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OCR for page 466
Sulfur
Sulfur (S) has been used in several forms since antiquity, but not until
recently has there been a real understanding of its biological signifi-
cance. The annual world "harvest" of sulfur is more than 27 billion kg
obtained from underground deposits of elemental sulfur and trapped
hydrogen sulfide gas, from the manufacture of petroleum products, and
from reclamation of combustion products of sulfurous fossil fuels.
About 80 percent of the annual production of sulfur is used for the
production of sulfuric acid, which in turn is used for the manufacture
of phosphate fertilizer, synthetic fibers such as rayon (100 kg cellulose
requires 3~50 kg carbon disulfide), pesticides and white pigments
(Brieger and Teisinger, 1966), in steel processing, in bleaching agents
for paper pulp, sugar and vegetable oils, in preservation of beverages
and foods, and in vulcanizing of rubber products (Leclercq, 1972~.
While the literature on sulfur chemistry is voluminous, the reviews
on this topic by Roy and Trudinger (1970), Senning (1972), Nickless
(1968), Young and Maw (1958), and du Vigneaud (1952) are note-
worthy. The nutritional aspects of sulfur have been reviewed by Baker
(1977), Muth and Oldfield (1970), and Goodrich (19781. While the indus-
trial hazards of organic and inorganic forms of sulfur have been often
investigated, limited information is available regarding the potential for
or effects of sulfur contamination of feedstuffs.
466
OCR for page 467
Sulfur
ESSENTIALITY
467
Sulfur is required for the formation of the many sulfur-containing com-
pounds found in essentially all body cells and, therefore, is an essential
nutrient. The important body sulfur compounds include the sulfur-
containing amino acids (methionine, cysteine, cystine, homocysteine,
cystathionine, taurine, and cysteic acid), thiamin, biotin, lipoic acid,
coenzyme A, glutathione, chondroitin sulfate, fibrinogen, heparin,
ergothionine, and estrogens. The sulfur in the mammalian body repre-
sents about 0.15 percent of body weight. Fortunately, all of the above
sulfur compounds, except thiamin and biotin, can be synthesized in
viva from one essential amino acid, methionine. Approximately 50
percent of the total requirement for sulfur-containing amino acids can
be provided by cystine. These amino acids are therefore involved in
acid-base balance of intra- and extracellular fluids, protein synthesis,
lipid and carbohydrate metabolism, collagen and connective tissue for-
mation through disulfide bonds between and within polypeptide chains,
blood-clotting, enzyme synthesis, and endocrine function (Baker,
1977).
METABOLISM
The metabolism of sulfur differs markedly between monogastrics and
ruminants, and an understanding of this difference is basic to an appre-
ciation of the sulfur cycle (Postgate, 1968) and of the nutritional value
of sulfur compounds. The major terrestrial source of sulfur is mineral
sulfide, which is converted to inorganic sulfate by weathering and to
organic sulfur by microbial action in the soil (Young and Maw, 1958~.
Inorganic sulfate is taken up by higher plants and converted to organic
sulfur in the form of the sulfur-containing amino acids, which in turn
serve as an organic sulfur source for both monogastric and ruminant
animals. Many bacteria, including the microbial flora of the ruminant,
are also able to convert inorganic sulfur to organic sulfur in the form of
methionine, cysteine, and cystine and hence for the many functions of
sulfur in the body. Monogastric animals have few, if any, intestinal
assimilatory bacteria to form organic sulfur from inorganic sources and,
therefore, must rely upon exogenous sulfur amino acid sources for their
requirement of organic sulfur. Both ruminants and nonruminants can
utilize inorganic sulfate in the formation of sulfate esters required in the
synthesis of mucopolysaccharides. Absorption by active transport of
the inorganic sulfate takes place in the small intestine, especially the
OCR for page 468
468 MINERAL TOLERANCE OF DOMESTIC ANIMALS
ileum (Dziewiatkowski, 1970~. Organic forms of sulfur are readily ab-
sorbed in the small intestine. The absorption mechanism is very eff~-
cient. Morrow et al. (1952) demonstrated that rats excreted, in the
urine, 41 to 64 percent of an oral dose of inorganic sulfate 35S within 8
hours of administration. The sulfur status of animals has been measured
by balance studies (Walker and Cook, 1967), by serum sulfate levels
(Bray, 1965), and by serum amino-acid levels (Schelling and Hatfield,
1968~.
SOURCES
Inorganic sulfur compounds have the potential for contaminating food
supplies and/or interfering with biological systems, albeit primarily by
industrial exposure of humans. Elemental sulfur (flowers of sulfur) is
used topically as a fungicide, karyolytic agent, and parasiticide. Hydro-
gen sulfide exposure (for humans) is frequent around shale oil plants
and from sewer gas developed from the putrefaction of organic matter.
