title: Amelioration of cyclophosphamide induced myelosuppression and oxidative stress by cinnamic acid.
abstract: Cinnamic acid (C9H8O2), is a major constituent of the oriental Ayurvedic plant Cinnamomum cassia (Family: Lauraceae). This phenolic acid has been reported to possess various pharmacological properties of which its antioxidant activity is a prime one. Therefore it is rational to hypothesize that it may ameliorate myelosuppression and oxidative stress induced by cyclophosphamide, a widely used chemotherapeutic agent. Commercial cyclophosphamide, Endoxan, was administered intraperitoneally to Swiss albino mice (50mg/kg) pretreated with 15, 30 and 60mg/kg doses of cinnamic acid orally at alternate days for 15days. Cinnamic acid pre-treatment was found to reduce cyclophosphamide induced hypocellularity in the bone marrow and spleen. This recovery was also reflected in the peripheral blood count. Amelioration of hypocellularity could be correlated with the modulation of cell cycle phase distribution. Cinnamic acid pre-treatment reduced bone marrow and hepatic oxidative stress as evident by lipid peroxidation and activity assays of antioxidant enzymes such as superoxide dismutase, catalase and glutathione-S-transferase. The present study indicates that cinnamic acid pretreatment has protective influence on the myelosuppression and oxidative stress induced by cyclophosphamide. This investigation is an attempt and is the first of its kind to establish cinnamic acid as an agent whose consumption provides protection to normal cells from the toxic effects of a widely used anti-cancer drug.
authors.affiliation: Department of Zoology, West Bengal State University, Berunanpukuria, Malikapur, North-24 Parganas, Barasat, Kolkata 7000126, West Bengal, India.
authors.forename: Kartick
authors.initials: K
authors.lastname: Patra
authors.forename: Samadrita
authors.initials: S
authors.lastname: Bose
authors.forename: Shehnaz
authors.initials: S
authors.lastname: Sarkar
authors.forename: Jyotirmoy
authors.initials: J
authors.lastname: Rakshit
authors.forename: Samarjit
authors.initials: S
authors.lastname: Jana
authors.forename: Avik
authors.initials: A
authors.lastname: Mukherjee
authors.forename: Abhishek
authors.initials: A
authors.lastname: Roy
authors.forename: Deba Prasad
authors.initials: DP
authors.lastname: Mandal
authors.forename: Shamee
authors.initials: S
authors.lastname: Bhattacharjee
mesh_terms: D000818:Animals; D018906:Antineoplastic Agents, Alkylating / Q000633:toxicity*; D001772:Blood Cell Count; D001853:Bone Marrow / Q000187:drug effects* / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D002453:Cell Cycle / Q000187:drug effects; D002934:Cinnamates / Q000494:pharmacology*; D003520:Cyclophosphamide / Q000633:toxicity*; D005434:Flow Cytometry; D005982:Glutathione Transferase / Q000378:metabolism; D051379:Mice; D018384:Oxidative Stress / Q000187:drug effects* / Q000502:physiology; D011897:Random Allocation; D013154:Spleen / Q000187:drug effects* / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D018906:Antineoplastic Agents, Alkylating; D002934:Cinnamates; D017392:Thiobarbituric Acid Reactive Substances; C029010:cinnamic acid; D003520:Cyclophosphamide; D002374:Catalase; D013482:Superoxide Dismutase; D005982:Glutathione Transferase