A model for the induction of aplastic anemia by subcutaneous administration of benzene in mice

Lezama, Rodolfo Velasco; Escorcia, Eduardo Barrera; Torres, Antonio Muñoz; Aguilar, Rafaela Tapia; Ramı́rez, Claudia; Lorenzana, Mario García; Monroy, Verónica; Rule, Miguel Betancourt

doi:10.1016/s0300-483x(01)00371-7

Cited by 31 publications

(21 citation statements)

References 20 publications

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“…Methods for blood cell counts have been described previously (Velasco Lezama et al 2001). Briefly, whole blood was diluted in Gower's liquid (1:200) in red cell pipettes for erythrocyte (RBC) counts, and blood was diluted in Turk's solution (1:20) for leukocyte (WBC) quantification.…”

Section: Sample Analysis Blood Cell Countsmentioning

confidence: 99%

Amifostine Protects Bone Marrow from Benzene-Induced Hematotoxicity in Mice

et al. 2007

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Benzene is one of the most widely used industrial chemical agents. Long-term benzene exposure causes bone marrow aplasia and leads to a wide range of hematopoietic disorders including aplastic anaemia (AA). There are currently no effective approaches to protect people from benzene-induced hematotoxicity and AA. In addition, current treatments for AA have limitations with short- and long-term risks. Protective agents and new therapeutic approaches, therefore, are needed to prevent and treat the disease. Amifostine is a well-known cytoprotective agent and has been widely used in clinical for protecting normal tissues from the toxic effects of chemotherapy and radiotherapy. The authors utilized an established mouse model to determine the protective effect of amifostine on benzene-induced bone marrow hematotoxicity. Whole-blood cell count, morphological and histopathological alterations in the bone marrow and spleen, as well as the production of inducible toxic oxidative species were examined and compared among the mouse groups. Amifostine treatment in benzene-exposed mice significantly improved blood cell counts, and morphological and histopathological signs of hematotoxicity in the bone marrow as well as in the spleen. Moreover, amifostine prevented benzene-induced bone marrow and spleen cell apoptosis and rescinded the inhibition of cell proliferation induced by benzene exposure. Finally, amifostine significantly inhibited the levels of reactive oxidative species and lipid peroxidation induced by benzene exposure. These data suggest that amifostine appears to have substantial protective effect on benzene-induced bone marrow hematotoxicity.

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Section: Sample Analysis Blood Cell Countsmentioning

confidence: 99%

Amifostine Protects Bone Marrow from Benzene-Induced Hematotoxicity in Mice

et al. 2007

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“…Administration of benzene through inhalation or injection produced hematopoietic damage in C57BL/6 (B6), 9,10 Swiss, 11 Kunming, 12 CD1, 13 and 129/Sv mice, 14 as well as in rats. 15 Velasco et al 13 subcutaneously injected 2 ml/kg (1940 mg/kg) benzene to CD1 male mice at either 5 days or 3 days per week for a total of 10, 15, and 20 injections, respectively. Mice that received 15 and 20 injections at 5 daily injections per week showed lethargy and irritability with 42% body weight loss and 68% spleen weight loss.…”

Section: Benzene Induced Bm Failurementioning

confidence: 99%

“…While both injection schedules induced aplastic anemia, the disease was masked by spleen toxicity in the group receiving 5 daily injections per week. 13 Inhalation of benzene vapor for 2.5 months induced aplastic anemia in Kunming mice with significant declines in erythroid progenitor cell counts and phosphoribosylpyrophosphate synthetase activity in colony-forming units (CFU)-erythroid. Treatment with a Chinese prescription, Sheng-Mai injection, brought erythroid progenitor cell counts and phosphoribosylpyrophosphate synthetase activity in CFU-erythroids to normal levels.…”

Section: Benzene Induced Bm Failurementioning

confidence: 99%