Industrial exposure to carbon~sulfur compounds occurs in the manu-
facture of viscose, rubber, and insecticides (Sorbo, 19721. Sulfur di-
oxide is a major component of industrial smog as a result of combustion
of coal and petroleum. Additional sources of sulfur dioxide are paper
bleaches, fumigants, and refrigerants. Sodium sulfides are used as food
and pharmaceutical preservatives. The thiosulfates, used in antimy-
cotic and antiparasitic agents, are also used as antidotes for cyanide
toxicity and have been used in clinical medicine to measure extracellu-
lar fluid space and gIomerular filtration rates. Exposure to sulfuric acid,
the intermediate in the manufacturing of the many sulfur compounds
mentioned, is usually limited to aerosols generated in electroplating and
battery charging. Ammonium persulfate is used as an alternative to
nitrogen bichloride as a bleaching agent for flour, because the latter
causes necrologic problems in dogs consuming products containing
American-processed flour (Lewis, 1954~. Additional inorganic sulfur
sources include sulfate salts used in mineral supplements, dicalcium
phosphate, water supplies (Larson, 1959), fish by-products, cement
kiln dust, sulfur-coated urea used as a slow-release nitrogen fertilizer
for cranberry bogs, and sodium metabisulfide and sulfur dioxide used
as silage preservatives.
The organic sources of sulfur include methionine, an essential sulfur-
containing amino acid; dimethyl sulfoxide, a powerful solvent to trans-
port medication to poorly vascularized tissues such as the lens and the
articulations (Caldwell et al., 1967~; and the high-sulfur feed ingredients
.
OCR for page 469
Sulfur
469
such as feathers, viscera, and fecal waste used in some contemporary
livestock diets.
TOXICOSIS
The toxicity of sulfur is dependent upon its form and route of adminis-
tration. Whereas elemental sulfur is considered one of the least toxic
elements, hydrogen sulfide rivals cyanide in toxicity. Fitzhugh et al.
(1946) reviewed the chronic toxicity of sulfites.
LOW LEVELS
The ejects of long-term feeding of sulfur dioxide (SO2) to cattle have
been investigated by Weigand et al. (19721. Lactating cows fed between
1X and 20 g of sulfur as SO2 daily for 110 days exhibited no deleterious
effects on milk production or butterfat level. The mean sulfide levels of
the milk or blood were not significantly different between treated and
control cattle, and no changes in hematology, behavior, body tempera-
ture, heart rate, or rumen motility could be attributed to the SO2 treat-
ments.
The toxic effects of sodium metabisulfite (Na2S2Os) and sulfur di-
oxide, two silage preservatives, have been investigated by Luedke et
al. (1959) with rumen-fistulated cattle. A cow given 80 g of sodium
metabisulfite, equal to 26.5 g sulfur per day for 180 days, seemed
unaffected by the treatment and, in fact, completed a gestation and
calved normally during the treatment. A second cow given sulfur as
sodium metabisulfite on a schedule of 26.5 g per day for 2 days, 40 g per
day for the next 2 days, and 53 g per day for the next 2 days stopped
eating on the sixth day of the experiment. Supplementation was ceased
and the cow appeared normal again within 6 days. Another cow admin-
istered sodium metabisulfite on a schedule of 26.5 g per day for 1 week,
40 g per day for the second week, and 53 g per day for the third week
was unable to stand on the eighteenth day after receiving 673 g of the
sulfur. Other cows and heifers on similar schedules died after 16 to 21
days on experiment and after receiving 56~658 g sulfur as sodium
metabisulfite or sulfur dioxide. These cattle had exhibited anorexia,
weight loss, constipation, diarrhea, and depression. At necropsy, pul-
monary emphysema, cardiac petechiation, congestion of the central
nervous system, acute catarrhal enteritis, and hepatic necrosis were
present in the treated cows.
Alhassan and Satter (1968) have investigated the effects of intraru-
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470 MINERAL TOLERANCE OF DOMESTIC ANIMALS
menally administered sodium sulfite in cattle. These investigators ad-
ministered 15 g of sulfur as Na2SO3 per day per cow and gradually
increased this dosage to 50 g of sulfur per cow daily. These amounts of
sulfur caused partial to complete anorexia, depression of milk fat from
3.7 to 2.4 percent, and a depression of the ruminal acetat~butyrate
ratio. Weeth and Hunter (1971) provided Hereford cattle with drinking
water containing 1,240 ppm sulfur as Na2SO4 for 30-day trials. This
level of sulfur caused reduced feed and water intakes, weight loss,
diuresis, and hemoconcentration.
Upton et al. (1970) fed 2,200 ppm sulfur as sodium sulfate to sheep
without effect and found fecal sulfur correlated well with dry matter
intake. Marcilese et al. (1969) fed wethers the equivalent of 0.5 g sulfur
per day as sodium sulfate for indefinite periods without any adverse
effects. Lewis (1954) found that rumen-fistulated wethers given 4, 8, or
15 g of sulfur daily as sodium sulfate via the fistula exhibited no toxic
effects from the treatments, even though there was a marked elevation
in rumen sulfate concentration.
