in milk from rats (Garcia et al.,
1974a,b).
Mercury concentration in hair and feathers of animals has been
highly correlated with tissue turnover of mercury (Nelson et al., 1971;
Herigstad e! al., 1972; Skerfving, 1972; Huckabee et al., 1973), and
these tissues are major excretion routes that should be included in
estimates of mercury retention (Hollies e' al., 1975~. Accumulation of
mercury in hair and feathers could cause contamination of processed
hair and feather meals used as protein supplements for livestock.
OCR for page 309
Mercury
TOXICOSIS
309
Mercury toxicosis has been reviewed by Mills (1974), Buck (1975),
Neathery and Miller (1975), Ammerman et al. (1977), and Gruber et al.
(1978~. Accumulation of metalloproteins during mercury intoxication to
intolerable tissue threshold levels could be responsible for renal cortical
tubular epithelial damage and subsequent renal failure (Fowler, 1972~.
Epithelial damage has been reported also in intestinal walls following
mercury dosage to rats and swine (Norseth and Clarkson, 1971; Piper
et al., 1971~. Lysosomes were the major sites of renal tubular mercury
deposition in rats fed HgCI2 or ClI3HgOH (Fowler et al., 1975; Madsen
and Christensen, 1975~. Ingestion of 20 ppm mercury by rats appeared
to result in exocytosis of the lysosomal material into the tubular lumen.
These effects were thought to be involved in the appearance of urinary
protein. Mercurials have a high affinity for sulfllydry! groups altering
SH-containing molecules (MacGregor and Clarkson, 19741.
LOW LEVELS
The onset of chronic mercury toxicosis is variable and slow. The mani-
festations include dysfunction of the central nervous, digestive, geni-
tourinary, respiratory, and muscular systems, as well as skin and visual
problems (D'Itri, 1971~. Daily consumption of methylmercury at 0.1 mg
mercury per kilogram of body weight was tolerated by ~week-old
calves for 90 days, but 0.2~.4 mg/kg produced methy~mercury toxi-
cosis in 75 days (Herigstad et al., 1972~. Methylmercury dicyandiamide
was toxic for cattle and sheep at 0.225 mg mercury per kilogram of body
weight. Animals displayed signs of incoordination and unsteady gait
within 40 to 60 days (Wright et al., 1973~.
Tryphonas and Nielsen (1970) fed pigs phenylmercuric chloride for
90 days and observed no problems with 0.19 me mercury per kilogram
of body weight; but increased tissue accumulation of mercury occurred
with 0.38 and 0.76 mg/kg, while 2.28 and 4.56 mg mercury per kilogram
resulted in weight loss and kidney and colon necrosis.
With 0.075 or 0.150 mg mercury as methylmercury dicyandiamide
per kilogram of body weight, chickens showed increased mercury accu-
mulation in tissues (wright et al., 19731. Miller et al. (1967) fed mercuric
chloride and phenylmercuric acetate to day-old chicks at 2 or 20 ppm
mercury. Feeding 2 ppm as either form produced mercury accumula-
tion in the liver and kidney in 20 days; however, 20 ppm mercury
produced the same result in 5 days. Laying hens given 10 ppm mercury
as CH3HgC1 for 70 days accumulated 55 percent of the mercury in the
OCR for page 310
310 MINERAL TOLERANCE OF DOMESTIC ANIMALS
eggs with 80 percent of that amount associated with the albumin (Sell
et al., 1974~. Methylmercury dicyandiamide (33 ppm mercury) pro-
duced a death rate in 30 days of 90 percent in pheasants, 85 percent in
ducks, and 7.5 percent in chickens (Gardiner, 1972~. Daily consumption
of 1 ppm mercury as mercuric or methy~mercuric chloride by mice for
life did not affect health and longevity, but 5 ppm was toxic (Schroeder
and Mitchener, 1975~. Daily consumption of greater than 1 mg mercury
per kilogram of body weight as alky~nercur~als was tox~c.for rats and
young swine (Tryphonas and Nielsen, 1970, 1973; Khera and Taba-
cova, 19731.
Adult mink were not affected by 0.1 ppm mercury as CH3HgC! for 93
days, but 1.1 ppm increased tissue mercury and levels from 1.S to 15
ppm proved lethal (Wobeser e' al., 1976b). Sperm from steelhead trout
exposed to 1 ppm or greater mercury as CH3HgC1 showed decreased
ability to fertilize eggs (McIntyre, 1973~. Mercury in the axial muscle of
large benthopelagic fish taken at 2,500 m deep ranged from 0.03 to 0.76
ppm on a wet weight basis (Barber et at., 19721. Tuna and swordfish
have been found to have tissue levels of mercury in excess of 0.5 ppm
(Ganther et al., 19721.
HIGH LEVELS
Comparisons among species for tolerance to cumulative toxic elements
indicate that tissue saturation kinetics are related to body mass and
duration of exposure. With high body burdens of methylmercury,
pathology of many tissues may be simultaneous, but nerve tissue is
particularly vulnerable and critical. Ultrastructural pathology usually
occurs well in advance of the clinical signs for peripheral neuropathy.
