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Abstract(s)
The contribution of vanadate oligomers to the acute
histological effects of vanadium was analyzed in the heart,
kidney, and liver of Halobatrachus didactylus (Schneider,
1801).A sublethal vanadium dose(5mM,1mL/kg)in the form
of metavanadate(containing ortho and metameric species)or in
the form of decavanadate (containing only decameric species)
was intraperitoneally administered by injection, and specimens
of H. didactylus were sacrificed at one and seven days postinjection.
Sections of heart ventricle and renal and hepatic tissue
were stained with hematoxylin-eosin and examined by light
microscopy to identify vanadium-induced tissue injury. In addition,
PicroSirius-stained ventricular sections were analyzed
by bipolarized light microscopy to determine the fraction of
myocardium occupied by the ventricular wall structural elements
(collagen I, collagen III, and cardiac muscle). Both
vanadate solutions produced similar effects in the renal tissue.
Morphological alterations included damaged renal tubules
showing disorganized epithelial cells in different states of
necrosis. Reabsorbed renal tubules and hyperchromatic interstitial
tissue were also observed. The hepatic tissue presented
hyperchromatic and hypertrophied nuclei, along with necrotic
and hypertrophied hepatocytes, and more severe changes were
observed in the liver with exposure to decavanadate. Vanadate
oligomers promoted evident tissue lesions in the kidney and
liver, but not in the cardiac tissue. However, cardiac tissue
structural changes were produced. For example, decavanadate
induced a hypertrophy of the ventricle due to a decrease in the
percentage of myocardium occupied by collagen fibers. In
general, decavanadate was shown to be more toxic than metavanadate.
Description
Keywords
Vanadate Stress in vivo