L' Estrange et al. (1969) fed 40 kg wethers either sodium sulfate,
sodium bisulfite, ammonium bisulfite, sulfuric acid, or ammonium sul-
fate to create 1 percent sulfur diets. The sodium sulfate and sodium
bisulfite caused a 22 percent decrease in voluntary feed intake, while
the other sulfur sources decreased feed intake by 44 percent. The
sulfuric acid-supplemented diet caused a decrease in rumen pH.
L'Estrange and Murphy (1972) found similar effects of sulfuric acid
when added to sheep diets at the rate of 320 mEq/kg of grass.
L,Estrange e! al. (1972) also found graded levels of dietary sulfur (0.5,
1.0, and 1.5 percent) added-to pelleted grass meal for wethers decreased
feed intake and increased the apparent digestibility of the diets over a
14-day feeding trial.
Sodium disulfite has been used in the processing of sugarcane pulp
(Kaemmerer, 1972), which has been incorporated into ruminant ra-
tions. Kaemmerer et al. (1972) studied the effects of 0.5 percent sulfur
as sodium disulfite in sheep diets consisting of hay, sugar pulp, and
oatmeal in ratios of 5:~:2. Sheep fed this diet tolerated the supplemental
sulfur without signs of ill health, although there was indication of in-
creased incidence of renal cysts in the sulfur-supplemented sheep.
Bird (1972) has studied the effects of ruminal infusions of sulfate
solutions in sheep. In one experiment, continuous infusions of sulfate
sulfur at rates of 0 to 6 g daily for up to 8 days were given. A significant
decrease in the dry matter intake and mmen motility appeared when the
infusion rate reached 2.93 g per day. At 6 g per day there was complete
anorexia within 3 to 9 days, followed by Lumen stasis, impaction, and
OCR for page 471
Sulfur
471
a foul odor (H2S) on the breath of the sheep. In additional studies with
sheep, Peirce (1960) provided 3- to Year-old wethers with drinking
water containing 0.1 to 0.5 percent sodium sulfate for 15 months. The
drinking water for each Coup was isonatremic. No adverse effects on
general health, food intake, weight gain, or wool production were ob-
served in any of the sheep regardless of their level of sulfur intake,
which ranged between 1.3 and 6.5 g per day.
Paterson et al. (1979) have given sows drinking water containing up
to 664 ppm sulfur, as Na2S04, from 30 days postbreeding to 28 days of
lactation and found no significant effect on reproduction. These investi-
gators have also provided weanling pigs with drinking water containing
600 ppm sulfur as Na2SO4. This level of sulfur caused loose feces and
increased incidence of diarrhea, but no differences in average daily gain
or feed conversion ratios.
The effects of inhaled sulfur compounds have been studied in several
species. O'Donoghue (1961) reported an experiment in which swine
were exposed to 0- 470 ppm of H2S in an inhalation chamber. The pigs
appeared barely able to detect the odor of 0.9 ppm H2S, seemed to lose
their sense of smell at 28 ppm H2S, were markedly affected by 47-188
ppm H2S, and were killed by 470 ppm H2S. In subsequent studies,
O'Donoghue and Graesser (1962) exposed 2-week-old pigs to sulfur
dioxide atmospheres equal to ~20 ppm sulfur for 6.5 hours and sacri-
ficed the pigs after 70 days. Signs exhibited by the pigs in the sulfur
dioxide chambers included irritation of the eyes, excessive blinking,
serous nasal discharge, and hyperpnea. The pigs, however, appeared
to adapt to the conditions. Pigs exposed to the 1~20 ppm levels of
sulfur dioxide had pulmonary induration (fibrosis) when examined at
necropsy.
The toxicity of ammonium persulfate [(NH4~2S2O~l, used as a bleach-
ing agent in processing of flour, has been studied in dogs (Arnold and
Goble, 1950~. Dietary levels of 0.04 to 0.28 percent sulfur were fed for
as long as 16 months without noticeable effect on gross appearance,
weight gains, renal function, or hematology and without gross or micro-
scopic lesions observed upon necropsy.
Anderson and Chen ( 1940) studied the toxicosis of some thiocyanates
in dogs. Sodium and potassium thiocyanates appeared to be similarly
toxic with the no-e~ect level as high as 9.1 mg sulfur/kg per day orally
for more than 3 months. Sulfur intake of 12.2 mg/lcg per day caused
--death in 45 days, while sulfur at 3~41 mg/kg per day caused deaths of
the dogs within 4 days.
The eject of inhaled carbon disulf~de (CS2) in rabbits was studied by
Scheel (19671. Atmospheres of 926 ppm sulfur as carbon disulf~de for 6
OCR for page 472
472 MINERAL TOLERANCE OF DOMESTIC ANIMALS
hours per day, 5 days per week, for 8 weeks caused reduced weight
gains, loss of muscle control, necrologic damage, and marked increases
in the copper levels of the thyroid, pancreas, and spinal cord. The
altered copper metabolism of the central nervous system tissues may
account for the central nervous system disturbances associated with
carbon disulf~de toxicosis in humans.
Guinea pigs have been exposed to atmospheres of 2.5 to 9.0 ppm
super as sulfur dioxide in respiratory chambers for ~15 days
(O'Donoghue and Graesser, 1962~. These exposures caused reduced
weight gains, but no other pathologic disturbances were detected.