The acute signs that result from ingestion of mercury include nausea,
vomiting of blood-stained mucus, severe gastrointestinal irritation and
abdominal pain, shock, and cardiac arrhythmias. From 1 day to 2
weeks following exposure, reactions include excessive salivation, foul
breath, loose teeth, soft spongy gums, and a blue-black gum line caused
by a mercury-su~ydryl complex. Death is usually caused by uremia
(D 'Itri, 1971~. The primary clinical lesion in mercury toxicosis is acute
renal failure due to injury in renal epithelial tubular cortical tissue
(Burger and Siegel, 1975; Preuss et al., 1975~. Buck (1975) described
clinical signs that were similar for cattle acutely poisoned with organic
or inorganic mercury exposure. From the onset of clinical signs, the
average time to death was 20 days but ranged from 1 to 43 days.
Palmer et al. (1973) produced mercury toxicosis in cattle, sheep, and
turkeys with an alkylmercury fungicide administered daily in capsules.
Cattle and sheep receiving 0.48 mg mercury per kilogram of body
OCR for page 311
Mercury 31 1
weight,died within 7 to 27 and 13 to 31 days, respectively. Turkeys
developed weakness and incoordination in 13 to 14 days with 0.16 mg
mercury per kilogram of body weight.
Pigs tolerated a single oral dose of 2.5 mg mercury per kilogram of
body weight as methylmercury dicyandiamide. With 5 and 10 mg/kg,
anorexia, reduced gain, central nervous system depression, vomiting,
muscular tremors, and increased tissue mercury concentration were
observed. Death occurred in 7.5 to 29 days, 7 days, 24 hours, and 12
hours for 20, 40, 80, and 160 mg/kg of body weight, respectively (Piper
et al., 1971~.
Differences in tolerance to organic mercury among sex and strain of
chicks, swine, and rats have been reported (Miller et al., 1970; Piper et
al., 1971; Parizek et al., 19741. When hens were fed 10 ppm mercury as
CH3HgC1 for 10 days, eggs contained 55 percent of the total hen dose
after 70 days (Sell et al., 1974~. Egg mercury levels increased sharply
to 12 days and declined during the next 58 days. At lo ppm, mercury
methylmercury produced 50 percent mortality in 16 weeks with
Japanese quail (El-Begearmi et al., 19741. Dietary methy~mercury was
acutely toxic at 20 ppm for Japanese quad] (Stoewsand et al., 19741. In
Japanese quail and chicks, however, 25 ppm mercury as mercuric ion
had no effect on growth, fertility, or egg hatchability but did increase
mortality (Thaxton and Parkhurst, 1973a; Thaxton e' al., 19741.
FACIORS INFLUENCING TOXICITY
Studies with one broiler strain and three White Leghorn strains indicate
genetic differences in the degree of tissue concentration of mercury
from dietary fish meals (March et al., 1974~. Mercuric chloride up to 500
ppm expresses a more toxic effect in Japanese quail when incorporated
in the diet as a dry salt rather than as a solution, regardless of the
solvent system (ethanol, methanol, or water) (El-Begearmi et al., 1979~.
Selenite or selenate administered to rats orally or parenterally (Parizek
et al., 1974) or Japanese quad! (El-Begearmi et al., 1977a) reduced acute
or chronic toxicosis of mercuric-or methylmercuric ions by redistribu-
tion of tissue mercury as opposed to increased excretion of the element.
Dietary selenium (S ppm selenium) protected rats against toxicity of
otherwise acute lethal doses of methylmercury and mercuric mercury
(Potter and Matrone, 19741. Selenite increased the percentage of mer-
cury retained in liver and spleen but decreased that in kidney compared
with animals untreated with selenium. In selenium-deficient rats in-
jected simultaneously with 75SeO32~ and 203Hg2+, a protein of
sulfLydrylselenium-mercuric components was identified in plasma 20
hours postinje-ction, suggesting that the protein was formed after
OCR for page 312
312 MINERAL TOLERANCE OF DOMESTIC ANIMALS
isotopes were metabolized (Burk et al., 1974~. Reduction of. kidney
mercury with redistribution in other tissues appears to reduce toxicosis
(Ganther and Sunde, 1974; Stillings et al., 1974; Klassen, 1975b). Simi-
lar results were repotted with rats receiving selenium and organic or
inorganic mercury (Chen et al., 1974; Moff~tt and Clary, 1974; Chen et
al., 197Sa; Ohi et al., 1975~. It has been postulated that cystine or thiols
provide protei~sulfur binding sites for mercury, that selenium cata-
lyzes mercury to change to a less damaging form, or that selenium
reacts directly with mercury.
