Amifostine protects bone marrow from benzene-induced hematotoxicity in mice.
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 Moreover, amifostine prevented benzene-induced bone marrow and spleen cell apoptosis and rescinded the inhibition of cell proliferation induced by benzene exposure.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.
Yu
Kang
K
Hemotology and Oncology Research Institute, the First Affiliated Hospital of Wenzhou MedicalCollege, 2 Fu-Xue Xiang,Wenzhou, Zhejiang Province, China 325000. yukang62@126.com
Yang
Kai-Yan
KY
Ren
Xing-Zhou
XZ
Chen
Yi
Y
Liu
Xin-Hua
XH
D000395:Air Pollutants, Occupational / Q000633:toxicity*; D004999:Amifostine / Q000627:therapeutic use*; D000741:Anemia, Aplastic / Q000139:chemically induced / Q000473:pathology / Q000517:prevention & control*; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D001554:Benzene / Q000633:toxicity*; D001853:Bone Marrow / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D001854:Bone Marrow Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D018890:Chemoprevention; D004195:Disease Models, Animal; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D011837:Radiation-Protective Agents / Q000627:therapeutic use*; D017382:Reactive Oxygen Species / Q000378:metabolism; D013154:Spleen / Q000187:drug effects / Q000473:pathology
D000395:Air Pollutants, Occupational; D018809:Proliferating Cell Nuclear Antigen; D011837:Radiation-Protective Agents; D017382:Reactive Oxygen Species; D001554:Benzene; D004999:Amifostine