Optimal level of inorganic sulfur, as sodium sulfate, in semipurified
diets for male rats has been reported to be 0.02 percent when the total
dietary sulfur is maintained at 0.67 percent (Smith, 19731. When the
total sulfur-containing amino acid content of test diets for growing rats
was 0.14 percent (from peanut protein), Brown and Gamatero (1970)
found improved net weight gain, feed efficiency, and protein efficiency
ratios as supplemental SO4 levels increased from 0.002 percent to 0.1
percent.
The effects of inhaled sulfur dioxide upon fertility of rats have been
evaluated by Mamatashvili (1970), who found exposures of female rats
to 0.15 mg SO2/mm3 equal to 0.075 mg sulfur /mm3 for 72 days caused
no changes in estrous cycles or fertility. Concentrations of 4 mg/mm3 (2
mg sulfur/mm3) had some detrimental effect on these parameters.
Relevant studies of toxicity of organic sulfur compounds pertain to
excess dietary sulfur-containing amino acids, especially methionine. In
fact, it is well accepted that methionine given in excess of its dietary
requirement is the most toxic of the amino acids (Snetsinger and Scott,
1961~. Daniel and Waisman (1969) fed diets providing 0.21, 0.64, and
1.07 percent sulfur from ~-methionine to growing rats. The high
c-methionine levels initially caused severe growth depression;
however, metabolic adaptation occurred and was believed related to
altered hepatic enzyme ratios. Cohen et al. (1958) found similar growth
depression effects from D~-methionine and homocysteine but con-
cluded the effects were not associated with excess sulfur. A curious
hemosiderin deposition in the spleen was associated with the excess
dietary methionine (Klavins et al., 1965~.
The relative toxicities of organic sulfur compounds for chicks have
been evaluated by Katz and Baker (1975~. Methionine and homo-
cysteine were very toxic, while cysteine was found relatively nontoxic.
When diets contained the minimal required levels of threonine and
glycine, 0.52 and 0.51 percent, respectively, methionine at 1.25 percent
OCR for page 473
Sulfur 473
of the diet (equal to 2,690 ppm sulfur) caused a 40 percent reduction in
growth rate of the chicks. Sasse and Baker (1974) studied the effect of
increasing levels of K2SO4 equal to 37-370 ppm sulfur in the diets of
chickens and noted a plateauing effect on growth and feed efficiency at
the 185 and 370 ppm levels.
HIGH LEVELS
Acute sulfur toxicosis in cattle has been reported by Coghlin (19441.
This incident stemmed from excessive use of liquid sulfur as a top
dressing on green chop in an effort to control lice and ringworm. An
estimated 1.36 kg of liquid sulfur were added to the feed for 25 head of
cattle. Signs of toxicosis were muscular twitching, restlessness, diar-
rhea, recumbent attitude, and dyspnea. All animals that became recum-
bent appeared to be blind, became comatose, and died. Luedke et al.
(1959) found that single oral doses of 53~1,860 g sulfur as sodium
bisulf~te administered to adult cattle caused death within 16 days.
Acute sulfur toxicosis in sheep was accidentally induced (White,
1964) when excessive quantities of sublimated sulfur (flowers of sulfur)
were mixed with a concentrate mix and fed to 480 sheep for treatment
of contagious ovine ecthyma. It was estimated that the sheep consumed
an average of 62 g sulfur instead of the anticipated 15 g per sheep.
Evidence of toxicosis occurred within 24 hours and included colicky
pain, depressed attitude, dyspnea, pyrexia, recumbency, H2S odor of
the breath, and about 5 percent mortality within 3 days. Postmortem
examination revealed the sulfur-toxic sheep had severe enteritis, peri-
toneal effusions, darkened kidneys, and generalized petechial
hemorrhages.
Several acute sulfur toxicity studies have been conducted with dogs.
Dougherty et al. (1943) reported on administering hydrogen sulfide
(H2S) per rectum to dogs. Hydrogen sulfide administered at the rate of
3.6 cc/min was not lethal, but rates of 4.1 to 10 cc/min were fatal to dogs
breathing air. Dogs breathing 90 percent oxygen and 10 percent carbon
dioxide tolerated doses up to 22 cc hydrogen sulfide per minute ad-
ministered per rectum. Gilman et al. (1946) intravenously administered
single doses of sodium tetrathionate to dogs at rates equal to 59-350 mg
sulfur per kilogram. The lowest level was without effect but the highest
levels caused death within 3 days.
The acute toxic effects of intraperitoneally administered sodium
bisulf~te have been investigated in several species (Wilkins et al., 1968),
because it is used as an antioxidant in peritoneal dialysis solutions. The
OCR for page 474
474 MINERAL TOLERANCE OF DOMESTIC ANIMALS
dosage range of 17~393 mg/kg of body weight of dog was used, and the
arm for -administered sodium bisulfite was calculated to be 244 mg/kg.
