The contribution of decameric vanadate species to vanadate toxic effects in cardiac muscle was studied following an intravenous administration of a decavanadate solution (1 mM total vanadium) in Sparus aurata. Although decameric vanadate is unstable in the assay medium, it decomposes with a half-life time of 16 allowing studying its effects not only in vitro but also in vivo. After 1, 6 and 12 h upon decavanadate administration the increase of vanadium in blood plasma, red blood cells and in cardiac mitochondria and cytosol is not affected in comparison to the administration of a metavanadate solution containing labile oxovanadates. Cardiac tissue lipid peroxidation increases up to 20%, 1, 6 and 12 h after metavanadate administration, whilst for decavanadate no effects were observed except 1 h after treatment (+20%). Metavanadate administration clearly differs from decavanadate by enhancing, 12 h after exposure, mitochondrial superoxide dismutase (SOD) activity (+115%) and not affecting catalase (CAT) activity whereas decavanadate increases SOD activity by 20% and decreases (À55%) mitochondrial CAT activity. At early times of exposure, 1 and 6 h, the only effect observed upon decavanadate administration was the increase by 20% of SOD activity. In conclusion, decavanadate has a different response pattern of lipid peroxidation and oxidative stress markers, in spite of the same vanadium distribution in cardiac cells observed after decavanadate and metavanadate administration. It is suggested that once formed decameric vanadate species has a different reactivity than vanadate, thus, pointing out that the differential contribution of vanadium oligomers should be taken into account to rationalize in vivo vanadate toxicity.

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Abstract. 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 (5 mM, 1 mL/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.

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The purpose of this work is to calculate end‐systolic and end‐diastolic volumes of Halobatrachus didactylus ventricles, from two‐dimensional (2D) echocardiographic images, comparing four different linear methods, and to derive systolic indices of ventricular function—fractional shortening, ejection fraction, stroke volume, and cardiac output independent of the Fick principle. Echocardiography provided high resolution images of cardiac structures and allowed accurate linear measurements. The Simpson algorithm proved to be the best method of calculating ventricle volumes. As a corollary, ventricular mass can be derived from echocardiographic volume data. This noninvasive method promises wide utilization in experimental comparative cardiovascular biology. J. Exp. Zool. 286:585–595, 2000. © 2000 Wiley‐Liss, Inc.