OBJECTIVES: 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. DESIGN AND 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.
OBJECTIVES: To evaluate the antioxidant status and repair capacity in breast cancerpatients as well as the relationship between these parameters and expression of critical proteins in breast cancer tissue. DESIGN AND METHODS: Blood samples were obtained from 25 female breast cancerpatients 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 cancerpatients 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 cancerpatients and suggest that the regulation of DNA repair is sensitive to cellular redox state and can be modulated by ER/PR status.
Authors: Antonio Luiz Gomes Júnior; Marcia Fernanda Correia Jardim Paz; Laís Iasmin Soares da Silva; Simone da Costa e Silva Carvalho; André Luiz Pinho Sobral; Kátia da Conceição Machado; Paulo Michel Pinheiro Ferreira; Prabodh Satyal; Rivelilson Mendes de Freitas; Ana Amélia de Carvalho Melo Cavalcante Journal: Oxid Med Cell Longev Date: 2015-10-20 Impact factor: 6.543