The arm for -administered sodium bisulfite in other species was found
to be 300 mg/kg for rabbits, 65~740 mg/kg for rats, and 675 mg/kg for
mice. Hauschild (1960) found the oral administration of 2.5 mg H2SO3
per kilogram of body weight, intravenous administration of 30 mg
NaHSO3 per kilogram of body weight, and the subcutaneous adminis-
tration of 90~1 ,000 mg NaHSO3 per kilogram of body weight to be fatal
in the dog.
The acute toxic effects of sodium tetrathionate administered intra-
venously to dogs have been investigated by Gilmanet al. (1946~. Doses
of 60 mg sulfur per kilogram as tetrathionate did not cause death, but
all higher doses used (25~500 mg/kg) caused death in 2 to 9 days. Acute
lethal doses caused vomition, hyperpnea, ataxia, and anorexia, while
sublethal doses produced proximal tubular necrosis. The data of Gil-
man et al. (1946) also indicate that rabbits are more sensitive to sodium
tetrathionate toxicosis than dogs. All rabbits given 48 mg sulfur per
kilogram or more as sodium tetrathionate intravenously died. Saunders
and Wills (1954) administered sulfur as sodium tetrathionate to rabbits
intravenously at the rates of 4.8 to 48 mg/kg via the femoral vein. Doses
between 36 and 48 mg/kg caused proximal tubule necrosis, as was also
observed in dogs by Gilman et al. (1946~.
There appears to be a critical toxic level for sodium bisulfite in
rabbits. The ~D50 for intravenously administered sulfur as sodium bisul-
fite in rabbits was found to be 20 mg/kg (Hoppe and Goble, 1951), with
death due to thrombosis and respiratory failure. Approximately two-
thirds of the lasso' however, was injected 3 times per day, 5 days per
week, for 8 weeks without apparent toxicosis. Rabbits seem more
sensitive to sulfur as sodium bisulfite than some other laboratory
animals, because the calculated arm levels for hamsters, rats, and mice
are 30, 3S, and 42 mg/kg, respectively.
Guinea pigs were found more susceptible to H2SO4 mists than several
other laboratory animal species Freon et at., 19501. Exposure to H2SO4
mist concentrations equal to 7.2 ppm sulfur for 2.75 hours caused death
in guinea pigs, whereas other species (cats, rabbits, rats, and mice)
survived the equivalent of 38 ppm for 7 hours. The morphologic effects
of the H2SO4 mists in.the guinea pigs included labored breathing, pul-
monary congestion, emphysema, pulmonary edema, and degeneration
of the respiratory epithelium.
The arm for intraperitoneally administered sulfur compounds,
Na2S 9H2O, Na2SO3 7H2O, NaHSO4 H2O, and Na2S2O3 in mice were
OCR for page 475
Sulfur
475
found by Nofre et al. (1963) to be 53, 277, 193, and 226 mg/kg, respec-
tively. These investigators concluded the sulfur ion was 202 times as
toxic as the chloride ion.
An accidental case of acute sulfur toxicosis in the horse (Ales, 1907)
resulted from the use of a flowers of sulfur gruel given orally as a
systemic adjunct to the topical treatment for collar gall in the horse.
One and one-half kilograms of flowers of sulfur were given to a total of
five horses, and therefore, the individual dosage approximated 300 g
per horse. Within 3 hours, the treated horses developed violent colic,
collapsed to the ground, and developed foetid diarrhea, H2S odor of the
feces, a feeble, thready pulse, and red-brown urine. Death occurred
within a few hours in at least one horse. The surviving horses had
unquenchable thirst and diarrhea for 2 days.
FACTORS AFE;ECTING TOXICITY
The literature leaves most matters on this topic to speculation. If one
determines that factors that increase the requirement for sulfur-
containing amino acids in turn decrease the susceptibility of the
organisms to sulfur toxicity, then increased dietary protein level, in-
creased dietary energy level, and increased environmental temperature
would all be factors which decrease the toxicity to sulfur.
The toxicity of sulfur in large part is determined by the enzyme
systems of the exposed organism, and especially by whether the or-
ganism has the capacity to form hydrogen sulfide from the inorganic
sulfate sources presented. The rate of exposure becomes a critical
factor in terms of the organ~sm's ability to safely metabolize the toxic
agent or its intermediates (Mudd et al., 19671.
Wolf and Varandani (1960) demonstrated that vitamin A deficiency
impairs the ability of the gut mucosa of rats to incorporate sulfate ions
and glucose into mucopolysaccharides. This is due to an inhibition of
sulfotransferases by the vitamin A deficiency.
The rate of excretion of intraperitoneally injected 35S sulfate is
greatly increased by the simultaneous subcutaneous administration of
2-naphthylamine or 2-naphthol; therefore, these compounds should de-
crease the toxicity of sulfur (Laidlaw and Young, 19481. Sodium azide,
as well as sodium fluoride, inhibit the transfer of sulfate from the
mucosal to the serosal surfaces of the intestine. These compounds.
therefore, would also be expected to reduce the toxicity of sulfur
(Dziewiatkowski, 19701. Whether high dietary copper levels reduce the
toxicity of sulfur in a manner opposite to that in which sulfate and
OCR for page 476
476 MINERAL TOLERANCE OF DOMESTIC ANIMALS
molybdenum induce copper deficiencies appears not to have been
demonstrated. It may be that elevated dietary copper and molybdenum
levels would also decrease the toxicity of sulfur.
