title: Oxidative stress and hematological profiles of advanced breast cancer patients subjected to paclitaxel or doxorubicin chemotherapy.
abstract: Several adverse effects of chemotherapy treatments have been described, and most of these effects are associated with direct interactions between blood cells and indirect effects generated during the oxidative metabolism of antineoplastic drugs. In this study we evaluated the oxidative systemic status and hematological profiles of breast cancer patients with advanced ductal infiltrative carcinoma treated with doxorubicin (DOX) or paclitaxel (PTX) within 1 h after chemotherapy. Blood analyses included evaluation of hemogram, pro-oxidative markers, and antioxidant status. The results showed that advanced breast cancer diseased (AD) patients without previous chemotherapy presented anemia and high oxidative stress status characterized by elevated levels of lipid peroxidation and nitric oxide, and reduced catalase activity when compared with controls. DOX-treated patients exhibited increased anemia and reduced antioxidant status, which was revealed by decreases in reduced glutathione levels and the total antioxidant capacity of plasma; however, these changes did not lead to further increases in lipid peroxidation or carbonyl proteins when compared with the AD group. PTX-treated patients also showed increased anemia, lactate dehydrogenase leakage, and enhanced lipid peroxidation. These data reveal for the first time that patients subjected to chemotherapy with DOX or PTX present immediate systemic oxidative stress and red blood cell oxidative injury with anemia development. These findings provide a new perspective on the systemic redox state of AD and patients subjected to chemotherapy regarding oxidative stress enhancement and its possible involvement in the aggravation of chronic anemia.
authors.affiliation: Laboratory of Pathophysiology and Free Radicals, Department of General Pathology-Center of Biological Science, State University of Londrina, Londrina, PR 86051-990, Brazil.
authors.forename: C
authors.initials: C
authors.lastname: Panis
authors.forename: A C S A
authors.initials: AC
authors.lastname: Herrera
authors.forename: V J
authors.initials: VJ
authors.lastname: Victorino
authors.forename: F C
authors.initials: FC
authors.lastname: Campos
authors.forename: L F
authors.initials: LF
authors.lastname: Freitas
authors.forename: T
authors.initials: T
authors.lastname: De Rossi
authors.forename: A N
authors.initials: AN
authors.lastname: Colado Simão
authors.forename: A L
authors.initials: AL
authors.lastname: Cecchini
authors.forename: R
authors.initials: R
authors.lastname: Cecchini
mesh_terms: D000328:Adult; D000368:Aged; D000975:Antioxidants / Q000378:metabolism; D001943:Breast Neoplasms / Q000097:blood* / Q000188:drug therapy / Q000473:pathology; D018270:Carcinoma, Ductal, Breast / Q000097:blood* / Q000188:drug therapy / Q000473:pathology; D002374:Catalase / Q000378:metabolism; D004912:Erythrocytes / Q000201:enzymology / Q000378:metabolism; D005260:Female; D005978:Glutathione / Q000378:metabolism; D006801:Humans; D015227:Lipid Peroxidation; D008875:Middle Aged; D009367:Neoplasm Staging; D009573:Nitrites / Q000378:metabolism; D018384:Oxidative Stress; D050050:Protein Carbonylation; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D000975:Antioxidants; D009573:Nitrites; D017392:Thiobarbituric Acid Reactive Substances; D002374:Catalase; D013482:Superoxide Dismutase; D005978:Glutathione