VANESSA JACOB VICTORINO
Projetos de Pesquisa
Unidades Organizacionais
LIM/51 - Laboratório de Emergências Clínicas, Hospital das Clínicas, Faculdade de Medicina
6 resultados
Resultados de Busca
Agora exibindo 1 - 6 de 6
- Clinical insights from adiponectin analysis in breast cancer patients reveal its anti-inflammatory properties in non-obese women(2014) PANIS, C.; HERRERA, A. C. S. A.; ARANOME, A. M. F.; VICTORINO, V. J.; MICHELLETI, P. L.; MORIMOTO, H. K.; CECCHINI, A. L.; SIMAO, A. N. C.; CECCHINI, R.Adiponectin is a cytokine reported as a determinant of poor prognosis in women with breast cancer. However, because data regarding its role in breast cancer have been obtained primarily from studies employing overweight or obese women, the adiponectin profile in non-obese women is poorly understood. In this study, we determined adiponectin levels in plasma from non-obese women with breast cancer and investigated a possible correlation with systemic inflammatory status. We determined the plasma adiponectin levels as well as biochemical and oxidative stress parameters in 80 women. Our results revealed that plasma adiponectin levels were affected by chemotherapy, estrogen receptor status, and disease progression. Adiponectin was positively correlated with antioxidant levels, without affecting either the metastatic behavior of disease or patient outcome. These findings highlight adiponectin as a novel player in the endocrine signaling that modulates the oxidative inflammatory response in human breast cancer, and contribute to the understanding of the role of adiponectin in pathological conditions in non-obese women.
- Trastuzumab-based chemotherapy modulates systemic redox homeostasis in women with HER2-positive breast cancer(2015) LEMOS, L. G. T.; VICTORINO, V. J.; HERRERA, A. C. S. A.; ARANOME, A. M. F.; CECCHINI, A. L.; SIMAO, A. N. C.; PANIS, C.; CECCHINI, R.Trastuzumab is an immunotargeting therapeutic against breast tumors with amplification of the human epithelial growth factor receptor 2 (HER2). HER2 patients naturally exhibit disruption in the pro-oxidant inflammatory profiling; however, the impact of trastuzumab-based chemotherapy in modulating this process is still unknown. Here we determined the systemic pro-inflammatory profile of women diagnosed with HER2-amplified tumors, undergoing trastuzumab-based chemotherapy (TZ), and compared the results with that of healthy controls (CTR) and untreated patients with HER2-amplified breast cancer (CA). The plasmatic inflammatory profile was assessed by evaluating pro-oxidant parameters such as lipid peroxidation, total antioxidant capacity (TRAP), levels of advanced oxidation protein products (AOPPs), nitric oxide (NO), C-reactive protein (CRP), and total thiol content. Markers of cardiac damage were also assessed. Our findings showed increased NO levels in TZ than that in either CA or CTR groups. Furthermore, TZ augmented TRAP and reduced total thiol than that of the CA group. Our data also revealed that AOPP levels were significantly higher in the TZ than the CA group. AOPP and the MB fraction of creatine-kinase (CKMB) levels were positively correlated in TZ patients. These findings suggest that trastuzumab-associated chemotherapy can modulate the pro-inflammatory markers of HER2-positive breast cancer patients to the levels found in healthy controls.
- Post-translational modifications disclose a dual role for redox stress in cardiovascular pathophysiology(2015) VICTORINO, Vanessa Jacob; MENCALHA, Andre Luiz; PANIS, CarolinaAlthough some of the redox changes that occur in biological components may result in deleterious events, this process has recently been tackled as a modulatory event. Advances in our understanding regarding the role of some oxidative/nitrosative reactions revealed that proteins can be structurally and functionally modified by chemical reactions, an epigenetic event known as post-translational modification (PTM). PTMs can function as an ""on-off switch"" for signaling cascades, and are dependent on the specific generation of redox components such as reactive oxygen species (ROS) and nitric oxide (NO). NO-driven modifications regulate a wide range of cellular processes and have been highlighted as an epigenetic event that protects proteins from proteolytic degradation. On the other hand, ROS-driven modifications are implicated in cell damage in a number of pathological conditions, especially in the cardiovascular system. Therefore, while mitochondrial uncoupling yields the massive production of ROS in the heart, some cellular redox-sensitive pathways trigger PTMs that may play a cardioprotective role. In this review, we present an overview of the oxidative/nitrosative milieu in cardiac pathologies and address the role of the main redox-driven FTMs as epigenetic events in cardioprotection, as well as its regulatory function in cardiomyocyte signaling. Improved understanding of the role of these FTMs in cardiovascular disease can help direct some approaches for future clinical research regarding health risk assessment, as well as inform strategies for disease treatment and prevention.
- Impact of Tumor Removal on the Systemic Oxidative Profile of Patients With Breast Cancer Discloses Lipid Peroxidation at Diagnosis as a Putative Marker of Disease Recurrence(2014) HERRERA, Ana Cristina S.; VICTORINO, Vanessa J.; CAMPOS, Fernanda C.; VERENITACH, Beatriz D.; LEMOS, Lauana T.; ARANOME, Adrian M. F.; OLIVEIRA, Sayonara R.; CECCHINI, Alessandra L.; SIMAO, Andrea Name C.; ABDELHAY, Eliana; PANIS, Carolina; CECCHINI, RubensThis study highlights the systemic oxidative changes that occur in women with invasive breast cancer at diagnosis that are indicative of disease recurrence in a 5-year follow-up, before the primary tumor removal. Background: Recent studies have suggested a regulatory role for some of the metabolites derived from oxidative stress in breast cancer. In this way, cancer-induced oxidative changes could modify the breast environment and potentially trigger systemic responses that may affect disease prognosis and recurrence. In this study, we investigated the systemic oxidative profile of women with early breast cancer bearing the primary tumor and after tumor withdrawal, and its long-term implications. Patients and Methods: Plasma samples were collected at diagnosis, and the systemic oxidative profile was determined by evaluating the lipid peroxidation, total antioxidant capacity of plasma (TRAP), malondialdehyde (MDA), protein carbonylation, and hydroperoxides. Nitric oxide, vascular endothelial growth factor (VEGF), and tumor necrosis factor alpha (TNF-alpha) levels were further measured. We also evaluated the impact of the oxidative profiling at diagnosis on disease recurrence in a 5-year follow-up. Results: Enhanced oxidative stress was detected in patients bearing the primary tumors, characterized by high lipid peroxidation, TRAP consumption, high carbonyl content, and elevated VEGF and TNF-a levels. After tumor removal, the systemic oxidative status presented attenuation in lipid peroxidation, MDA, VEGF, and TNF-a. The 5-year recurrence analysis indicated that all patients who recidivated presented high levels of lipid peroxidation measured by chemiluminescence at diagnosis. Conclusions: Our data suggest that the presence of the primary tumor is indicative of the systemic pro-oxidant status of breast cancer and demonstrates a role for lipid peroxidation in disease recurrence, highlighting the need for a metabolic follow-up of patients with cancer at diagnosis before tumor removal.
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.