Frontiers in nutrition · 2026
Daily intake of antioxidants ameliorates PM2.5-induced neuronal injury in mice.
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Huang Taida, Li Hui, Huang Xiaomin, Li Bo, Zhang Hongyi, Bai Xu, Oliver Brian G, Tian Meilin, Yi Chenju, Li Dan, Chen Hui
Аннотация
OBJECTIVE: Fine particulate matter (PM2.5) within polluted air is a significant health risk and a strong oxidant. Even exposure to low-level PM2.5 (at or below the WHO standard) is linked to neuroinflammatory, oxidative stress and the development of neurological disorders in the long term. This study aimed to investigate the prophylactic effects of antioxidant supplementation on mitigating sub-chronic exposure to low-level PM2.5-induced brain pathology in mice.
MATERIALS AND METHODS: Mice were exposed to traffic-derived PM2.5 (5 μg/day) collected from a highway in Sydney, Australia, once daily for 3 weeks, while receiving antioxidant, vitamin C (10 mM) or N-acetylcysteine (NAC, 40 mM), via drinking water. Oxidative stress and neuronal loss were assessed across different brain regions. In vitro experiments were conducted to evaluate neuronal integrity and mitochondrial function by VC and NAC treatment in PM2.5-exposed primary neurons.
RESULTS: Sub-chronic PM2.5 exposure increased lipid peroxidation and reduced neurofilament density in the cortex, hippocampus, and thalamus, which were mitigated by VC and NAC supplementation. Although oxidative stress (ROS accumulation and increase in 4-HNE) was prevented in all brain regions by VC and NAC, neurofilament loss remained. In vitro, VC and NAC reduced mitochondrial ROS production, which in turn improved neuronal and synaptic survival, suggesting mitochondria-dependent oxidative stress plays a central role in PM2.5-induced neurotoxicity at least in the cortex and hippocampus.
CONCLUSION: Mitochondria-dependent oxidative stress is a key mechanism underlying PM2.5-induced neurotoxicity, which can be attenuated by VC and NAC supplementation. This highlights a potential prophylactic strategy to partially protect the brain from polluted air.
MATERIALS AND METHODS: Mice were exposed to traffic-derived PM2.5 (5 μg/day) collected from a highway in Sydney, Australia, once daily for 3 weeks, while receiving antioxidant, vitamin C (10 mM) or N-acetylcysteine (NAC, 40 mM), via drinking water. Oxidative stress and neuronal loss were assessed across different brain regions. In vitro experiments were conducted to evaluate neuronal integrity and mitochondrial function by VC and NAC treatment in PM2.5-exposed primary neurons.
RESULTS: Sub-chronic PM2.5 exposure increased lipid peroxidation and reduced neurofilament density in the cortex, hippocampus, and thalamus, which were mitigated by VC and NAC supplementation. Although oxidative stress (ROS accumulation and increase in 4-HNE) was prevented in all brain regions by VC and NAC, neurofilament loss remained. In vitro, VC and NAC reduced mitochondrial ROS production, which in turn improved neuronal and synaptic survival, suggesting mitochondria-dependent oxidative stress plays a central role in PM2.5-induced neurotoxicity at least in the cortex and hippocampus.
CONCLUSION: Mitochondria-dependent oxidative stress is a key mechanism underlying PM2.5-induced neurotoxicity, which can be attenuated by VC and NAC supplementation. This highlights a potential prophylactic strategy to partially protect the brain from polluted air.