Chemistry Reference
In-Depth Information
increased mortality were also observed (Halverson,
1966). The composition of the diet is of importance for
the chronic toxicity of selenium. In early experiments
it was realized that selenium was less toxic with high
protein content in the diet (Moxon, 1943). Methionine
might be an essential factor for this effect. A combina-
tion of methionine and tocopherol (or other antioxi-
dants) alleviated liver damage caused by 10 mg Se/kg,
given as selenate for 8 weeks (Levander and Morris,
1970). Other factors of importance are certain glyco-
sides, isolated from linseed oil, which have protected
against growth depression caused by 9 mg Se/kg diet
given as selenite (Palmer
et al
., 1980).
Selenium is known to accumulate in the anterior
pituitary and in selenium-treated animals (15 mg
sodium selenite/L drinking water) the growth hor-
mone and somatomedin C secretion on stimulation
was decreased, indicating that growth retardation in
selenium-treated rats could be mediated by reduced
GH and somatomedin C production (Thorlacius-
Ussing
et al
., 1987).
Twenty female long-tailed macaques received nasogas-
tric intubation of 0-600
kg caused, in some cattle, mild to severe forms of alkali
disease. No signifi cant neurological, renal, or hepatic
lesions developed. According to the authors, this sup-
ports the contention that blind staggers is caused by
factors other than excessive dietary selenium (O'Toole
and Raisbeck, 1995).
In male buffalo calves after repeated oral adminis-
tration of 0.3 mg selenourea/kg (providing 0.19 mg/
Se kg) for 75 days, selenosis was induced and sele-
nium increased from 0.70
µ
g/mL blood on day 0 to
3.12
g/mL on day 75. Signs occurred when Se levels
were about 2.0
µ
µ
g/mL and were prominent above 2.5-
2.6
g/mL (Deore
et al
., 2002).
In crossbred cow calves given sodium selenite
(0.25 mg/kg bw) for 16 weeks the treatment resulted
in characteristic signs of subchronic selenosis (i.e., alo-
pecia, cracking, and enlargement of hooves, interdig-
ital lesions, ring formation on the coronet region, and
gangrene at tip of the tail). The treatment resulted in a
signifi cant rise of blood selenium levels and concurrent
increase in erythrocytic glutathione peroxidase activ-
ity. Blood glutathione levels were lowered. Selenosis
caused oxidative stress as evidenced by increased lipid
peroxidation. Glutathione-S-transferase, glutathione
reductase, superoxide dismutase, and catalase activities
were signifi cantly increased (Kaur
et al
., 2003).
Pigs were fed sodium selenite or Se-enriched yeast,
added at 0, 5, 10, 15, or 20 mg/kg Se to corn-soybean
meal diets for 12 weeks. The results suggest that die-
tary Se from inorganic or organic sources was toxic at
5 mg/kg Se, but subsequent selenosis were more severe
and occurred sooner with sodium selenite. Decreased
weight gain, hair loss (alopecia), and separation of the
hoofs, increased plasma GOT activity, and other effects
were reported (Kim and Mahan, 2001).
In controlled feeding trials comparing seleno-
DL-methionine with
Astragalus bisulcatus
or sodium
selenate, growing swine developed signs of Se toxic-
ity including paralysis. Signs were more severe and
occurred sooner in the
A. bisulcatus
group (Panter
et al
.,
1996).
µ
g/kg/day L-selenomethionine
for up to 30 consecutive days. Two animals given 600
µ
g/
kg/day died. The incidence of anorexia, gastrointesti-
nal distress, mucocutaneous toxicity, and frequency
of reduced body temperature increased with time
and dose. At higher doses, disturbances in menstrua-
tion occurred. Also reproductive toxicity was noted.
The maximum tolerated dose was 150
µ
µ
g/kg/day
(Cukierski
et al
., 1989).
7.2.2 Domestic Animals
A chronic syndrome described in livestock and
horses is “alkali disease.” This disease has been asso-
ciated with the consumption of grains or plants con-
taining 5-25 mg Se/kg for periods of less than a month
(Moxon, 1943). The disease is characterized by lack of
vitality, loss of appetite, emaciation, deformation, and
shedding of hooves, loss of long hair, and erosions of
joints of the long bones. In more advanced cases, liver
cirrhosis may develop.
The syndrome “blind staggers” in livestock has also
been associated with the consumption of selenium in
accumulator plants. Characteristics of the syndrome are
impaired vision, depressed appetite, and a tendency to
“wander” in circles. This latter stage is characterized
by various degrees of paralysis, and death results from
respiratory failure (Moxon, 1943). However, the classifi -
cation of blind staggers has been questioned. Seventeen
yearling steers were fed 0.15, 0.28, and 0.8 mg Se/kg
bw as selenomethionine or selenite for 120 days; 0.28
and 0.8 mg selenomethionine/kg and 0.8 mg selenite/
7.2.3 Humans
7.2.3.1 Exposure to Supplements
Two individuals took selenium-containing yeast
at doses of 200 and 400
g selenium daily for 18
months. Together with dietary intake, they received
approximately 350 and 600
µ
g/day. Marginal hema-
tological changes and a borderline increase in serum
ALAT were seen (Schrauzer and White, 1978).
A small group of patients with rheumatoid arthritis
receiving 250
µ
g Se as organic selenium in addition to
selenium from food for 6 months had decreased levels
µ
