Protective effect of arjunolic acid against arsenic‐induced oxidative stress in mouse brain

Abstract

Arsenic, a notoriously poisonous metalloid, is ubiquitous in the environment, and it affects nearly all organ systems of animals including humans. The present study was designed to investigate the preventive role of a triterpenoid saponin, arjunolic acid against arsenic-induced oxidative damage in murine brain. Sodium arsenite was selected as a source of arsenic for this study. The free-radical-scavenging activity and the in vivo antioxidant power of arjunolic acid were determined from its 2,2-diphenyl-1-picryl hydrazyl radical scavenging ability and ferric reducing/antioxidant power assay, respectively. Oral administration of sodium arsenite at a dose of 10 mg/kg body weight for 2 days significantly decreased the activities of antioxidant enzymes, superoxide dismutase, catalase, glutathione-S-transferase, glutathione reductase and glutathione peroxidase, the level of cellular metabolites, reduced glutathione, total thiols and increased the level of oxidized glutathione. In addition, it enhanced the levels of lipid peroxidation end products and protein carbonyl content. Treatment with arjunolic acid at a dose of 20 mg/kg body weight for 4 days prior to arsenic administration almost normalized above indices. Histological findings due to arsenic intoxication and arjunolic acid treatment supported the other biochemical changes in murine brains. Results of 2,2-diphenyl-1-picryl hydrazyl radical scavenging and ferric reducing/antioxidant power assays clearly showed the in vitro radical scavenging as well as the in vivo antioxidant power of arjunolic acid, respectively. The effect of a well-established antioxidant, vitamin C, has been included in the study as a positive control. Combining all, results suggest that arjunolic acid possessed the ability to ameliorate arsenic-induced oxidative insult in murine brain and is probably due to its antioxidant activity.

Mangiferin, a Natural Xanthone, Protects Murine Liver in Pb(II) Induced Hepatic Damage and Cell Death via MAP Kinase, NF-κB and Mitochondria Dependent Pathways

“…Activities of antioxidant enzymes (CAT, SOD, GST, GP X and GR) in the liver tissue of the experimental mice were determined following the methods as described elsewhere [68], [69].…”

Terpene Compounds in Nature: A Review of Their Potential Antioxidant Activity

“…In an animal model with rats, El-Missiry and Shalaby [55] showed that concomitant treatments with the tetraterpene ß-carotene (131) protected against cadmiuminduced oxidative stress in brain with a concomitant increase in both enzymatic (SOD, GST) and non-enzymatic (GSH) antioxidant status, a decrease in LDH activity and lipid peroxidation and an increase of ATPase activity. Pretreatments with the triterpene arjunolic acid (108) recovered almost completely from reduced antioxidant protection (SOD, CAT, GR, GPx GST, GSH) and increased oxidative damage (lipid peroxidation and protein carbonyl content), mainly via radical scavenging, in murine brain treated with arsenic [56].…”

Arsenic-Induced Hepatic Toxicity and Its Attenuation by Fruit Extract of Emblica officinalis (Amla) in Mice

“…The antioxidant activity found in fruit extract of E. officinalis maintain the endogenous antioxidant, thus reduced oxidative stress and alleviate the pathological changes caused by arsenic in liver. Oxidative effects of arsenic have been found to be counteracted by plant extracts and pharmacological agents due to their antioxidant potential and metal binding property [35,36]. GSH has been considered to be an important intracellular reductant for arsenic methylation and transport [37], which in turn help the removal of arsenic from the body.…”