Direct contact with particulate matter increases oxidative stress in different brain structures

Fagundes, Lucas Sagrillo; Fleck, Alan da Silveira; Zanchi, Ana Claudia; Saldiva, Paulo Hilário Nascimento; Rhoden, Cláudia Ramos

doi:10.3109/08958378.2015.1060278

Cited by 60 publications

(21 citation statements)

References 36 publications

(41 reference statements)

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“…However, SOD, an antioxidant in vivo, significantly decreased after 6-month PM2.5 exposure. The results suggested that long-term exposure to moderate concentrations of PM2.5 can indeed affect balance of oxidation and antioxidation, which is consistent with previous study [21].…”

Section: Discussionsupporting

confidence: 92%

Ambient PM2.5 induces brain injury through PI3K/AKT/FoxO1 pathway

Song

Pan

et al. 2020

Preprint

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Background Fine particulate matter (PM 2.5 )-induced neurological and mental diseases, such as cognitive impairment and stroke, tend to cause disability. In this study, we plan to find the appropriate biological indicators reflecting the early effects of PM 2.5 exposure and explore the toxicity of inhaling PM 2.5 along with its pathological mechanism on nervous system. Methods Male C57BL/6 mice were divided into 6 groups and exposed to concentrated PM 2.5 or filtered air for 2, 4 and 6 months, respectively. Their performances of ethology were tested by Morris water maze, elevated plus maze and buried food pellet test. Weight of whole brain and olfactory bulbs were recorded when the mice were sacrificed and the brain structure was observed by HE staining. ROS, SOD, IL-6, TNF-α, IL-1β, BDNF, β-hydroxybutyric, IgG, albumin, fibrinogen and plasminogen were tested. The mRNA expressions of the cortex were detected by RNA sequencing and real-time PCR, and the corresponding proteins were detected by Western blot. Results The spatial learning memory ability were impaired and the mice performed anxiously after PM 2.5 exposure. Relative brain weight decreased along with age and PM 2.5 inhaled exposure exceeded the process. But neuronal morphology, inflammatory cytokines, ROS, β-hydroxybutyric, BDNF, IgG and fibrinogen did not change. Intriguingly, SOD and albumin decreased, while plasminogen increased after PM 2.5 exposure. PI3K-AKT-FoxO1 pathway was activated after 6-month PM 2.5 exposure. Conclusion Albumin, A/G value and plasminogen are main serum indicators of early-stage (2 month) PM 2.5 exposure, and long-term (6 month) PM 2.5 exposure induced brain injury potentially through the activation of PI3K/AKT/FoxO1 pathway.

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Section: Discussionsupporting

confidence: 92%

Ambient PM2.5 induces brain injury through PI3K/AKT/FoxO1 pathway

Song

Pan

et al. 2020

Preprint

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“…3B). In contrast, others have previously shown that PM increases oxidative stress in the brain (Mohan Kumar et al 2008; Sagrillo Fagundes et al 2015), and that oxidative stress plays a primary role in DEP neurotoxicity (Block et al 2004). Thus, the possibility that some forms of oxidative stress may be involved in the microglia-mediated effects of DEP warrants further investigations.…”

Section: Discussionmentioning

confidence: 91%

Microglia mediate diesel exhaust particle-induced cerebellar neuronal toxicity through neuroinflammatory mechanisms

