ascorbic-acid and Cardiotoxicity

The present study was conducted to investigate the role of vitamin C versus platelet-rich plasma (PRP) against sodium fluoride (NaF)-induced cardiotoxicity and cell death in rats' myocardium. Previous studies suggest that NaF decreased cellular viability and intracellular antioxidant power.. The present study revealed that NaF administration caused histological alterations in the cardiac muscle and increased the accumulation of intracellular reactive oxygen species, the expression of inducible nitric oxide synthases and proliferating cell nuclear antigen as well as collagen deposition in cardiac tissue. As supported by colorimetric analysis, an elevation in malondialdehyde level and a decrease in both superoxide dismutase (SOD) and thioredoxin-1 oxidoreductase (TrX) levels were seen, whereas molecular analysis revealed a decrease in Keap1 and an increase in Nrf2 and HO-1 gene expression. Pretreatment with vitamin C and PRP prior to NaF administration significantly improved the altered parameters and enhanced the cellular antioxidant capability of myocardium resulting in protection of cardiac muscle from NaF-induced cytotoxicity and apoptotic cell death.. The cyto-protective activity of PRP was found to be comparable to that of the known antioxidant, vitamin C.

Topics: Animals; Antioxidants; Ascorbic Acid; Cardiotoxicity; Kelch-Like ECH-Associated Protein 1; NF-E2-Related Factor 2; Oxidative Stress; Platelet-Rich Plasma; Rats; Sodium Fluoride

Arsenic trioxide (As

Topics: alpha-Tocopherol; Animals; Antioxidants; Apoptosis; Arsenic Trioxide; Arsenicals; Ascorbic Acid; Cardiotoxicity; Cell Line; Cytoprotection; Heart Diseases; Membrane Potential, Mitochondrial; Mitochondria, Heart; Myocytes, Cardiac; NF-E2-Related Factor 2; Oxidative Stress; Oxides; Proto-Oncogene Proteins c-bcl-2; Rats; Signal Transduction

Pharmacodynamic interactions of three anthracycline antibiotics namely doxorubicin (DXH), epirubicin (EpiDXH) and daunorubicin (DNR) with DNA in the absence and presence of ascorbic acid (AA) as natural additive were monitored under physiological conditions (pH = 7.4, 4.7 and T = 309.5K). Route-1 (Anthracycline-AA-DNA) and Route-2 (Anthracycline-DNA-AA) were adopted to see the interactional behavior by cyclic voltammetry (CV) and UV-visible spectroscopy. In comparison to Route-2; voltammetric and spectral responses as well as binding constant (Kb) and Gibb's free energy change (ΔG) values revealed strongest and more favorable interaction of anthracycline-AA complex with DNA via Route-1. Kb, s (binding site sizes) and ΔG evaluated from experimental (CV, UV-Vis) and theoretical (molecular docking) findings showed enhanced binding strength of tertiary complexes as compared to binary drug-DNA complexes. The results were found comparatively better at pH 7.4. Consistency was observed in binding parameters evaluated from experimental and theoretical techniques. Diffusion coefficients (Do) and heterogeneous electron transfer rate constant (ks,h) confirmed the formation of complexes via slow diffusion kinetics. Percent cell inhibition (%Cinh) of anthracyclines for non-small cell cancer cell lines (NSCCLs) H-1299 and H-157 were evaluated higher in the presence of AA which further complimented experimental and theoretical results.

Topics: Antibiotics, Antineoplastic; Antioxidants; Ascorbic Acid; Cardiotoxicity; Cell Line, Tumor; Cell Proliferation; Daunorubicin; DNA; Doxorubicin; Drug Interactions; Epirubicin; Humans; Hydrogen-Ion Concentration; Molecular Docking Simulation; Neoplasms

Topics: AMP-Activated Protein Kinases; Animals; Antioxidants; Arterial Pressure; Ascorbic Acid; Cardiotoxicity; Doxorubicin; Drug Synergism; Glucosides; Glutathione; Glutathione Peroxidase; Heart Rate; Male; Malondialdehyde; Myocardium; Oxidative Stress; PPAR gamma; Rats; Rats, Sprague-Dawley; Stilbenes; Superoxide Dismutase

