Investigating and comparing the effects of lead poisoning in the rate of Flt3 gene expression in Acute Myeloid Leukemia (AML) and the value of its proteins synthesis in adult male rats


Nowadays, cancer is undoubtedly one of the main and most common causes of human mortality. Recent studies have proved the origin and genetic source of many types of cancers. One of the main causes of genetic changes leading to the prevalence of cancer is exposure to various environmental pollutants in the living environment. The present study aims to investigate the possible effects of poisoning with lead compounds on the expression of an important gene of flt3 involved in the development of Leukemia in healthy rats. A total of 48 male rats were used in this study. Animals were generally divided into 6 groups, including control group, 300 mg / sodium sulfide poisoning group, 600 mg / sodium sulfide poisoning group, 30 mg / lead acetate poisoning group, 60 mg / lead acetate poisoning group, 600 mg / sodium sulfide plus 60 mg / lead acetate poisoning group. In this study, gavage was performed on rats for four months and blood samples were taken after this time. Using protein measurement kits, the value of protein was measured and it was found that in the group that received 600 mg / sodium sulfide plus 60 mg / lead acetate, the value of protein and gene expression increased significantly compared to other groups.


  • Adolfsson J, Mansson R, Buza-Vidas N, Hultquist A, Liuba K, Jensen CT, Bryder D, Yang L, Borge OJ, Thoren LA, et al. (2005) Identification of Flt3+ lympho-myeloid stem cells lacking erythromegakaryocytic potential a revised road map for adult blood lineage commitment. Cell 121: 295-306.
  • Armstrong SA, Mabon ME, Silverman LB, Li A, Gribben JG, Fox EA, Sallan SE, Korsmeyer SJ (2004) FLT3 mutations in childhood acute lymphoblastic leukemia. Blood, 103(9): 3544-3546.
  • Ashry KM, El-Sayed YS, Khamiss RM, El-Ashmawy IM (2010) Oxidative stress and immunotoxic effects of lead and their amelioration with myrrh (Commiphora molmol) emulsion. Food Chem Toxicol. Jan;48(1): 236-41.
  • Bannon A (2000) Ommen (2003) Health Effects. P. 168.
  • Betz BL, Hess JL (2010) Acute myeloid leukemia diagnosis in the 21st century. Arch Pathol Lab Med 134:1427–33.
  • Fracasso ME, Perbellini L, Solda S, Talamini G, Franceschetti P (2002) Lead induced Francastel C, Schubeler D, Martin DI and Groudine M. Nuclear compartmentalization and gene activity. Nat Rev Mol Cell Biol; 1(2): 137-43.
  • Fuller PJ, Chu S, Fikret S, Burger HG (2002) Molecular pathogenesis of granulosa cell tumours. Mol Cell Endocrinol, 191: 89–96.
  • Howlader N, Noone AM, Krapcho M, Neyman N, et al. (eds). (2011) SEER Cancer.Statistics Review, 1975-2008, National Cancer Institute. Bethesda, MD. Available at: based on November 2010 SEER data submission, posted to the SEER website.
  • Jadidi R, et al. (2014) Parents a dead end life: The main experiences of parents of children with leukemia. Iranian journal of nursing and midwifery research 19(6): 600.
  • Kharfan-Dabaja MA, Patel SA, Osunkoya AO, Kojouri K, Kamble R, Yang J, et al. (2006) Expression of the vascular endothelial growth factor receptors 1 and 2 in acute myeloid leukemia: incidence and feasibility of immunohistochemical staining. Clin Lab Haematol. Aug;28(4): 254-8.
  • Lemmon MA, Schlessinger J (2010) Cell signaling by receptor tyrosine kinases. Cell 141(7): 1117-34.
  • Pakin DM (2006) The Global Health Burden of Infection-Associated Cancers in the years 2002. Int J Cancer 118(12): 3030-44.
  • Tachdjian G, Aboura A, Lapierre JM, Viguei F (2002) Cytogenetic analysis from DNA by comparative genomic hybridization. Ann Genet. 43: 147-154.
  • Zuo Z, Chandra P, Wen YH, Koeppen H (2009) Molecular diagnostics of acute myeloid leukaemia. Diagn Histopathol 15: 531–539.


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