title: Association of low repair efficiency with high hormone receptors expression and SOD activity in breast cancer patients.
abstract: OBJECTIVE
  To evaluate the antioxidant status and repair capacity in breast cancer patients as well as the relationship between these parameters and expression of critical proteins in breast cancer tissue.
  
  
  METHODS
  Blood samples were obtained from 25 female breast cancer patients and 19 healthy women. The antioxidant status was determined by the concentration of thiobarbituric-reactive substances (TBARS) and activity of superoxide dismutase (SOD) and catalase (CAT). The basal DNA damage and repair capacity in lymphocytes were evaluated by comet assay. The expression of p53, c-erbB2, Ki-67, estrogen receptor (ER) and progesterone receptor (PR) in cancer tissue was detected by immunohistochemical staining.
  
  
  RESULTS
  The breast cancer patients presented significantly elevated endogenous DNA damage in lymphocytes and lower susceptibility to DNA damage induced by H(2)O(2) when compared to the control group. There is a negative correlation between TBARS and sensitivity to peroxide induced DNA damage in patients. The percentage of residual damage after H(2)O(2) treatment followed by 3h of post-incubation is significantly higher in patients and also correlates positively with SOD activity, ER and PR expression and negatively with the basal DNA damage.
  
  
  CONCLUSIONS
  Our results demonstrate low repair capacity in lymphocytes of breast cancer patients and suggest that the regulation of DNA repair is sensitive to cellular redox state and can be modulated by ER/PR status.
authors.affiliation: Departamento de Biofísica, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil.
authors.forename: Mateus H
authors.initials: MH
authors.lastname: Agnoletto
authors.forename: Temenouga N
authors.initials: TN
authors.lastname: Guecheva
authors.forename: Fernanda
authors.initials: F
authors.lastname: Dondé
authors.forename: Adriana F
authors.initials: AF
authors.lastname: de Oliveira
authors.forename: Fabio
authors.initials: F
authors.lastname: Franke
authors.forename: Carina
authors.initials: C
authors.lastname: Cassini
authors.forename: Mirian
authors.initials: M
authors.lastname: Salvador
authors.forename: João A P
authors.initials: JA
authors.lastname: Henriques
authors.forename: Jenifer
authors.initials: J
authors.lastname: Saffi
mesh_terms: D001943:Breast Neoplasms / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D002374:Catalase / Q000378:metabolism; D020552:Comet Assay; D004249:DNA Damage; D004260:DNA Repair; D005260:Female; D006801:Humans; D006861:Hydrogen Peroxide / Q000494:pharmacology; D007150:Immunohistochemistry; D019394:Ki-67 Antigen / Q000032:analysis; D008214:Lymphocytes / Q000187:drug effects / Q000378:metabolism; D008875:Middle Aged; D011960:Receptors, Estrogen / Q000378:metabolism*; D011980:Receptors, Progesterone / Q000378:metabolism*; D013482:Superoxide Dismutase / Q000097:blood*; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000032:analysis
chemical_list: D019394:Ki-67 Antigen; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D017392:Thiobarbituric Acid Reactive Substances; D016159:Tumor Suppressor Protein p53; D006861:Hydrogen Peroxide; D002374:Catalase; D013482:Superoxide Dismutase