Análise do estresse oxidativo em gliomas e glioblastomas

Abstract

Central nervous system (CNS) tumors are debilitating and often fatal. Among them, gliomas and particularly a subtype known as glioblastoma, affect brain tissue and are notably aggressive, requiring prompt intervention. These tumors induce several systemic changes in the patient’s body, including disruption of oxidative stress balance. Oxidative stress refers to the equilibrium between oxidant molecules—known as reactive oxygen species (ROS)—and the body’s antioxidant defense mechanisms. Oxidants can chemically alter various molecules, and if these alterations are harmful, they may lead to cellular membrane damage, DNA mutations, and other cellular injuries. The consequences of oxidative imbalance are widely studied in the context of cancer, as they may contribute to both the onset and persistence of carcinogenesis. Understanding the relationship between oxidative stress and CNS tumors is therefore crucial for improving diagnosis and treatment. This cross-sectional, case-control study involved blood sample collection from 34 patients diagnosed with glioma or glioblastoma between 2022 and 2024. Oxidative stress profiles were assessed in the laboratory through markers such as TBARS, myeloperoxidase, catalase, total thiols, and nonprotein thiols. A control group of 9 healthy volunteers underwent the same analyses. The results showed a general increase in oxidative stress among glioma and glioblastoma patients compared to the control group, with notable differences: low-grade gliomas presented lower levels of oxidative stress markers compared to glioblastomas, suggesting better protection against oxidative damage, which may contribute to longer survival and greater treatment resistance. In contrast, glioblastomas, classified as high-grade tumors, exhibited higher levels of oxidative stress and lower antioxidant protection, correlating with their aggressive clinical behavior. These findings align with current literature and highlight the potential of targeting key oxidative stress-related molecules—particularly catalase, glutathione, and myeloperoxidase—to alter disease progression and enhance treatment efficacy.