The addition of 5 ppm selenium as Na2SeO3 to diets containing 20
ppm mercury as CH3HgC! reduced the death rate in Japanese quail by
7X percent (Stoewsand et al., 1974~. Other authors have indicated that
simultaneous equimolar ratios of selenium and mercury are necessary
to prevent toxicity of either (Ganther and Sunde, 1974; Moff'tt and
CIary, 1974~. Selenium as sodium selen~te at 8 ppm alleviated reduction
in egg production induced by feeding 20 ppm mercury as CH3HgC! in
Japanese quail, but not in chickens (Sell, 1977~. Either 4 or 8 ppm
selenium partially prevented decreased egg production and hatchability
in chickens produced by 10 ppm mercury as CH3HgC1 (Emerick e! al.,
1976~. Selenium as Na2SeO3 at 0.5 ppm increased weight gain in rats
receiving 1, 5, 10, and 25 ppm mercury as CH3HgOH in drinking water
(Ganther et al., 1972~.
Blackstone et al. (1974) fed maintenance levels of ascorbic acid to
guinea pigs and provided mercuric ion (8 mg mercury per kilogram of
body weight as HgCl2) in drinking water. Ascorbic acid levels were
depressed in brain, adrenals, and spleen. Mercury deposition in kidney
and liver increased with ascorbic acid level.
Vitamin E has been shown to protect against the toxic effects of
methy~mercury in Japanese quad! (Welsh and Soares, 1975) and rats
(Welsh, 1976, 1979) and organic mercury in Japanese quail (El-
Begearmi et al., 1977b).
The specif~c antidote for mercury poisoning is dimercaprol, which
can be used in conjunction with proteins such as milk and eggs to bind
mercury still in the gastrointestinal tract. Gastric ravage with sodium
formaIdehyde sulfoxalate will reduce d~valent mercury to the less toxic
monovalent form (Siegmund and Fraser, 1973~.
TISSUE LEVELS
Samples of kidney and liver obtained from slaughter animals in Canada
(pork, poultry, and beef) ranged from undetectable (~0.01 ppm) to
OCR for page 313
Mercury
31-3
0.097 ppm mercury in wet tissue for 265 samples (Prior, 19761. Muscle
accounted for 72 percent and liver 7 percent of a tracer dose of methyl-
mercury in ruminants 1 week following ingestion (Neathery et al.,
1974~. At 24 days following an 8-day exposure, milk of goats accounted
for 1.22 and 0.22 percent of total oral organic and inorganic mercury,
respectively (Sell and Davidson, 1975~. Similar results were reported
for CH32°3Hg in milk of rats (Garcia et al., 1974a,b). Mercury content
of cow's milk may range from 3 to 10 ppb (Mullen et al., 1975; Rob et
al., 1975~. Methy~mercury (CH3Hg+) comprises 75 to 90 percent of
mercury in fish and is transferred through the food chain with the C-Hg
bond intact. The methylmercury was not removed by boiling fish
(Westoo, 19661. When breast of ducks that had received single ore]
doses of methy~mercury was cooked by dry or moist heat, mercury
levels of meat and drippings were not different on a dry matter basis
from uncooked meat (Hough and Zabik, 1973~.
MAXIMUM TOLERABLE LEVELS
Dairy calves tolerated mercury as methylmercury at a level of 0.1 mg
per kilogram of body weight (about 3 ppm in their diet) for 90 days
without visible adverse effects, while a level of 0.2 mg/kg resulted in
toxicosis. Yearling sheep receiving 0.22 mg mercury per kilogram of
body weight orally as methylmercury dicyandiamide exhibited incoor-
dination and unsteady gait after 4~50 days of exposure. Swine have
received 0.38 mg mercury per kilogram of body weight daily by capsule
in the form of either phenylmercuric chloride or methylmercuric
dicyandiamide for 6~90 days without visible adverse effects. In-
creased mercury in tissue and signs of mercury toxicosis occurred with
a level of 0.76 mg/kg body weight. Chickens, turkeys, ducks, and
pheasants tolerated 3.3 ppm supplemental dietary mercury without
evidence of adverse effects, although increased tissue mercury has
been shown at levels lower than this. Elemental mercury was tolerated
at considerably higher levels than this by Japanese quail. Daily con-
sumption of drinking water containing 1 ppm mercury as CH3HgC1 by
mice did not affect health or longevity, but 5 ppm of either CH3HgC1 or
HgCl2 resulted in toxicosis and death.
The suggested maximum tolerable dietary level for domestic animals
is 2 ppm mercury for both the organic and inorganic forms. Research
with several species indicates that animals can tolerate higher dietary
quantities of the inorganic form, but the maximum tolerable level for
this form was not increased because of the possibility of elevated tissue
OCR for page 314
314 MINERAL TOLERANCE OF DOMESTIC ANIMALS
levels of the element. Studies with rats and mice support the proposed
tolerance level for domestic animals, but limited research with mink
suggests that this species is much more sensitive to mercury.
SUMMARY
Mercury toxicity has received considerable attention.because of
poisonings that have occurred in the human population. The metal is
not essential in animal or human nutrition, and its level of concentra-
tion in living organisms depends on the type of organism and the form
of mercury to which the organism is exposed. Biomethylation of inor-
gan~c mercury occurs in the environment or the animal and increases
He potential for toxicity. Animals can be exposed to mercury contam'-
nation from air, soil, or water, while the major feed sources are fish
protein concentrates or the accidental use of treated seed grain.
