Alternations of cardiac biomarkers in White Pekin ducks intoxicated with arsenic and its amelioration by use of ginger
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Published:2023-08-02
Issue:3
Volume:93
Page:329-340
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ISSN:0372-5480
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Container-title:Veterinarski arhiv
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language:
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Short-container-title:Vet. Arh
Author:
Kumar Panda Santosh, ,Kumar Dhirendra,Rani Jena Geeta,Chandra Patra Ramesh,Kumar Panda Susen,Sethy Kamdev,Kant Mishra Surya,Kumar Swain Bijaya,Kumar Naik Prafulla,Beura Chandrakant,Gupta Ritu
Abstract
Cardiotoxicity is an imperative issue in the assessment of heavy metal consumption and inorganic arsenic (As). These have a cardiotoxic effect which is evaluated by biochemical, and oxidative-antioxidant tests, and by the Nrf2- HO-1 pathway. Dried ginger powder is recognized for its efficient antioxidant activities and as a protector of the cardiovascular system from toxic damage caused by heavy metals. However, the possible function of ginger against As in heart via heme oxygenase-1 (HO-1) and nuclear factor erythroid 2-related factor (Nrf2) is unclear. A total of 120 White Pekin ducks were randomly distributed into groups comprising 24 birds in each. Each group comprised 3 replicates having 8 birds in each replicate. The time period of this study was 90 days. The groups were the control [Group I] whereas groups II to IV were fed a basal diet including arsenic at 28 mg/L. Dried ginger powder as an ameliorative agent was mixed with the basal diet and fed at 0.1, 0.3 and 1 g/kg feed to groups III, IV and V, respectively. In the current experiment, dried ginger powder decreased As-induced reactive oxygen species (ROSs) production, oxidative injury and pathological modifications. In addition, cardiac dysfunction factors, intracellular calcium (Ca2+), As accumulation and cAMP deficiency levels were noticed in ducks; these alternations were attenuated by ginger. Furthermore, ginger significantly altered the down regulation of both HO-1 and Nrf2 gene expressions caused by As. Thus, the proven protective role of ginger against As-induced cardiotoxicity may be a consequence of the maintenance of redox homeostasis, i.e. the Nrf2-HO-1 pathway and by enabling As efflux.
Publisher
Faculty of Veterinary Medicine, University of Zagreb
Subject
General Veterinary