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<p>Ozone gas (O₃) has emerged as a promising therapeutic agent for various pathological conditions, including neurodegenerative diseases (NDs). These illnesses are associated with the accumulation of neurotoxic metabolites by microglia, including tryptophan catabolites. This study aimed to investigate the effects of O₃ exposure on BV-2 microglial cells in the presence or absence of quinolinic acid (QA). O₃ at increasing concentrations (5, 12, 20, 40, and 70&#xa0;µg/mL) was added in cell culture medium, both under baseline conditions and following exposure to QA (1.5 mM) for 24&#xa0;h. Spectrophotometry and flow cytometry were performed to assess cell viability, apoptosis, reactive oxygen species (ROS), nitric oxide (NO), mitochondrial membrane potential (ΔΨm), lipid peroxidation (TBARS), and the activities of superoxide dismutase (SOD) and cytochrome <i>c</i> oxidase (COX). qRT-PCR assessed TNF-α gene expression levels. O₃ exposure enhanced cell viability without inducing oxidative/nitrosative stress or DNA damage in BV-2 cells. In addition, 12&#xa0;µg/mL of O₃ significantly improved cell viability and alleviated oxidative stress and inflammation induced by QA by normalizing SOD activity, reducing lipid peroxidation, and TNF-α gene expression. Nevertheless, O₃ did not restore COX activity nor prevent the hyperpolarization observed under co-treatment conditions. The results suggest that O₃ exerts a biphasic effect, depending on the cellular redox state. This study provides critical insights into the complex mechanisms underlying ozone action in glial cells, highlighting its potential for developing new therapeutic strategies for NDs.</p> Graphical Abstract <p></p>

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Protective Effects of Ozone against Quinolinic Acid-Induced Redox Imbalance in Murine BV-2 Microglial Cells

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月16日

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  • Pedro Henrique Zatti,
  • Nicole Peyrot da Silva,
  • Marina Rigotti,
  • Fernando Joel Scariot,
  • Carolina Bordin Davidson,
  • Alencar Kolinski Machado,
  • Catia Santos Branco

摘要

Ozone gas (O₃) has emerged as a promising therapeutic agent for various pathological conditions, including neurodegenerative diseases (NDs). These illnesses are associated with the accumulation of neurotoxic metabolites by microglia, including tryptophan catabolites. This study aimed to investigate the effects of O₃ exposure on BV-2 microglial cells in the presence or absence of quinolinic acid (QA). O₃ at increasing concentrations (5, 12, 20, 40, and 70 µg/mL) was added in cell culture medium, both under baseline conditions and following exposure to QA (1.5 mM) for 24 h. Spectrophotometry and flow cytometry were performed to assess cell viability, apoptosis, reactive oxygen species (ROS), nitric oxide (NO), mitochondrial membrane potential (ΔΨm), lipid peroxidation (TBARS), and the activities of superoxide dismutase (SOD) and cytochrome c oxidase (COX). qRT-PCR assessed TNF-α gene expression levels. O₃ exposure enhanced cell viability without inducing oxidative/nitrosative stress or DNA damage in BV-2 cells. In addition, 12 µg/mL of O₃ significantly improved cell viability and alleviated oxidative stress and inflammation induced by QA by normalizing SOD activity, reducing lipid peroxidation, and TNF-α gene expression. Nevertheless, O₃ did not restore COX activity nor prevent the hyperpolarization observed under co-treatment conditions. The results suggest that O₃ exerts a biphasic effect, depending on the cellular redox state. This study provides critical insights into the complex mechanisms underlying ozone action in glial cells, highlighting its potential for developing new therapeutic strategies for NDs.

Graphical Abstract