Acute toxic signs include nausea, vomiting, severe gastrointestinal
imitation and pain, shock, and cardiac arrhythmias. Death usually re-
sults from uremia, caused by damage to renal epithelial tubular cortical
tissue. Dietary selenium has been reported to decrease mercury tox~c-
ity.
OCR for page 317
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322 MINERAL TOLERANCE OF DOMESTIC ANIMALS
REFERENCES
Alberg, G., L. Ekman, R. Falk, U. Greitz, G. Persson, and J. Snibs. 1969. Metabolism
of methyl mercury (203Hg) compounds in man. Arch. Environ. Health 19:478.
Al-Fayadh, H., A. W. R. Mehdi, K. Al-Soudi, A. K. Al-Khazraji, N. A. Al-Jiboori, and
S. Al-Muraib. 1976. Effects of feeding ethyl mercury chloride to chickens. Poult. Sci.
55:772.
A'nmerman, C. B., S. M. Miller, K. R. Fick, and S.L. Hansard II. 1977. Contaminating
elements in mineral supplements and their potential toxicity: A review. J. Anim. Sci.
44:485.
Annett, C. S., F. M. D'Itri, J. R. Ford, and H. H. Prince. 1975. Mercury in fish and water
fowl from Lake Ball, Ontario. J. Environ. Qual. 4:219.
Ansari, M. S., W. J. Miller, R. P. Gentry, M. W. Neathery, and P. E. Stake. 1973. Tissue
203Hg distribution in young Holstein calves after single tracer oral doses in organic and
inorganic forms. J. Anim. Sci. 36:415.
Bakir, F., S. F. Damluji, L. Amin-Zaki, M. Murtadha, A. Khalidi, N. Y. Al-Rawi, S.
Tikriti, H. I. Dhahir, T. W. Clarkson, J. C. Smith, and R. A. Doherty. 1973. Methyl-
mercury poisoning in Iraq. Science 681:230.
Barber, R. T., A. Vijayakumar, and F. A. Cross. 1972. Mercury concentrations in recent
and ninety-year-old benthopelagic fish. Science 178:636.
Berlin, M., J. Carlson, and T. Norseth. 197S. The dose-dependence of methylmercury
metabolism. Arch. Environ. Health 30:307.
Billings, C. E., and W. R. Matson. 1972. Mercury emissions from coal combustion.
Science 176:1232.
Blackstone, S., R. J. Hurley, and R. E. Hughes. 1974. Some inter-relationships between
vitamin C (~-ascorbic acid) and mercury in the guinea pig. Food Cosmet. Toxicol.
12:5 1 1 .
Buck, W. B. 1975. Toxic materials and neurological diseases in cattle. J. Am. Vet. Med.
Assoc. 166:222.
Bulger, R. E., and F. L. Siegel. 1975. Alterations of the renal papilla during mercuric
chloride-induced acute tubular necrosis. Lab. Invest. 33:712.
Burk, R. F., K. A. Foster, P. M. Greenfield, and K. W. Kiker. 1974. Binding of simul-
taneously administered inorganic selenium and mercury to a rat plasma protein. Proc.
Soc. Exp. Biol. Med. 145:782.
Chang, C. W. J., R. M. Nakamura, and C. C. Brooks. 1977. Effect of varied dietary levels
and forms of mercury on swine. J. Anim. Sci. 45:279.
Chen, R. W., H. E. Ganther, and W. G. Hoekstra. 1973. Studies on the binding of methyl
mercury by thionein. Biochem. Biophys. Res. Commun. 51:383.
Chen, R. W., P. D. Whanger, and S. C. Fang. 1974. Diversion of mercury binding in rat
tissues by selenium: A possible mechanism of protection. Pharmacol. Res. Commun.
6:571.
Chen, R. W., V. L. Lacy, and P. D. Whanger. 1975a. Effect of selenium on methylmer-
cury binding to subcellular and soluble proteins in rat tissues. Res. Commun. Chem.
Pathol. Pharmacol. 12:297.
Chen, R. W., P. D. Whanger, and P. H. Weswig. 1975b. Selenium-induced redistnbution
of cadm~um binding to tissue proteins: A possible mechanism of protection against
cadmium toxicity. Bioinorg. Chem. 4:125.
Clarkson, T. W. 1970. Epidemiological aspects of lead and mercury contamination of
food. Presented at a Symposium on "Chemical Contaminants in Foods --Hazard or
Not?" sponsored by the Food and Drug Directorate, Department of National Health
OCR for page 323
Mercury
323
and Welfare, Ottawa, Ontario, and held in Ottawa on June 1~19, 1970. Also published
as "Epidemiological and experimental aspects of lead and mercury contamination of
food." Food Cosmet. Toxicol. 9:229, April 1971.
Clarkson, T. W., L. Magos, and G. G. Berg. 1973. Mercury compounds. Science
176: 1074.
Clarkson, T. W., L. Amin-Zaki, and S. K. Al-Tikriti. 1976. An outbreak of methylmer-
cury poisoning due to consumption of contaminated grain. Fed. Proc. 35:2395.
Colucci, A. V., D. Winge, and J. Krasno. 1975. Cadmium accumulation in rat liver. Arch.
Environ. Health 80:153.
