title: Hemoglobin induces colon cancer cell proliferation by release of reactive oxygen species.
abstract: OBJECTIVE
  To study whether hemoglobin could amplify colon cancer cell proliferation via reactive oxygen species (ROS) production.
  
  
  METHODS
  Colon cancer cell line HT-29 was grown in the conventional method using RPMI1640 media. The viability of the cells was measured using the colorimetric MTT [3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide] assay after adding hemoglobin. We determined reactive oxygen species levels to be indicators of oxidative stress in HT 29 cell lines with and without hemoglobin and/or 5-fluorouracil (5-FU), 5'-deoxy-5-fluorouridine (5-DFUR) using fluorometric dichlorofluorescin diacetate (DCFH-DA) assay.
  
  
  RESULTS
  Cellular proliferation was increased with hemoglobin in a concentration-dependent manner. A significant increment on ROS levels was found in HT 29 cells following hemoglobin incubation. The cytotoxic effects of 5-FU and 5-DFUR were significantly blunted by administration of hemoglobin. There was a slight increase of peroxiredoxin 1, superoxide dismutase 1 concentration according to different hemoglobin concentrations.
  
  
  CONCLUSIONS
  Hemoglobin has a cellular proliferative effect on HT-29 colon cancer cell line by production of ROS. Also, hemoglobin abates cytotoxic effects of chemotherapeutic agents such as 5-FU and 5-DFUR.
authors.affiliation: Department of Surgery, Ewha Womans University Mokdong Hospital, 158-710, 911-1, Mokdong, Yangcheonku, Seoul, Korea. ralee@ewha.ac.kr
authors.forename: Ryung-Ah
authors.initials: RA
authors.lastname: Lee
authors.forename: Hyun-Ah
authors.initials: HA
authors.lastname: Kim
authors.forename: Bo-Young
authors.initials: BY
authors.lastname: Kang
authors.forename: Kwang-Ho
authors.initials: KH
authors.lastname: Kim
mesh_terms: D000964:Antimetabolites, Antineoplastic / Q000494:pharmacology; D000069287:Capecitabine; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects*; D003110:Colonic Neoplasms / Q000378:metabolism* / Q000473:pathology*; D003841:Deoxycytidine / Q000031:analogs & derivatives / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D005472:Fluorouracil / Q000494:pharmacology; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D019073:HT29 Cells; D006454:Hemoglobins / Q000502:physiology*; D006801:Humans; D018384:Oxidative Stress; D010544:Peroxidases / Q000235:genetics / Q000378:metabolism; D054464:Peroxiredoxins; D017382:Reactive Oxygen Species / Q000378:metabolism*; D013482:Superoxide Dismutase / Q000235:genetics / Q000378:metabolism
chemical_list: D000964:Antimetabolites, Antineoplastic; D006454:Hemoglobins; D017382:Reactive Oxygen Species; D003841:Deoxycytidine; D000069287:Capecitabine; D010544:Peroxidases; C515940:PRDX1 protein, human; D054464:Peroxiredoxins; D013482:Superoxide Dismutase; D005472:Fluorouracil