Abstract:
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Abstract
Benzene is an organic compound and it has been classified as Class A carcinogen. At the start of the 20th century, it has been widely used in many industrial and commercial products e.g. printing, shoe industry, rubber industry, etc. Benzene has been reported for causing various diseases including aplastic anemia, leukemogenesis and hematological malignancies in humans. Benzene toxic metabolites (1.4 benzoquinone) in the liver or in the bone marrow can lead to traumatic bone marrow injury and hepatotoxicity, subsequently cause Leukemias. In benzene-induced leukemia, oxidative DNA Damage and chromosomal mutations occur by the change in function of Topoisomerase II. Deviant activation of STAT proteins and dysregulation of STAT pathway is associated with leukemogenesis. Current chemotherapeutics for the treatment of leukemia have been limited by high cost and severe side effects. Therefore there is an urgent need for the discovery of new biologically active compounds for treatment of Leukemia. Among various medicinal plants, Crithmum maritimum L. belongs to the family of Apiaceae and has been used traditionally for the treatment of various ailments including obesity, scurvy, Urinary tract infections, gastrointestinal problems, and Kidney problems. To validate the ethno pharmacological and anti-leukemic effects of phenolic extracts of Crithmum maritimum L. against benzene induced leukemia, extract of Crithmum maritimum L. has been prepared and tested on Leukemic model of Balb/c mice. Cytotoxicity of the extract against leukemia has been evaluated through a number of experiments. Annexin V assay in flow cytometry has been used to detect the apoptotic effect of Crithmum maritimum L. on Leukemic cells in Balb/c strain comparative to FDA approved Chemotherapeutic drug Cyclophosphamide. Annexin V has the affinity to bind with phosphatidylserine and ability to detect apoptotic cells by binding with phosphatidylserine, by flow cytometry. Translocation of phosphatidylserine (PS) from the inner region to outer layer of plasma membrane renders some alterations in plasma membrane due to early stages of apoptosis, due to which PS opens up at cell surface.
