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Oxidative stress in toadfish (Halobactrachus didactylus) cardiac muscle Acute exposure to vanadate oligomers
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Vanadate solutions as ‘metavanadate’ (containing ortho and metavanadate species) and ‘decavanadate’ (containing manly decameric
species) (5 mM; 1 mg/kg) were injected intraperitoneously in Halobatrachus didactylus (toadfish), in order to evaluate the contribution of
decameric vanadate species to vanadium (V) intoxication on the cardiac tissue. Following short-term exposure (1 and 7 days), different
changes on antioxidant enzyme activities—superoxide dismutase (SOD), catalase (CAT), selenium-glutathione peroxidase (Se-GPx), total
glutathione peroxidase (GPx), lipid peroxidation and subcellular vanadium distribution were observed in mitochondrial and cytosolic
fractions of heart ventricle toadfish. After 1 day of vanadium intoxication, SOD, CAT and Se-GPx activities were decreased up to 25%,
by both vanadate solutions, except mitochondrial CAT activity that increased (123%) upon decavanadate administration. After 7 days of
exposure, decavanadate versus metavanadate solutions promoted different effects mainly on cytosolic CAT activity (256% versus25%),
mitochondrial CAT activity (210% versus110%) and total GPx activity (11% versus235%), whereas lipid peroxidation products were
significantly increased (182%) upon 500mM decavanadate intoxication. Accumulation of vanadium in total (0.13760.011mg/g) and
mitochondrial (0.02260.001mg/g) fractions was observed upon 7 days of metavanadate exposure, whereas for decavanadate, the
concentration of vanadium increased in cytosolic (0.02060.005mg/g) and mitochondrial (0.02160.009mg/g) fractions. It is concluded
that decameric vanadate species are responsible for a strong increase on lipid peroxidation and a decrease in cytosolic catalase activity
thus contributing to oxidative stress responses upon vanadate intoxication, in the toadfish heart.
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Oxidative stress Vanadate