The Food and Drug Administration recently warned of the fatal cardiovascular risks of azithromycin in humans. In addition, a recently published study documented azithromycin-induced cardiotoxicity in rats. This study aimed to justify the exact cardiovascular events accompanying azithromycin administration in rats, focusing on electrocardiographic, biochemical, and histopathological changes. In addition, the underlying mechanisms were studied regarding reactive oxygen species production, cytokine release, and apoptotic cell-death. Finally, the supposed protective effects of both carvedilol and vitamin C were assessed. Four groups of rats were used: (1) control, (2) azithromycin, (3) azithromycin + carvedilol, and (4) azithromycin + vitamin C. Azithromycin resulted in marked atrophy of cardiac muscle fibers and electrocardiographic segment alteration. It increased the heart rate, lactate dehydrogenase, creatine phosphokinase, malondialdehyde, nitric oxide, interleukin-1 beta (IL1-β), tumor necrosis factor alpha (TNF-α), nuclear factor kappa beta (NF-κB), and caspase-3. It decreased reduced glutathione, glutathione peroxidase, and superoxide dismutase. Carvedilol and vitamin C prevented most of the azithromycin-induced electrocardiographic and histopathological changes. Carvedilol and vitamin C decreased lactate dehydrogenase, malondialdehyde, IL1-β, TNF-α, NF-κB, and caspase-3. Both agents increased glutathione peroxidase. This study shows that both carvedilol and vitamin C protect against azithromycin-induced cardiotoxicity through antioxidant, immunomodulatory, and antiapoptotic mechanisms.

Topics: Animals; Anti-Bacterial Agents; Ascorbic Acid; Azithromycin; Carbazoles; Cardiotoxicity; Carvedilol; Caspase 3; Electrocardiography; Interleukin-1beta; Male; NF-kappa B; Propanolamines; Random Allocation; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species; Tumor Necrosis Factor-alpha

Tilmicosin (TIL) is a long-acting macrolide antibiotic approved for the treatment of cattle with Bovine Respiratory Disease. However, overdose of TIL has been reported to induce cardiotoxicity. The purpose of our experiment was to evaluate the protective effects of Commiphora molmol (mirazid (MRZ); myrrh) and (or) ascorbic acid (AA) against TIL-induced cardiotoxicity in mice. MRZ and AA were orally administered using stomach gavage, either alone or in combination for 5 consecutive days, followed with a single TIL overdose. TIL overdose induced a significant increase in serum levels of cardiac damage biomarkers (AST, LDH, CK, CK-MB, and cTnT), as well as cardiac lipid peroxidation, but cardiac levels of antioxidant biomarkers (GSH, SOD, CAT, and TAC) were decreased. Both MRZ and AA tended to normalize the elevated serum levels of cardiac injury biomarkers. Furthermore, MRZ and AA reduced TIL-induced lipid peroxidation and oxidative stress parameters. MRZ and AA combined produced a synergistic cardioprotective effect. We conclude that myrrh and (or) vitamin C administration minimizes the toxic effects of TIL through their free-radical-scavenging and potent antioxidant activities.

Topics: Animals; Ascorbic Acid; Cardiotonic Agents; Cardiotoxicity; Commiphora; Drug Synergism; Lipid Peroxidation; Male; Mice; Myocardium; Oxidative Stress; Resins, Plant; Tylosin

Topics: Administration, Intravenous; Ascorbic Acid; Cardiotoxicity; Diuresis; Diuretics; Tidal Volume; Vital Capacity

Topics: Administration, Intravenous; Ascorbic Acid; Cardiotoxicity; Diuresis; Diuretics; Mercury; Mercury Poisoning; Psychotherapy

Topics: Administration, Intravenous; Ascorbic Acid; Cardiotoxicity; Diuresis; Diuretics; Mercury; Mercury Poisoning; Psychotherapy