2016

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In addition to the well-established effects of air pollution on the cardiovascular and respiratory systems, emerging evidence has implicated it in inducing negative effects on the central nervous system. Diesel exhaust particulate matter (DEP), a major component of air pollution, is a complex mixture of numerous toxicants. Limited studies have shown that DEP-induced dopaminergic neuron dysfunction is mediated by microglia, the resident immune cells of the brain. Here we show that mouse microglia similarly mediate primary cerebellar granule neuron (CGN) death in vitro. While DEP (0, 25, 50, 100 µg/2 cm2) had no effect on CGN viability after 24 h of treatment, in the presence of primary cortical microglia neuronal cell death increased by 2–3-fold after co-treatment with DEP, suggesting that microglia are important contributors to DEP-induced CGN neurotoxicity. DEP (50 µg/2 cm2) treatment of primary microglia for 24 h resulted in morphological changes indicative of microglia activation, suggesting that DEP may induce the release of cytotoxic factors. Microglia-conditioned medium after 24 h treatment with DEP, was also toxic to CGNs. DEP caused a significant increase in reactive oxygen species in microglia, however, antioxidants failed to protect neurons from DEP/microglia-induced toxicity. DEP increased mRNA levels of the pro-inflammatory cytokines IL-6 and IL1-β, and the release of IL-6. The antibiotic minocycline (50 µM) and the peroxisome proliferator-activated receptor-γ agonist pioglitazone (50 µM) attenuated DEP-induced CGN death in the co-culture system. Microglia and CGNs from male mice appeared to be somewhat more susceptible to DEP neurotoxicity than cells from female mice possibly because of lower paraoxonase-2 expression. Together, these results suggest that microglia-induced neuroinflammation may play a critical role in modulating the effect of DEP on neuronal viability.

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“…Previous animal experiments showed that neurochemicals and behavior changed in rodents after exposure to air pollutants (Yin et al, ; Fagundes et al, ). It has been reported that atmospheric particulates cause inflammation of the brain via activation of the c‐Jun N‐terminal kinase (JNK) pathway and the NF‐κB pathway.…”

Section: Mechanisms Of Particles‐induced Neurotoxicitymentioning

confidence: 98%

“…PM: particulate matter, ROS: reactive oxygen species, CNS: central nervous system, BBB: brain-blood barrier, ER: endoplasmic reticulum. 2013; Fagundes et al, 2015). It has been reported that atmospheric particulates cause inflammation of the brain via activation of the c-Jun N-terminal kinase ( JNK) pathway and the NF-κB pathway.…”

Section: Neuroinflammation and Bbb Damagementioning

confidence: 99%

Toxicity of inhaled particulate matter on the central nervous system: neuroinflammation, neuropsychological effects and neurodegenerative disease

2017

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Particulate matter (PM) combined with meteorological factors cause the haze, which brings inconvenience to people's daily life and deeply endanger people's health. Accumulating literature, to date, reported that PM are closely related to cardiopulmonary disease. Outpatient visits and admissions as a result of asthma and heart attacks gradually increase with an elevated concentration of PM. Owing to its special physicochemical property, the brain could be a potential target beyond the cardiopulmonary system. Possible routes of PM to the brain via a direct route or stimulation of pro-inflammatory cytokines have been reported in several documents concerning toxicity of engineered nanoparticles in rodents. Recent studies have demonstrated that PM have implications in oxidative stress, inflammation, dysfunction of cellular organelles, as well as the disturbance of protein homeostasis, promoting neuron loss and exaggerating the burden of central nervous system (CNS). Moreover, the smallest particles (nano-sized particles), which were involved in inflammation, reactive oxygen species (ROS), microglial activation and neuron loss, may accelerate the process of the neurodevelopmental disorder and neurodegenerative disease. Potential or other undiscovered mechanisms are not mutually exclusive but complementary aspects of each other. Epidemiology studies have shown that exposure to PM could bring about neurotoxicity and play a significant role in the etiology of CNS disease, which has been gradually corroborated by in vivo and in vitro studies. This review highlights research advances on the health effects of PM with an emphasis on neurotoxicity. With the hope of enhancing awareness in the public and calling for prevention and protective measures, it is a critical topic that requires proceeding exploration. Copyright © 2017 John Wiley & Sons, Ltd.

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Direct contact with particulate matter increases oxidative stress in different brain structures

Cited by 60 publications

References 36 publications

Ambient PM2.5 induces brain injury through PI3K/AKT/FoxO1 pathway

Ambient PM2.5 induces brain injury through PI3K/AKT/FoxO1 pathway

Microglia mediate diesel exhaust particle-induced cerebellar neuronal toxicity through neuroinflammatory mechanisms

Toxicity of inhaled particulate matter on the central nervous system: neuroinflammation, neuropsychological effects and neurodegenerative disease

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