Cousins, R. J. 1974. Influence of cadmium on the synthesis of liver and kidney cadmium-
binding protein. In W. G. Hoekstra, J. W. Suttie, H. E. Ganther, and W. Mertz (eds.).
Trace Element Metabolism in Animals 2. University Parlc Press, Baltimore, Md.
Curley, A., V. A. Sedlak, E. F. Girting, 11. E. Hawk, W. F. Barthel, P. E. Pierce, and
W. H. Likosky. 1971. Organic mercury identified as the cause of poisoning in humans
and hogs. Science 172:65.
D'Itri, F. M. 1971. Lee Environmental Mercury Problem. Michigan Legislative Report
HR~24. Lansing.
El-Begearmi M., H. E. Ganther, and M. L. Sunde. 1974. Effect of some sulfur amino
acids, selenium and arsenic on mercury toxicity using Japanese quail. Poult. Sci.
53:1921. (Abstr.)
El-Begearmi, M. M., M. L. Sunde, and H. E. Ganther. 1977a. A mutual protective effect
of mercury and selenium in Japanese quail. Poult. Sci. 56:313.
El-Begearmi, M. M., H. E. Ganther, and M. L. Sunde. 1977b. Protective effect of vitamin
E against inorganic mercury and methylmercury toxicity. Poult. Sci. 56:1711.
El-Begearmi, M. M., H. E. Ganther, and M. L. Sunde. 1979. Toxicity of mercuric
chloride as affected by method of incorporation into the diet. Fed. Proc. 38:869.
(Abstr.)
Ellis, R. W., and S. C. Fang. 1967. Elimination, tissue accumulation and cellular incor-
poration of mercury in rats receiving an oral dose of mercury-203-labeled phenylmer-
curic acetate and mercuric acetate. Toxicol. Appl. Pharmacol. 11:104.
Emerick, R. J., S. Palmer, C. W. Carlson, and R. A. Nelson. 1976. Mercury-selenium
interrelationships in laying hens. Fed. Proc. 35:577. (Abstr.)
Fitzhugh, O. G., A. A. Nelson, E. P. Laug, and F. M. Kunze. 1950. Chronic oral
toxicities of mercun-phenyl and mercuric salts. IMP Arch. Ind. Hyg. Occup. Med.
2:433.
Fowler, B. A. 1972. Ultrastructural evidence for nephropathy induced by long-term
exposure to small amounts of methyl mercury. Science 175:780.
Fowler, B. A., and G. F. Nordberg. 1975. The renal toxicity of cadmium metallothionein.
Int. Conf. Heavy Metals Environ. Toronto, Canada (Abstr.).
Fowler, B. A., H. W. Brown, G. W. Lucier, and M. R. Krigman. 1975. The effects of
chronic oral methyl mercury exposure on the Iysosome system of rat kidney. Lab.
Invest. 32:313.
Gage. J. C. 1975. Mechanisms for the biodegradation of organic mercury compounds:
We actions of ascorbate and of soluble proteins. Toxicol. Appl. Pharmacol. 32:225.
Ganther, H. E., and M. L. Sunde. 1974. Effect of tuna fish and selenium on the toxicity
of methylmercury: A progress report. J. Food Sci. 39:1.
Ganther, H. E., C. Goudie, M. L. Sunde, M. J. Kopecky, P. Wagner, S. H. Oh, and W.
G. Hoekstra. 1972. Selenium: Relation to decreased toxicity of methylmercury added
to diets containing tuna. Science 175:1122.
Garcia, J. D., M. G. Yang, J. H. C. Wang, and P. S. Bela. 1974a. Carbo~mercury bond
OCR for page 324
324 MINERAL TOLERANCE OF DOMESTIC ANIMALS
breakage in milk, cerebrum, liver and kidney of rats fed methyl mercuric chloride.
Proc. Soc. Exp. Biol. Med. 146:190.
Garcia, J. D., M. G. Yang, J. H. C. Wang, and P. S. Belo. 1974b. Translocation and fluxes
of mercury in neonatal and maternal rats treated with methyl mercuric chloride during
gestation. Proc. Sci. Exp. Biol. Med. 147:224.
Gardiner, E. E. 1972. Differences between ducks, pheasants and chickens in tissue
mercury retention, depletion and tolerance to increasing levels of dietary mercury.
Can. J. Anim. Sci. 52:419.
Gruber, T. A., P. Costigan, G. T. Wilkinson, and A. A. Seawright. 1978. Chronic
methylmercunalism in the cat. Aust. Vet. J. 54:155.
Hammond, P. B. 1973. Metabolism and metabolic action of lead and other heavy metals.
Clin. Toxicol. 6:353.
Haq, I. U. 1963. Agrosan poisoning in man. Br. J. Med. 5345:1579.
Hengstad, R. R., C. K. Whitehair, N. Beyer, O. Mickelsen, and M. J. Zabik. 1972.
Chronic methylmercury toxicosis in calves. J. Am. Vet. Med. Assoc. 160:173.
Hill, E. F., and C. S. Shaffner. 1976. Sexual maturation and productivity of Japanese
quail fed graded concentrations of mercuric chloride. Poult. Sci. 55:1449.
