Arsenic-induced oxidative myocardial injury: protective role of arjunolic acid.
Arsenic, one of the most harmful metalloids, is ubiquitous in the environment. The present study has been carried out to investigate the protective role of a triterpenoid saponin, arjunolic acid (AA) against arsenic-induced cardiac oxidative damage. In the study, NaAsO2 was chosen as the source of arsenic. The free radical scavenging activity and the effect of AA on the intracellular antioxidant power were determined from its 2,2-diphenyl-1-picryl hydrazyl radical scavenging ability and ferric reducing/antioxidant power assay, respectively. Oral administration of NaAsO2 at a dose of 10 mg/kg body weight for 2 days caused significant accumulation of arsenic in cardiac tissues of the experimental mice in association with the reduction in cardiac antioxidant enzymes activities, namely superoxide dismutase, catalase, glutathione-S-transferase, glutathione reductase and glutathione peroxidase. Arsenic intoxication also decreased the cardiac glutathione (GSH) and total thiol contents and increased the levels of oxidized glutathione (GSSG), lipid peroxidation end products and protein carbonyl content. Treatment with AA at a dose of 20 mg/kg body weight for 4 days prior to NaAsO2 intoxication protected the cardiac tissue from arsenic-induced oxidative impairment. In addition to oxidative stress, arsenic administration increased total cholesterol level as well as the reduced high-density lipoprotein cholesterol level in the sera of the experimental mice. AA pretreatment, however, could prevent this hyperlipidemia. Histological studies on the ultrastructural changes in cardiac tissue supported the protective activity of AA also. Combining all, results suggest that AA could protect cardiac tissues against arsenic-induced oxidative stress probably due to its antioxidant property.
Manna
Prasenjit
P
Department of Chemistry, Bose Institute, 93/1, Acharya Prafulla Chandra Road, Kolkata 700009, West Bengal, India.
Sinha
Mahua
M
Sil
Parames C
PC
D000818:Animals; D020261:Arsenic Poisoning / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D018053:Arsenites / Q000633:toxicity*; D018890:Chemoprevention; D002784:Cholesterol / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004791:Enzyme Inhibitors / Q000633:toxicity*; D016166:Free Radical Scavengers / Q000494:pharmacology / Q000627:therapeutic use*; D006321:Heart / Q000187:drug effects*; D006801:Humans; D006949:Hyperlipidemias / Q000139:chemically induced / Q000378:metabolism / Q000517:prevention & control; D008297:Male; D051379:Mice; D009205:Myocarditis / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D009206:Myocardium / Q000201:enzymology / Q000473:pathology; D018384:Oxidative Stress / Q000187:drug effects; D010088:Oxidoreductases / Q000378:metabolism; D017670:Sodium Compounds / Q000633:toxicity*; D014315:Triterpenes / Q000494:pharmacology / Q000627:therapeutic use*
D018053:Arsenites; D004791:Enzyme Inhibitors; D016166:Free Radical Scavengers; D017670:Sodium Compounds; D014315:Triterpenes; C061640:arjunolic acid; C017947:sodium arsenite; D002784:Cholesterol; D010088:Oxidoreductases