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Table of Contents | |
- ANTIMONY
-
- Title
Effects of antimony on rats following 90-day exposure via
drinking water.
Author
Poon R; Chu I; Lecavalier P; Valli VE; Foster W; Gupta S; Thomas B
Address
Bureau of Chemical Hazards, Environmental Health Directorate, Health Canada,
Environmental Health Center, Tunney's Pasture, Ottawa, Canada.
Source
Food Chem Toxicol, 36(1):21-35 1998 Jan
Abstract
The subchronic toxicity of antimony in drinking water was
studied in the rat. Male and female Sprague-Dawley rats (127-135 g body weight,
15 animals per group) were exposed to a soluble trivalent antimony
salt, potassium antimony tartrate, in drinking water at
concentrations of 0.5, 5, 50 and 500 ppm for 13 wk. Control rats received tap
water as drinking water. An additional 10 male and 10 female rats were included
in each of the control and 500 ppm groups and were given tap water for a further
4-wk recovery period after the 13-week treatment period. During treatment, the
highest dose animals of both sexes consumed significantly less water and showed
suppressed body weight gain. During recovery, water intake was quickly restored
to that of the control groups and body weight gain was accelerated. At
termination, one highest dose male had a cirrhotic liver, and three highest dose
males exhibited gross haematuria. Female rats showed a dose-related decrease in
serum glucose starting at 5 ppm, and rats of both sexes in the highest dose
group had slightly decreased alkaline phosphatase activity and creatinine. The
highest dose males had decreased red blood cell and platelet counts and
increased mean corpuscular volume. Hepatic glutathione S-transferase activity
was increased in the highest dose males and females and
ethoxyresorufin-O-deethylase activity was increased in the highest dose males.
In the highest dose groups, mild adaptive histological changes were observed in
the thyroid, liver and pituitary gland of both sexes, and
in the spleen of male rats and thymus of female rats. After a 4-wk
recovery period, the pituitary gland of both sexes appeared normal and the
changes in the liver and thyroid of both sexes became less severe. On the other
hand, minimal changes persisted in the spleen of both sexes and in the thymus of
males. Tissue antimony levels were dose-related and follow the
order: red blood cells > > spleen, liver > kidney > brain, fat >
serum. After the recovery period, antimony level in the highest
dose animals decreased for all tissues except the spleen, which remained the
same as before recovery. A NOAEL of 0.5 ppm antimony in drinking
water, equivalent to an average intake of 0.06 mg/kg body weight/day, was
established on the basis of the histological and biochemical changes observed at
5.0 ppm.
- Title
Increased biliary excretion of glutathione is generated by the
glutathione-dependent hepatobiliary transport of antimony and bismuth.
Author
Gyurasics A; Koszor´us L; Varga F; Gregus Z
Address
Department of Pharmacology, University Medical School of P´ecs, Hungary.
Source
Biochem Pharmacol, 44(7):1275-81 1992 Oct 6
Abstract
We have recently demonstrated that the hepatobiliary transport of arsenic is
glutathione-dependent and is associated with a profound increase in biliary
excretion of glutathione (GSH), hepatic GSH depletion and diminished GSH
conjugation (Gyurasics A, Varga F and Gregus Z, Biochem Pharmacol 41: 937-944
and Gyurasics A, Varga F and Gregus Z, Biochem Pharmacol 42: 465-468, 1991).
The present studies in rats aimed to determine whether antimony and bismuth,
other metalloids in group Va of the periodic table, also possess similar
properties. Antimony potassium tartrate (25-100 mumol/kg, i.v.) and bismuth
ammonium citrate (50-200 mumol/kg, i.v.) increased up to 50- and 4-fold,
respectively, the biliary excretion of non-protein thiols (NPSH). This
resulted mainly from increased hepatobiliary transport of GSH as suggested by
a close parallelism in the biliary excretion of NPSH and GSH after antimony or
bismuth administration. Within 2 hr, rats excreted into bile 55
and 3% of the dose of antimony (50 mumol/kg, i.v.) and bismuth
(150 mumol/kg, i.v.), respectively. The time courses of the biliary excretion
of these metalloids and NPSH or GSH were strikingly similar suggesting
co-ordinate hepatobiliary transport of the metalloids and GSH. However, at the
peak of their excretion, each molecule of antimony or bismuth
resulted in a co-transport of approximately three molecules of GSH. Diethyl
maleate, indocyanine green and sulfobromophthalein (BSP), which decreased
biliary excretion of GSH, significantly diminished excretion of antimony and bismuth
into bile indicating that hepatobiliary transport of these metalloids is GSH-dependent.
Administration of antimony, but not bismuth, decreased hepatic
GSH level by 30% and reduced the GSH conjugation and biliary excretion of BSP.
These studies demonstrate that the hepatobiliary transport of trivalent
antimony and bismuth is GSH-dependent similarly to the
hepatobiliary transport of trivalent arsenic. Proportionally to their biliary
excretion rates, these metalloids generate increased biliary excretion of GSH
probably because they are transported from liver to bile as unstable GSH
complexes. The significant loss of hepatic GSH into bile as induced by arsenic
or antimony may compromise conjugation of xenobiotics with GSH.
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