Hollins, J. G., R. F. Willes, F. R. Bryce, S. M. Charbonneau, and I. C. Munro. 1975. The
whole body retention and tissue distribution of 203Hg methylmercury in adult cats.
Toxicol. Appl. Pharmacol. 33:438.
Hough, E. J., and M. E. Zabik. 1973. Mercury residues in duck breast tissue after moist
and dry heat cooking. J. Sci. Food Agric. 24:107.
Huckabee, J. W., F. O. Cartan, G. S. Kenhington, and F. J. Camenzind. 1973. Mercury
concentration in the hair of coyotes and rodents in Jackson Hole, Wyoming. Bull.
Environ. Contam. Toxicol. 9:37.
Johnels, A. G. 1967. Mercury content of Exox lucius as indicator of pollution. Oikos.
18:323.
Khan, J. M. 1974. Compartmental analysis for the evaluation of biological half-lives of
cadmium and mercury in mouse organs. Environ. Res. 7:54.
Khera, K. S., and S. A. Tabacova. 1973. Effects of methylmercunc chlonde on the
progency of mice and rats treated before or during gestation. Food Cosmet. Toxicol.
11:245.
Klaasen, C. D. 197Sa. Biliary excretion of mercury compounds. Toxicol. Appl. Pharma-
col. 33:356.
Klaasen, C. D. 1975b. Effect of spisonolactone on the distribution of mercury. Toxicol.
Appl. Pharmacol. 33:336.
MacGregor, J. T., and T. W. Clarkson. 1974. Distribution, tissue binding and toxicity of
mercurials. Adv. Exp. Med. Biol. 48:463.
Madsen, K., and E. I. Christensen. 1975. Effects of mercury on kidney Iysosome func-
tion. Int. Conf. Heavy Metals Environ. Toronto, Canada.
Magat, W., and J. L. Sell. 1979. Distnbution of mercury and selenium in egg components
and egg-white proteins. Proc. Soc. Exp. Biol. Med. 161:458.
Magos, L. 1968. The uptake of mercury by the brain. Br. J. Ind. Med. 2S:3 15.
March, B. E., R. Soong, E. Bilinski, and R. E. E. Jonas. 1974. Effect on chickens of
chronic exposure to mercury at low levels through dietary fish meal. Poult. Sci.
53:2175.
McIntyre, J. D. 1973. Toxicity of methyl mercury for steelhead trout sperm. Bull. En-
viron. Conf. Toxicol. 9:98.
Miller, V. L., D. V. Larkin, G. E. Bearse, and C. M. Hamilton. 1967. The effects of
dosage and administration of two mercurials on mercury retention in two strains of
chickens. Poult. Sci. 46:142.
OCR for page 325
Mercury
325
Miller, V. L., G. E. Bearse, and E. Csonka. 1970. Mercury retention in several strains
and strain crosses of chickens. Poult. Sci. 49:1101.
Mills, C. F. 1974. Trace element interactions: Effect of dietary composition on the
development of imbalance and toxicity. In W. G. Hoekstra, J. W. Suttie, H. E.
Ganther, and W. Mertz (eds.). Trace Element Metabolism in Animals 2. University
Park Press, Baltimore, Md.
Moffitt, A. E., Jr., and J. J. CIary. 1974. Selenite-induced binding of inorganic mercury
in blood and other tissues in the rat. Res. Commun. Chem. Pathol. Pharmacol. 7:593.
Mullen, A. L., R. E. Stanley, S. R. Lloyd, and A. A. Moghessi. 1975. Absorption,
distribution and milk secretion of radionuclides by the dairy cow. IV. Inorganic radio-
mercury. Health Phys. 28:685.
Neathery, M. W., and W. J. Miller. 1975 . Metabolism and toxicity of cadmium, mercury
and lead in animals: A review. J. Dairy Sci. 58:1767.
Neathery, M. W., W. J. Miller, R. P. Gentry, P. E. Stake, and D. M. Blackman. 1974.
Cadmium-109 and methyl mercury-203 metabolism, tissue distribution and secretion
into milk of cows. J. Dairy Sci. 57:1177.
Nelson, N., T. C. Byerly, A. C. Kolbye, Jr., L. T. Kurland, R. E. Shapiro, S. I. Shibko,
W. H. Stickel, J. E. Thompson, L. A. Vanden Berg, and A. Weissler. 1971. Hazards
of mercury. Environ. Res. 4:1.
Nordberg, G. F., and M. Nordberg. 1975. Metabolism and toxicity of metallothionein-
bound cadmium. Int. Conf. Heavy Metals Environ. Toronto, Canada.
Norseth, T. 1974. The effect of diethyldithiocarbamate on biliary transport, excretion and
organic distribution of mercury in the rat after exposure to methylmercuric chlonde.
Acta Pharmacol. Toxicol. 34:76.
Norseth, T., and T. W. Clarkson. 1970. Studies on the biotransformation of 203Hg-
labelled methyl mercury chloride in rats. Arch. Environ. Health 21:717.
