Redox Report · 2017 · 23 citations · 21 references
Life SciencesPharmacologyToxicologyAnalytical ToxicologyHeavy Metal ToxicologyRedox BiochemistryAntioxidant DefenseArsenic ToxicologyCardiotoxicity ManagementOxidative StressOxidative Stress In NeurotoxicityReactive Oxygen SpeciesCardioprotective TherapyCardiotoxicityInorganic Arsenic ToxicityLipid Peroxidation MarkersMechanisms Of Arsenic ToxicityMechanisms Of Cardiac InjuryOxidative Stress In Cardiovascular DiseaseOxidized Glutathione
OBJECTIVES: induced cardiotoxicity. METHODS: for evaluating its cardioprotective efficacy. RESULTS: resulted in deposition of arsenic in heart tissue, increased cardiac marker enzymes release, lipid peroxidation (LPO), oxidative insults and pathological damages in the heart. Co-treatment with FSO (500 mg/kg) significantly reduced the arsenic accumulation, cardiac marker enzymes, LPO and cardiac structural alterations. FSO treatment significantly improved cardiac glutathione content, antioxidant enzymes and reduced the pathological damages in cardiac tissue. Gas chromatographic-mass spectrometry analysis revealed that the major fatty acid content in the FSO is alpha-linolenic acid, which has a strong milieu in cardiac health. CONCLUSION: therapy.
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