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.