Norseth, T., and T. W. Clarkson. 1971. Intestinal transport of 203Hg-labeled methyl
mercury chlonde. Arch. Environ. Health 22:568.
Ohi, G., S. Nishigaki, H. Seki, Y. Tamura, T. Maki, H. Maeda, S. Ochiai, H. Yamada,
Y. Shimamura, and H. Yagyu. 1975. Interaction of dietary methylmercury and sele-
nium on accumulation and retention of these substances in rat organs. Toxicol. Appl.
Pharmacol. 32:527.
Ordonez, J. V., J. A. Carnllo, and M. Miranda. 1966. Epidemiolo~cal study of a disease
in the Guatemalan highlands believed to be encephalitis. Boll Of. Sanit. Panam. 60:510.
Palmer, J. S., F. C. Wright, and M. Haufler. 1973. Toxicologic and residual aspects of
an alkyl mercury fun'pcide to cattle, sheep and turkeys. Clin. Toxicol. 6:425.
Parizek, J., J. Kalouskova, A. Babicky, J. Benes, and L. Pavlik. 1974. Interaction of
selenium with mercury, cadmium and other toxic metals. In W. G. Hoekstra, J. W.
Suttie, H. E. Ganther, and W. Mertz (eds.). Trace Element Metabolism in Animals 2.
University Park Press, Baltimore, Md.
Parkhurst, C. R., and P. Thaxton. 1973. Toxicity of mercury to young chickens. I . Effect
on growth and mortality. Poult. Sci. 52:273.
Piotrowski, J. K., B. Trojanowska, J. M. Wisniewska-Knypl, and W. Bolanowska.
1974a. Mercury binding in the kidney and liver of rats repeatedly exposed to mercuric
chloride: Induction of metallothionein by mercury and cad~rnum. Toxicol. Appl. Phar-
macol. 27:11.
Piotrowski, J. K., B. Trojanowska, and A. Sapota. 1974b. Binding of cadmium and
mercury by metallothionein in the kidneys and liver of rats following repeated admini-
stration. Arch. Toxicol. 32:3S 1.
Piper, R. C., V. L. Miller, and E. O. Dickenson. 1971. Toxicity and distribution of
mercury in pigs with acute methylmercurialism. Am. J. Vet. Res. 32:263.
OCR for page 326
326 MINERAL TOLERANCE OF DOMESTIC ANIMALS
Potter, S., and G. Matrone. 1974. Effect of selenite on the toxicity of dietary methyl
mercury and mercuric chloride in the rat. J. Buts. 104:638.
Preuss, H. G., A. Tourkantonis, C. H. Hsu, P. S. Shim, P. Barzyk, F. Tio, and G. E.
Schriiner. 1975. Early events in various forms of experimental acute tubular necrosis
in rats. Lab. Invest. 32:286.
Prior, M. G. 1976. Lead and mercury residues in kidney and liver of Canadian slaughter
animals. Can. J. Comp. Med. 40:9.
Roh, J. K., R. L. Bradley, Jr., T. Richardson, and K. G. Weckel. 1975. Distribution and
removal of added mercury in milk. J. Dairy Sci. 58:1782.
Rubenstein, D. A., and J. H. Soares, Jr. 1979. The effect of selenium on the biliary
excretion and tissue deposition of two forms of mercury in the broiler chick. Poult. Sci.
58:1289.
Rucker, R. R., and D. F. Amend. 1969. Absorption and retention of organic mercurials
by rainbow trout and chinook and sockeye salmon. Prog. Fish Cult. 31:197.
Salvaterra, P., E. J. Massaro, J. B. Morganti, and B. A. Lown. 1975. Time~ependent
tissue/organ uptake and distribution of 203Hg in mice exposed to multiple sublethal
doses of methyl mercury. Toxicol. Appl. Pha~macol. 32:432.
Sasser, L. B., G. E. Jarboe, B. K. Walter, and B. J. Kelman. 1978. Absorption of
mercury from ligated segments of the rat gastrointestinal tract. Proc. Soc. Exp. Biol.
Med. 157:57.
Schroeder, H. A., and M. Mitchener. 1975. Life-term effects of mercury, methylmercury
and nine other trace metals on mice. J. Nutr. 105:452.
Scott' M. L., J. R. Zimmerman, S. Marinsky, P. A. Mullenhoff, G. L. Rumsey, and
R. W. Rice. 1975. Effects of Pcs's, DDr, and mercu~y compounds upon egg production,
hatchability and shell quality in chickens and Japanese quail. Poult. Sci. 54:350.
Sell, J. L. 1977. Comparative effects of selenium on metabolism of methylmercury by
chickens and quail: Tissue distribution and transfer into eggs. Poult. Sci. 56:939.
Sell, J. L., and K. L. Davidson. 1975. Metabolism of mercury, administration as methyl-
mercuric chloride or mercuric chloride by lactating ruminants. J. Agric. Food Chem.
23:803.
Sell, J. L., W. Guenter, and M. Sifri. 1974. Distribution of mercury among components
of eggs following the administration of methylmercuric chloride to chickens. J. Agric.
Food Chem. 22:248.
Shaikh, Z., and J. C. Smith. 1975. Mercury induced synthesis of renal metallothionein.