TISSUE LEVELS
The volatility of sulfur creates analytics errors unless appropriate pre-
cautions are taken, especially in analyzing certain vegetables. Masters
and McCance (1939) have published some values on the sulfur content
of tissues and edible animal by-products. Some selected values include
milk, 292 ppm; egg whites, 1,820 to 2,160 ppm; egg yolks, 1,649 to 2,010
ppm; rabbit muscle meat, 1,640 ppm; duck muscle meat, 3,950 ppm.
The nitroge~sulfur ratio is an important index of the biological value
of food substances. For meat and fish samples, the N-S ratios are quite
constant; therefore, by nitrogen analysis, one can indirectly calculate
quite accurately the sulfur content of feeds. The average N-S ratio is
lS.2: 1.0 for muscle meats and 13.8:1.0 for fish meats (Masters and
McCance, 1939~.
MAXIMUM TOLERABLE LEVELS
The data presented do not establish a very clear-cut, safe upper limit for
sulfur for any of the species or for any specific sulfur source. Interpret-
ing the combined data of Lewis (1954), Marcilese et al. (1969), and
L'Estrange et al. (1972), and considering the sheep representative of
sulfur metabolism in ruminants, it would appear that 0.4 percent is the
maximum tolerable level for dietary sulfur as sodium sulfate.
Data for monogastrics are not definitive either. Arnold and Goble
(1950) have fed dogs what would be comparable to 0.28 percent supple-
mental sulfur in the form of ammonium persulfate for 16 weeks without
apparent effect. In the case of the rat, Smith (1973) stated that the
optimal total sulfur level, inorganic and organic, for rat diets is about
0.69 percent. The toxic effects of dietary inorganic sulfate are believed
due to its conversion to hydrogen sulfide by the gastrointestinal flora in
both classes of animals represented, but monogastrics may be less
tolerant of this very toxic form of sulfur than ruminants.
OCR for page 480
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488 MINERAL TOLERANCE OF DOMESTIC ANIMALS
\
REFERENCES
Ales. 1907. Case of poisoning by sulphur in the horse. Vet. J. 63:254.
Alhassan, W. S., and L. D. Satter. 1968. Observations on sodium sulfite administration
to ruminant. J. Dairy Sci. 51:981.
Anderson, R. C., and K. K. Chen. 1940. Absorption and toxicity of sodium and potas-
sium thiocyanates. J. Am. Pharmacol. Assoc. 29:152.
Arnold, A., and F. C. Gable. 1950. Studies with dogs fed flour treated with ammonium
persulfate. Cereal Chem. 27:375.
Baker, D. H. 1977. Sulfur in non-ruminant nutrition. National Feed Ingredients Associa-
tion, West Des Moines, Iowa.
Bird, P. R. 1972. Sulfur metabolism and excretion studies in ruminants. X. Sulphide
toxicity in sheep. Aust. J. Biol. Sci. 25:1087.
Bray, A. C. 1965. Studies on the sulfur metabolism of sheep. Ph.D. thesis. University of
Western Australia, Nedlands.
Bneger, H., and J. Teisinger (eds.). 1966. Toxicology of Carbon Disulfide. Excerpta
Medica Foundation, Amsterdam.
Brown, R. G., and A. Gamatero. 1970. Effect of added sulfate on the utilization of peanut
protein by the rat. Can. J. Anim. Sci. 50:742.
Caldwell, A. D. S., P. G. T. Bye, and M. H. Biggs. 1967. Side effects of dimethyl
sulphoxide. Nature 215: 1 168.
Coghlin, C. L. 1944. Hydrogen sulfide poisoning in cattle. Can. J. Comp. Med. 8:1 11.
Cohen, H. P., H. C. Choitz, and C. P. Berg. 1958. Response of rats to diets high in
methionine and related compounds. J. Nutr. 64:555.
Daniel, R. G., and H. A. Waisman. 1969. Adaptation of the weanling rat to diets contain-
ing excess methionine. J. Nutr. 99:299.
Dougherty, R. W., R. Wong' and B. E. Christensen. 1943. Studies of hydroge~sulfide
poisoning. Am. J. Vet. Res. 4:254.
du Vigneaud, V. 1952. A Trail of Research in Sulfur Chemistry and Metabolism. Cornell
University Press, Ithaca, N.Y.
Dziewiatkowski, D. D. 1970. Metabolism of sulfate esters, p. 97. In 0. H. Muth and
J. E. Oldfield (eds.). Symposium: Sulfur in Nu~ition. AV! ~bbshing Co., Westport,
Conn.
Egan, D. A., and T. O. O'Cuill. 1968. An attempt to produce swayback in lambs born to
ewes dosed with high levels of molybdenum, inorganic sulphate and manganese
during pregnancy. Irish Vet. J. 22:28.
