الفهرس 
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Abstract
According to the WHO report issued on February 2012, Cancer is a leading cause of death worldwide, accounting [()f 7.6 million deaths (around 13% of all deaths) in 2008, and about 70% of all cancer deaths occurred in low- and middle-income countries (WHO 2012). Chemotherapy is one of the three most common treatment modalities for cancer, but most of the anticancer drugs cUlTently used in chemotherapy arc cytotoxic to nOl111al cells, leading to unwanted side effects. Therapentically effective doses of many anticancer drugs may produce ineversible changes in normal tissues. Therelore a search for compounds which can reduce the harmful side effects of anticancer drugs in normal tissues is necessary. (Sun & Peng, 2008)
Cyclophosphamide (CP). an alkylating agent used in the treatment of several cancers as well as an immunosuppressant in rheumatoid arthrit is and vasculit is. is one of the most effective antineoplastic drugs in the treatment of solid tumors as well as B cell malignant diseases; it is used against several cancers due to its broad spectrum efficacy (DolJery, 1999; Baumann & Preiss, 2001). Its cytotoxic effects arc the resu lr of chemically react ive metabolites that alkylate DNA and protein, producing cross-links (Hales, 1982; Hausen et al.. 200T).
Tbe injury ofnor111al tissues is the major limitation of using CP, which gives rise to numerous side effects. It bus been reported that oxidat ive stress mediated disl1lption of redox balance at1er CP exposure generates biochemical und physiological disturbances (Weijl et a1., 1997; Tripathi & .Jena, 200S; Pram ita et al., 2(09). As reviewed by Abraham and Sugumar (2008), CP may induce acute inflammation of the urinary bladder (Walker & Sommerkamp, 1998) and renal damage (Kopew:l, 200n, and less frequently, liver damage (Shaunak et al., 1988, Gustafsson et al., 1996), also therapy with cyclophosphamide (CP) can be complicated by the development oflung fibrosis (Kehrer & Margolin, 1997).
CP also exhibits unwanted risks for occupational exposure to tbe health care professionals due to its extensive use in clinics (Anderson et al., 1995; Reldwdevi et a1., 2007). Then, there is u need to protect normal tissue from chemotherapy-induced toxicity with th<.: absence of tumor protection and tumor growth stimulation properties. Several studies suggest that antioxidant supplementation can influence the response to chemotherapy as well as the development of adverse side effects that result ti’om treatment with CP (Zhang et al .. 2006; Bhatia et’al., 2008; Pramita et aI., 2009).
TQ has been shown to be the principal active ingredient of the seeds of Nigella sativa (Mahfouz & EI-Dakhakhny, 1960; Gali-Muhtasib et al., 2006), which possesses several properties including analgesic and anti-intlammatory actions (Houghton et al., 1995; Abdel¬Fattah et aI., 2000), protection against chemical induced carcinogenesis (Hassan & EI¬Dakhakhny, 1992; Worthen et al., 1998), and the inhibition of eicosanoids generation (Houghton et al., 1995). Moreover, it has been reported that TQ prevents oxidative injury in hepatocytes induced by carbon tetrachloride or tert-butyl hyDROPeroxide in various in vitro (Daba & Abdel-Rahman, 1998) and in vivo (Nagi et al., 1999; Mansour et aI., 2001) hepatotoxicity models, as well as acetic acid-induced colitis in rats (Mahgoub, 2003). It has been suggested that TQ may act as an antioxidant agent and prevent the membrane lipid peroxidation in hepatocytes (Mansour et al., 2002).
Therefore, the following study was conducted to detelmine whether a daily oral dose of TQ ameliorates CP-induced experimental lung, bladder and bone marrow toxicities in rats.