Int. Conf. Heavy Metals Environ. Toronto, Canada.
Shaikh, Z. A., R. L. Coleman, and O. J. Lucis. 1973. Sequestration of mercury by
cadmium-induced metallothionein. Trace Subst. Environ. Health 7:313.
Siegmund, O. H., and C. M. Fraser (eds.). 1973. The Merck Veterinary Manual, 4th ed.
Merck and Co., Inc., Rahway, N.J.
SIcerfving, S. 1972. Mercury in fish~ome toxicological considerations. Food Cosmet.
Toxicol. 10:545.
Skerfving, S. 1974. Methylmercury exposure, mercury levels in blood and hair, and
health status in Swedes consuming contaminated fish. Toxicology 2:3.
Soares, J. H., Jr., D. Miller, H. Lagally, B. R. Stillings, P. Bauersfeld, and S. Cuppett.
1973. The comparative effect of oral ingestion of methyl mercury on chicks and rats.
Poult. Sci. 52:452.
Stake, P. E., M. W. Neathery, W. J. Miller, and R. P. Gentry. 1975. 203Hg excretion and
tissue distribution in Holstein calves following single tracer intravenous doses of
methyl mercury chloride or mercuric chloride. J. Anim. Sci. 40:720.
Stillings, B. R., H. Lagally, P. Bauersfeld, and J. Soares. 1974. Effect of cystine, selen-
OCR for page 327
Mercury
327
ium and fish protein on the toxicity and metabolism of methylmercury in rats. Toxicol.
Appl. Pharmacol. 30:243.
Stoewsand, B. S., C. A. Bache, and D. J. Lisk. 1974. Dietary selenium protection of
methylmercury intoxication of Japanese quail. Bull. Environ. Contam. Toxicol.
11:152.
Thaxton, P., and C. R. Parkhurst. 1973a. Abnormal mating behavior and reproductive
dysfunction caused by mercury in Japanese quail. Proc. Soc. Exp. Biol. Med. 144:252.
Thaxton, P., and C. R. Parkhurst. 1973b. Toxicity of mercury to young chickens. 2. Gross
changes in organs. Poult. Sci. 52:277.
Thaxton, P., L. A. Cogburn, and C. R. Parkhurst. 1973. Dietary mercury as related to the
blood chemistry in young chickens. Poult. Sci. 52:1212.
Thaxton, P., P. S. Young, L. A. Cogburn, and C. R. Parkhurst. 1974. Hematology of
mercury compounds in young chickens. Mull. Environ. Contam. Toxicol. 12:46.
Thaxton, P., C. R. Parkhurst, L. A. Cogburn, and P. S. Young. 1975. Adrenal function
in chickens experiencing mercury toxicity. Poult. Sci. 54:578.
Tichy, M., J. Haurdova, and M. Cekrt. 1975. Comments on the mechanism of excretion
of mercury compounds via bile in rats. Arch. Toxicol. 33:267.
Tryphonas, L., and N. O. Nielsen. 1970. The pathology of arylmercurial poisoning in
swine. Can. J. Comp. Med. 34:181.
Tryphonas, L., and N. O. Nielsen. 1973. Pathology of chronic alkylmercurial poisoning
in swine. Am. J. Vet. Res. 34:379.
Underwood, E. J. 1977. Trace Elements in Human and Animal Nutrition, 4th ed. Aca-
demic Press, New York.
Webb, M. 1975. Toxicity of cadmiu~thionein. Int. Conf. Heavy Metals Environ.
Toronto, Canada (Abstr.).
Welsh, S. O. 1976. Influence of vitamin E on mercury poisoning in rats. Fed. Proc.
35:761. (Abstr.)
Welsh, S. O. 1979. The protective effect of vitamin E and N. N'-diphenyl-p-
phenylenediamine (DPPD) against methylmercury toxicity in the rat. J. Nutr. 109:1673.
Welsh, S. O., and J. H. Soares, Jr. 1975. The effects of selenium and vitamin E on methyl
mercury toxicity in the Japanese quail. Fed. Proc. 34:913 (Abstr.).
Westoo, G. 1966. Determination of methylmercury compounds in food stuffs. I. Methyl-
mercury compounds in fish, identification and determination. Acta Chem. Scand.
20:2131.
Wobeser, G., N. O. Nielsen, and B. Schiefer. 1976a. Mercury and mink. I. The use of
mercury contaminated fish as a food for ranch mink. Can. J. Comp. Med. 40:30.
Wobeser, G., N. O. Nielsen, and B. Schiefer. 1976b. Mercury and mink. II. Experimental
methyl mercury intoxication. Can. J. Comp. Med. 40:34.
Won, J. H. 1973. The concentration of mercury, cadmium, lead and copper in fish and
shell fish of Korea. Bull. Korean Fish. Soc. 6:1.
Wright, F. C., J. S. Palmer, and J. C. Riner. 1973. Accumulation of mercury in tissues
of cattle, sheep and chickens given the mercurial fungicide, Panogen 15 orally. J. Agric.
Food Chem. 21:414.
Representative terms from entire chapter:
body weight