Fitzhugh, O. G., L. F. Knudsen, and A. A. Nelson. 1946. The chronic toxicity of sulfites.
J. Pharmacol. Exp. Ther. 86:37.
Gilman, A., F. S. Philips, E. S. Koelle, R. P. Allen, and E. St. John. 1946. The metabolic
reduction and nephrotoxic action of tetrathionate in relation to a possible interaction
with sulfhydryl compounds. Am. J. Physiol. 147:115.
Goodrich, R. D. 1978. Sulphur in Ruminant Nutrition. National Feed Ingredients Asso-
ciation, West Des Moines, Iowa.
Harter, J. M., and D. H. Baker. 1978. Factors affecting methionine toxicity and its
alleviation in the chick. J. Nutr. 108:1061.
Hauschild, F. 1960. Pharmakologie und Grundlagen der Toxikologie. 2. Aufl. Leipsig. S
368.
Hoppe, J. O., and F. C. Goble. 1951. The intravenous toxicity of sodium bisulfite. J.
Pharmacol. Exp. Ther. 101:101.
Kaemmerer, K. Von. 1972. Zur toxikologischen Bedeutung von Sulfit bein Wiederkauer.
Zucker 25:123.
OCR for page 489
Sulfur 489
Kaemmerer, K. Van, E. Barke, and M. J. Seidler. 1972. Vertraglichkeit van Sulfit in
hoher Konzentration auf Trackenschnitzeln bei Schafen. Zucker 25:128.
Katz, R. S., and D. H. Balcer. 1975. Toxicity of various organic sulfur compounds for
chicks fed crystalline amino acid diets containing threonine and glycine at their
minimal dietary requirements for maximal growth. J. Anim. Sci. 41:1355.
Klavins, J. V., T. D. Kinney, and N. Kaufman. 1965. Histopathologic changes in methio-
nine excess. Arch. Pathol. 76:661.
Laidlaw, J. C., and L. Young. 1948. Studies on the synthesis of ethereal sulphatesin vivo.
Biochem. J. 42:1.
Larson, T. E. 1959. Mineral content of public ground water supplies in Illinois. Cir. 31.
State of Illinois, Water Survey Division, Urbana.
Leach, R. M., T. R. Zeigler, and L. C. Norris. 1960. The effect of dietary sulphate in the
growth rate of chicks fed a purified diet. Poult. Sci. 39:1577.
Leclercq, R. 1972. Commercially important sulfur compounds. In A. Senning, ed. Sulfur
in Organic and Inorganic Chemistry. Marcel Dekker, New York.
L'Estrange, J. L., and F. Murphy. 1972. Effect of dietary mineral acids on voluntary
intake, digestion, mineral metabolism and acid-base balance of sheep. Br. J. Nutr.
28:1.
L'Estrange, J. L., J. J. Clarke, and D. M. McAleese. 1969. Studies on high intake of
various sulphate salts and sulphuric acid in sheep. 1. Effects on voluntary fe~d intake,
digestibility and acid base balance. Irish J. Agric. Res. 8:133.
L'Estrange, J. L., P. K. Upton, and D. M. McAleese. 1972. Effects of die~y sulfate on
voluntary feed intake and metabolism of sheep. I. A comparison between different
levels of sodium sulphate and sodium chloride. Irish J. Agric. Res. 11:127.
Levitman, M. K. L. 1968. Morphological changes in the skeleton of rats under the
influence of incorporated Sulfur-35. Mater. Toksikol. Radioak. Veshchestv. 6:65.
Lewis, D. 1954. The reduction of sulphate in the rumen of the sheep. Biochem. J. 56:391.
Luedke, A. J., J. W. Bratzler, and H. W. Dunne. 1959. Sodium metabisulfite and sulfur
dioxide gas (silage preservative) poisoning in cattle. Am. J. Vet. Res. 20:690.
Mamatashvili, M. I. 1970. Toxic action of carbon monoxide, sulfur dioxide, and their
combinations on the fertility of rats. Gig. Sanit. 35:100.
Marcilese, N. A., C. B. Ammerman, R. M. Valsecchi, B. G. Dunavant, and G. K. Davis.
1969. Effect of dietary molybdenum and sulphate upon copper metabolism in sheep.
J. Nutr. 99:177.
Masters, M., and R. A. McCance. 1939. The sulfur content of foods. Biochem. J. 33:1304.
Morrow, P. E., H. C. Hodge, W. F. Neuman, E. A. Maynard, H. J. Blanchet, Jr., D. W.
Fassett, R. E. Birk, and S. Manrodt. 1952. The gastrointestinal non-absorption of
sodium cellulose sulfate labeled with s3s. J. Pharrnacol. Exp. Therap. 105:273.
Mudd, S. H., F. Irreverre, and L. Laster. 1967. Sulfite oxidase deficiency in man:
Demonstration of enzymatic defect. Science 156:1599.
Muth, O. H., and J. E. Oldfield (eds.). 1970. Symposium: Sulfur in Nutrition. AV] ~blish-
ing Co., Westport, Conn.
