Redistribution of subcellular calcium in rat liver on administration of vanadate

Gullapalli, Sharada; Shivaswamy, Vidya; Ramasarma, T.; Kurup, C. K. Ramakrishna

doi:10.1007/bf00221215

Cited by 11 publications

(1 citation statement)

References 24 publications

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“…The results of our study are well in congruence with this report. 32 Furthermore, it is also reported that stimulation of lipid peroxidation increases the intracellular content of calcium in isolated rat hepatocytes 33 therefore, it is suggestive that vanadium triggered Ca 2+ - dependent increase in lipid peroxidation. The coadministration (doxycycline + vanadium) to rats exhibited a significant decrease in calcium concentration.…”

Section: Discussionmentioning

confidence: 95%

Doxycycline: An Antibiotic Attenuates Oxidant Stress, Perturbation of Lipid Metabolites, and Antioxidants against Vanadium Toxicity in Rat Hepatocytes

Gassar

Mohamed

Emtawel

et al. 2022

Libyan International Medical University Journal

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Background The liver is target following exposure to pentavalent vanadium (V5+). Doxycycline is an antioxidant that prevents the progression of disease through inhibition of lipid peroxidation. Aim The present study was designed to evaluate the protective effects of doxycycline against vanadium-induced hepatoxicity. Methods Sixty two male Sprague-Dawley rats (250–300 g) were equally divided into the following four groups: control group (received 0.2 mL of physiological saline), doxycycline control group (received 4 mg/kg body weight on day 1 and 2 mg/kg body weight daily thereafter), vanadium group (received elemental vanadium 1.5 mg/kg-body weight in distilled water), and concomitantly treated group (doxycycline + vanadium) received (doxycycline 4 mg/kg body weight on day 1 and 2 mg/kg body weight thereafter + vanadium 1.5 mg/kg body weight), all given orally for 10 consecutive days. The rats were sacrificed by decapitation 24 hours after the last dose. The liver was removed rapidly and processed for the evaluation of metabolic variables: phospholipids, cholesterol, cerebrosides, gangliosides, reduced glutathione (GSH), vitamin C, calcium, acetylcholinesterase enzyme, and lipid peroxidation. Results Vanadium administration significantly reduced (−60 g) the body weight and significantly increased (+28%) the relative liver weight compared with controls. The rats exhibited neurological function deficits. Vanadium administration decreased the concentrations of metabolic variables compared with controls, cerebrosides (−50%), cholesterol (−39%), phospholipids (−18%), GSH (−45%), and inhibited acetylcholinesterase enzyme (–48%). Gangliosides (+ 38%), vitamin C (+ 20%), and calcium (+ 80%) were increased together with an enhancement (+64%) in lipid peroxidation. The combined treatment (vanadium and doxycycline) significantly increased (+25 g) the body weight and relative liver weight of rat was significantly reduced (+5%) compared with vanadium administered group. The levels of metabolic variables were significantly reversed in this group in the following order: cholesterol (+17%), phospholipids (+7%), vitamin C (−14%), acetylcholinesterase enzyme activity (−27%) together with inhibition (−16%) of lipid peroxidation. All levels were (p < 0.05). Doxycycline presented no effect on the levels of GSH, cerebrosides, and gangliosides. Conclusion Results of this study suggested vanadium-induced oxidation of lipids and sphingolipids in hepatocytes and much of GSH was consumed against high production of reactive oxygen species. Doxycycline protected against vanadium-induced oxidative damage that could be attributed to its free radical scavenging effects on membrane-bound lipids and acetylcholinesterase enzyme.

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Section: Discussionmentioning

confidence: 95%

Doxycycline: An Antibiotic Attenuates Oxidant Stress, Perturbation of Lipid Metabolites, and Antioxidants against Vanadium Toxicity in Rat Hepatocytes

Gassar

Mohamed

Emtawel

et al. 2022

Libyan International Medical University Journal

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Characterization of oxygen free radicals generated during vanadate-stimulated NADH oxidation

1992

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The oxidation of NADH and accompanying reduction of oxygen to H2O2 stimulated by polyvanadate was markedly inhibited by SOD and cytochrome c. The presence of decavanadate, the polymeric form, is necessary for obtaining the microsomal enzyme-catalyzed activity. The accompanying activity of reduction of cytochrome c was found to be SOD-insensitive and therefore does not represent superoxide formation. The reduction of cytochrome c by vanadyl sulfate was also SOD-insensitive. In the presence of H2O2, all the forms of vanadate were able to oxidize reduced cytochrome c, which was sensitive to mannitol, tris and also catalase, indicating H2O2-dependent generation of hydroxyl radicals. Using ESR and spin trapping technique only hydroxyl radicals, but not superoxide anion radicals, were detected during polyvanadate-dependent NADH oxidation.

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Effect of glucagon and some other alpha and beta adrenergic agonists and antagonists on alanine amino transferase of perfused rat liver

Begum

Datta

1991

Mol Cell Biochem

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Glucagon increased alanine amino transferase (AAT) activity in perfused rat liver by about 90% over control. Propranolol, the beta receptor antagonist, abolished the effect of glucagon on this enzyme. Well known beta receptor agonists like isoproterenol, norepinephrine and epinephrine also increased the enzyme activity under identical condition and the enhancement was similarly abolished by propranolol. These experiments suggest that the effect of glucagon on AAT was mediated through beta adrenergic receptor. However, the interesting observation was that phenylephrine, alpha receptor agonist and phenoxybenzamine and tolazoline, two alpha receptor antagonists, increased the AAT activity like glucagon in perfusion experiments and the effects of all these three agents were also abolished by propranolol. Glucagon, when perfused with phenoxybenzamine showed some additive effect. From all these results we are proposing that in our system phenoxybenzamine is acting as beta agonist although it is known to be an alpha antagonist.

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Redistribution of subcellular calcium in rat liver on administration of vanadate

Cited by 11 publications

References 24 publications

Doxycycline: An Antibiotic Attenuates Oxidant Stress, Perturbation of Lipid Metabolites, and Antioxidants against Vanadium Toxicity in Rat Hepatocytes

Doxycycline: An Antibiotic Attenuates Oxidant Stress, Perturbation of Lipid Metabolites, and Antioxidants against Vanadium Toxicity in Rat Hepatocytes

Characterization of oxygen free radicals generated during vanadate-stimulated NADH oxidation

Effect of glucagon and some other alpha and beta adrenergic agonists and antagonists on alanine amino transferase of perfused rat liver

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