VANESSA JACOB VICTORINO
Projetos de Pesquisa
Unidades Organizacionais
LIM/51 - Laboratório de Emergências Clínicas, Hospital das Clínicas, Faculdade de Medicina
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article 45 Citação(ões) na Scopus Mapping Oxidative Changes in Breast Cancer: Understanding the Basic to Reach the Clinics(2014) MENCALHA, Andre; VICTORINO, Vanessa Jacob; CECCHINI, Rubens; PANIS, CarolinaSince long, oxidative stress-driven modifications in breast cancer were faced as detrimental cellular events that cause obligatory cell damage. Recent studies show that the products generated during redox reactions are able to modulate pivotal processes regarding breast cancer survival, proposing a new way of looking at the events linked to oxidative stress. Therefore, it is necessary to understand the basis of oxidative stress generation in breast cancer by reviewing the two most important events that perpetuate the malignant transformation: mitochondrial dysfunction and DNA damage/misguided repair. In this context, the present review addresses the main events related with redox events reported in breast cancer studies, highlighting the impact of the oxidative environment on DNA damage and the role of the mitochondria as a determinant of oxidative modifications. In addition, we further discuss the main stand-out findings concerning the modulatory role of the metabolites derived from redox stresses, with a special focus on the oxidative changes detected in the breast cancer microenvironment and its systemic impact.- Systemic toxicity induced by paclitaxel in vivo is associated with the solvent cremophor EL through oxidative stress-driven mechanisms(2014) CAMPOS, Fernanda C.; VICTORINO, Vanessa J.; MARTINS-PINGE, Marli Cardoso; CECCHINI, Alessandra L.; PANIS, Carolina; CECCHINI, RubensThe toxic effects of paclitaxel (PTX) and its solubilizing agent cremophor EL (CREL) have been well established in vitro; however, the in vivo mechanisms underlying this toxicity remain unclear. Thus, the aim of this study was to analyze the in vivo toxicity induced by infusion of PTX and CREL and to investigate the involvement of oxidative stress as a potential mechanism for this toxicity. We treated male Wistar rats with PTX and/or CREL for 1 h using human-equivalent doses (PTX + CREL/ethanol + NaCl 175 mg/m(2) or CREL + ethanol + NaCl) and sacrificed immediately or 24 h after these drug infusions to systemic biochemical evaluations. Hidrosoluble vitamin E (vitE, Trolox) was added as a control in some groups. The oxidative profile was determined by measuring erythrocyte and plasma lipid peroxidation, superoxide dismutase and catalase activities, reduced glutathione (GSH) levels, red blood cell (RBC) counts, hemoglobin profile, plasma total radical-trapping antioxidant parameter (TRAP), plasma lipid peroxidation, nitric oxide levels and malondialdehyde levels. Our findings showed that CREL infusion triggered immediate high plasma lipid peroxidation and augmented TRAP, while PTX caused immediate TRAP consumption and metahemoglobin formation. Pronounced oxidative effects were detected 24 h after infusion, when CREL treatment enhanced RBC counts and plasma lipid peroxidation, increased catalase activity, and decreased TRAP levels. On the other hand, after 24 h, PTX-infused rats showed reduced catalase activity and reduced metahemoglobin levels. These data indicate the existence of a continuous oxidative stress generation during CREL-PTX treatment and highlight CREL as primarily responsible for the in vivo oxidative damage to RBCs.