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Arsenic-induced oxidative myocardial injury: protective role of arjunolic acid

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Abstract

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.

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Abbreviations

AA:

Arjunolic acid

CAT:

catalase

CDNB:

1-Chloro-2,4-dinitrobenzene

DNPH:

2,4-Dinitro phenyl hydrazine

DTNB:

5,5′-Dithiobis(2-nitrobenzoic acid) (Ellman’s reagent)

EDTA:

Ethylene diamine tetraacetic acid

NEM:

N-ethylmaleimide

FeCl3 :

Ferric chloride

FRAP:

Ferric reducing/antioxidant power

GPx:

Glutathione peroxidase

GR:

Glutathione reductase

GST:

Glutathione-S-transferase

HDL:

High-density lipoprotein

H2O2 :

Hydrogen peroxide

IR:

Infrared-spectroscopy

MDA:

Malondialdehyde

NADH:

Nicotinamide adenine dinucleotide reduced

NBT:

Nitro blue tetrazolium

NMR:

Nuclear magnetic resonance

GSSG:

Oxidized glutathione

KH2PO4 :

Potassium dihydrogen phosphate

PMT:

Phenazine methosulphate

ROS:

Reactive oxygen species

GSH:

Reduced glutathione

NaAsO2 :

Sodium arsenite

NaN3 :

Sodium azide

TA:

Terminalia arjuna

TCA:

Trichloro acetic acid

TBA:

Thiobarbituric acid

TPTZ:

2,4,6-Tripyridyl-1,3,5-triazine

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Acknowledgments

The authors are grateful to Mr. Prasanta Pal for his excellent technical assistance during the entire study.

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Correspondence to Parames C. Sil.

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P. Manna and M. Sinha contributed equally in this study.

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Manna, P., Sinha, M. & Sil, P.C. Arsenic-induced oxidative myocardial injury: protective role of arjunolic acid . Arch Toxicol 82, 137–149 (2008). https://doi.org/10.1007/s00204-007-0272-8

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