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ORIGINAL ARTICLE
Year : 2015  |  Volume : 7  |  Issue : 1  |  Page : 85-91

Effect of Butea monosperma leaf extracts on cyclophosphamide induced clastogenicity and oxidative stress in mice


Department of Pharmaceutical Sciences, Lovely Professional University, Punjab, India

Correspondence Address:
Asst. Prof. Bimlesh Kumar
Department of Pharmaceutical Sciences, 3B 204, Lovely Professional University, Jalandhar, Punjab
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0974-8490.147215

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Background: Butea monosperma is a medium sized deciduous tree of family Fabaceae. It is widely used by rural people in India to cure many disorders. It possesses antioxidant and anticancer activity which is a prerequisite for anticlastogenic activity. Objective: To evaluate the effect of Butea monosperma leaf extracts on cyclophosphamide induced clastogenicity and oxidative stress in mice. Materials and Methods: The present study assessed the role of aqueous and ethanolic leaf extracts of B. monosperma (AQEBM and ETEBM) on cyclophosphamide (CP) induced oxidative stress and DNA damage in mice using micronucleus assay for anticlastogenic activity and biochemical estimation of malondialdehyde (MDA) and glutathione (GSH) for antioxidant activity. The frequency of the micronucleated erythrocytes and mitotic index was studied in peripheral blood and bone marrow after 24 and 48 h of clastogenic exposure. Results: CP treatment led to a significant (P < 0.001) increase in the frequency of micronuclei and decrease in the mitotic index (MI) in bone marrow and peripheral blood cells. Moreover, CP also significantly increased the lipid peroxidation as evidenced by an increase in the MDA content and decreased the antioxidant enzyme (GSH) in mice liver. Pretreatment with AQEBM and ETEBM reduced the frequency of micronuclei and increased the MI in the bone marrow and peripheral blood cells and also restored the MDA and GSH levels in mice liver. Conclusion: The AQEBM and ETEBM do contain compounds capable of inhibiting the CP induced oxidative stress and subsequent DNA damage in both the peripheral blood and bone marrow cells in mice.


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