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Table of Contents | |
GADOLINIUM
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Redox Rep 1999;4(5):243-50 |
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Derangement of Kupffer cell functioning and
hepatotoxicity in hyperthyroid rats subjected to acute iron overload.
Boisier X, Schon M, Sepulveda A, Basualdo A, Cornejo P, Bosco C, Carrion
Y, Galleano M, Tapia G, Puntarulo S, Fernandez V, Videla LA
Programas de Farmacologia Molecular y Clinica, Facultad de Medicina,
Universidad de Chile, Santiago.
Liver oxidative stress, Kupffer cell functioning, and cell injury were
studied in control rats and in animals subjected to
L-3,3',5-tri-iodothyronine (T3) and/or acute iron overload. Thyroid
calorigenesis with increased rates of hepatic O2 uptake was not altered by
iron treatment, whereas iron enhanced serum and liver iron levels
independently of T3. Liver thiobarbituric acid reactants formation increased
by 5.8-, 5.7-, or 11.0-fold by T3, iron, or their combined treatment,
respectively. Iron enhanced the content of protein carbonyls independently
of T3 administration, whereas glutathione levels decreased in T3- and
iron-treated rats (54%) and in T3Fe-treated animals (71%). Colloidal carbon
infusion into perfused livers elicited a 109% and 68% increase in O2 uptake
in T3 and iron-treated rats over controls. This parameter was decreased
(78%) by the joint T3Fe administration and abolished by gadolinium chloride
(GdCl3) pretreatment in all experimental groups. Hyperthyroidism and
iron overload did not modify the sinusoidal efflux of lactate dehydrogenase,
whereas T3Fe-treated rats exhibited a 35-fold increase over control values,
with a 54% reduction by GdCl3 pretreatment. Histological studies showed a
slight increase in the number or size of Kupffer cells in hyperthyroid rats
or in iron overloaded animals, respectively. Kupffer cell hypertrophy and
hyperplasia with presence of inflammatory cells and increased hepatic
myeloperoxidase activity were found in T3Fe-treated rats. It is concluded
that hyperthyroidism increases the susceptibility of the liver to the toxic
effects of iron, which seems to be related to the development of a severe
oxidative stress status in the tissue, thus contributing to the concomitant
liver injury and impairment of Kupffer cell phagocytosis and
particle-induced respiratory burst activity.
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