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

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.

The Evaluation of the Ameliorative Effect of Montelukast Against Arsenic Trioxide-Induced Cardiotoxicity in Rats

“…These observations are in accordance with previous studies that revealed histological alterations in heart tissue after arsenic injection (8,32). Pretreatment with montelukast effectively prevented cardiomyocyte necrosis and preserved tissue morphology in As 2 O 3 -induced heart injury in rats, demonstrating the advantageous role of montelukast against As 2 O 3 -induced cardiotoxicity.…”

Oxidative stress-related liver dysfunction by sodium arsenite: Alleviation byPistacia lentiscusoil

“…In this study, the depletion in GSH levels was observed after arsenic treatment, which could be explained by an adaptive response to oxidative stress, hence GSH plays a fundamental role in detoxifying arsenic species as well as stimulates the excretion of methylated arsenic compounds, or GSH may be oxidised due to the interaction with the free radicals induced by arsenic (Vahter, 2002). Also, GSH can act as an electron donor for the conversion of arsenic (V) to arsenic (III) (Manna et al, 2008). The decrease in the activity of GPx might result directly from the decreased levels of GSH following As exposure since GPx activity depends on GSH level.…”

Arsenic: an ancient toxicant of continuous public health impact, from Iceman Ötzi until now

“…In an experimental study on rabbit aorta as Arch Toxicol (2012) 86:825-830 827 a cardiovascular target, Ma et al (2012) show that inflammatory responses play a critical role in the combined cardiovascular toxicity of As and F. Also, mechanisms involved in combined action of As and aryl hydrocarbon receptor ligands are being investigated (Anwar-Mohamed et al 2012). Indeed, with regard to the different manifestations of toxicity of arsenic (Singh et al 2011), cardiovascular disorders, such as hypertension, atherosclerosis and myocardial injury, are receiving increased interest (Manna et al 2008;Balakumar and Kaur 2009;Chen et al 2012). A mechanism likely to be involved is oxidative stress, connected with activation of eNOS and enhanced the phosphorylation of MLCK (Singh et al 2011).…”