Nickless, G. (ed.). 1968. Inorganic Sulphur Chemistry. Elsevier Publishing Co., New
York.
Nofre, C., H. Dufour, and H. Cier. 1963. Toxicite generale comparee des anions mine-
raux chez la souris. C. R. Acad. Sci. 257:791.
O'Donoghue, J. G. 1961. Hydrogen sulfide poisoning in swine. Can. J. Comp. Med. Vet.
Sci. 25:217.
O'Donoghue, J. G., and F. E. Graesser. 1962. Effects of sulphur dioxide on guinea pigs
and swine. Can. J. Comp. Med. Vet. Sci. 26:255.
OCR for page 490
490 MINERAL TOLERANCE OF DOMESTIC ANIMALS
Organesyan, N. M., and E. S. Gaidova. 1968. Morphological changes in rat organs
effected by the chronic administration of sulphur35. Mater. Toksikol. Radioak. Vesh-
chestv. 6:83.
Paterson, D. W., R. C. Wahlstrom, G. W. Libal, and O. E. Olson. 1979. Effects of sulfate
in water on swine reproduction and young pig performance. J. Anim. Sci. 49:664.
Peirce, A. W. 1960. Studies of salt tolerance of sheep. III. The tolerance of sheep for
mixtures of sodium chloride and sodium sulphate in'the drinking water. Aust. J. Agnc.
Res. 11:548.
Postgate, J. R. 1968. The Sulphur cycle, p. 259. In G. Nickless (ed.). Inorganic Sulphur
Chemistry. Elsevier Publishing Co., New York.
Roy, A. B., and P. A. Trudinger. 1970. The Biochemistry of Inorganic Compounds of
Sulphur. Cambridge University Press, England.
Sasse, C. E., and D. H. Baker. 1974. Factors affecting sulfate sulfur utilization by the
young chick. Poult. Sci. S3:652.
Saunders, J. P., and J. H. Wills. 1954. The nephrotoxic action of sodium tetrathionate.
J. Pharmacol. Exp. Ther. 112:197.
Scheel, L. D. 1967. Experimental carbon disulfide poisoning in rabbits: Its mechanisms
and similanties with human cases. In H. Brieger and J. Teisinger (eds.). Toxicology
of Carbon Disulfide. Exce~pta Medica Foundation, Amsterdam.
Schelling, G. T., and E. E. Hatfield. 1968. Effect of abomasally infused nitrogen sources
on nitrogen retention of growing lambs. J. Nutr. 96:319.
Senning, A. (ed.). 1972. Sulfur in Organic and Inorganic Chemistry. Marcel Dekker,
New York.
Smith, J. T. 1973. An optimal level of inorganic sulfate for the diet of a rat. J. Nutr.
103:1008.
Snetsinger, D. C., and H. M. Scott. 1961. The relative toxicity of intraperitoneally
injected amino acids and the effect of glycine and arginine thereon. Poult. Sci.
40:1681.
Sorbo, B. 1972. The pharmacology and toxicology of inorganic sulfur compounds, p. 143.
In A. Senning (ed.). Sulfur in Organic and Inorganic Chemistry. Marcel Dekker, New
York.
Treon, J. F., F. R. Dutra, J. Cappel, H. Sigmon, and W. Younker. 1950. Toxicity of
sulfuric acid mist. Arch. Ind. Hyg. Occup. Med. 2:716.
Upton, P. K., J. L. L'Estrange, and D. M. McAleese. 1970. Studies on high intake of
various sulphate salts and sulphuric acid in sheep. 2. Effects on the absorption,
excretion and retention of sulphur. Irish J. Agric. Res. 9:151.
Walker, D. M., and L. J. Cook. 1967. Nitrogen balance studies with the milk-fed la~nb.
4. Effect of different nitrogen and sulphur intakes on live weight gain and wool growth
and on nitrogen and sulphur balances. Br. J. Nutr. 21:237.
Weeth, H. J., and J. E. Hunter. 1971. Drinking of sulfate-water by cattle. J. Anin~. Sci.
32:277.
Weigand, E., M. Kirchgessner, W. Granzer, and G. Ranfft. 1972. Zur Futterung hoher
Sulfitmengen an Milchkuhe; SO2-Vertraglichkeit und SO2-gehalt der Milch. Zentra}bl.
Veterinaermed. Re'ihe A 19:490.
White, J. B. 1964. Sulphur poisoning in ewes. Vet. Rec. 76:278.
Wilkins, J. W., J. A. Greene, and J. M. Weller. 1968. Toxicity of intraperitoneal bisulfite.
Clin. Pharmacol. Ther. 9:328.
Wolf, G., and P. T. Varandani. 1960. Studies on the function of vitamin A in mucopoly-
saccharide biosynthesis. Biochim. Biophys. Acta 43:501.
Young, L., and G. A. Maw. 1958. The Metabolism of Sulphur Compounds. John Wiley
& Sons, New York.
Representative terms from entire chapter:
sulfur compounds
