Acute nitrogen dioxide inhalation induces mitochondrial dysfunction in rat brain

Yan, Wei; Ji, Xiaotong; Shi, Jing; Li, Guangke; Sang, Nan

doi:10.1016/j.envres.2015.02.022

Cited by 68 publications

(35 citation statements)

References 51 publications

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“…Indeed, as for the particles, in the gaseous phase, exposure to NO 2 generates oxidative stress. This finding was confirmed by Yan et al [34], who showed that the oxidative stress generated by exposure to NO 2 in the gas phase could be of mitochondrial origin. Indeed, these authors have shown that exposure to NO 2 induces overproduction of ROS from 2.5 ppm NO 2 , which represents a concentration well above that used in this study (0.2 and 0.3 ppm).…”

Section: Discussionsupporting

confidence: 62%

Toxicological Responses of Wistar Rats Exposed to Controlled Emissions of Carbon Monoxide and Nitrogen Dioxide

Tito¹,

Messan²,

Togbenou³

et al. 2019

World Journal of Research and Review

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The inhalation of pollutants of automobile origin induces blood disturbances, especially noncommunicable diseases, in humans. However, there are no studies highlighting the effects induced by car pollutants. From this perspective, this study aims to evaluate the effects of at least two (02) pollutants, carbon monoxide (CO) and nitrogen dioxide (NO 2), on oxidative stress and inflammation after a single exposure for four hours (04 h). Materials and methods: Ten male Wistar strain rats were randomly divided into two groups of five (05): the control group (179.00 ± 5.916 g) unexposed and the group exposed to CO and NO 2 (188.00 ± 13.13 g). CO and NO 2 were produced by the combustion gas oil using a device contained in a sealed metal box supplied with ambient air by a pump. The ranges of CO and NO 2 concentrations to which the rats were exposed varied between 35 and 45 ppm and between 0.2 and 0.3 ppm, respectively. The blood samples were taken at 24 hours after the end of the manipulations. A malondialdehyde (MDA) assay was performed on supernatant using the GENESYS 10S UV Visible Spectrophotometer. Tumour Necrosis factor alpha (TNF-α) levels in the supernatant stored at-80 ° C were examined with an ELISA kit. Results: The mean values of MDA (17,771 ± 6.624 nM / ml) and TNF-α (83,050 ± 7.483 μg / ml) observed in the exposed group were significantly higher (p ˂ 0.01) than those recorded in the control group (MDA (7.097 ± 1.882 nM / ml) and TNF-α (6.410 ± 3.160 μg / ml). Conclusion: Exposure to CO and NO 2 for at least 4 hours induces the overproduction of reactive oxygen species (ROS) and the exacerbation of inflammation.

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Section: Discussionsupporting

confidence: 62%

Toxicological Responses of Wistar Rats Exposed to Controlled Emissions of Carbon Monoxide and Nitrogen Dioxide

Tito¹,

Messan²,

Togbenou³

et al. 2019

World Journal of Research and Review

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“…Experimental literatures also provide evidence for neurotoxic effects of SO 2 exposure, such as oxidative stress and mitochondrial dysfunction in neuronal cells [28], neuronal insult and synaptic dysfunctions [29] and impairment of neuronal behavior in experimental animals [30]. Recently, an animal study reported that acute NO 2 inhalation induced mitochondrial morphological changes in rat cortex and the abnormality of mitochondrial energy metabolism [31], which is involved in the pathogenesis of various neurological disorders.…”

Section: Discussionmentioning

confidence: 99%

The impact of ambient air pollution on suicide mortality: a case-crossover study in Guangzhou, China

Lin

Song

et al. 2016

Environ Health

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BackgroundPreventing suicide is a global imperative. Although the effects of social and individual risk factors of suicide have been widely investigated, evidence of environmental effects of exposure to air pollution is scarce. We investigated the effects of ambient air pollution on suicide mortality in Guangzhou, China during 2003−2012.MethodsA conditional logistic regression analysis with a time-stratified case-crossover design was performed to assess the effects of daily exposure to three standard air pollutants, including particulate matter less than 10 μm in aerodynamic diameter (PM10), sulphur dioxide (SO2) and nitrogen dioxide (NO2), on suicide mortality, after adjusting for the confounding effects of daily mean temperature, relative humidity, atmospheric pressure and sunshine duration. Further analyses were stratified by season, gender, age group, educational attainment and suicide type.ResultsBetween 2003 and 2012, there were a total of 1 550 registered suicide deaths in Guangzhou. A significant increase in suicide risk were associated with interquartile-range increases in the concentration of air pollutant, with an odds ratio of 1.13 (95 % confidence interval (CI): 1.01, 1.27) and 1.15 (95 % CI: 1.03, 1.28) for PM10 and NO2 at lag 02, and 1.12 (95 % CI: 1.02, 1.23) for SO2 at lag 01, respectively. The suicide risks related to air pollution for males and people with high education level were higher than for females and those with low education level, respectively. Significant air pollution effects were found on violent suicide mortality and in cool season but not on non-violent suicide mortality or in warm season.ConclusionsSuicide risk was positively associated with ambient air pollution levels. This finding would provide important information for the health impact assessment of air pollution and for the development of effective strategies and interventions for the prevention of suicide.

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“…Protein was extracted and quantified according to a previously reported method [29]. Protein samples of 30 μg were then size-fractionated through sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and transferred to a nitrocellulose membrane.…”

Section: Western Blot Analysismentioning

confidence: 99%

“…After inoculation of the cells (1 × 10 6 cells/mL) into 35-mm petri dishes, the cells were treated with 0, 3, 10 or 30 μM buprofezin for 24 h. Intracellular ATP levels were determined with a Thermo Scientific Varioskan Flash (Thermo Fisher Scientific, USA) according to the manufacturer's instructions (Beyotime, China) [29]. Similarly, intrasellular pyruvate and lactate levels were determined according to the manufacturer's instructions (Nanjing Jiancheng Bioengineering Institute, China).…”

Section: Determination Of the Atp Pyruvate And Lactate Levelmentioning

confidence: 99%

Potential hepatic toxicity of buprofezin at sublethal concentrations: ROS-mediated conversion of energy metabolism

Zhu

et al. 2016

Journal of Hazardous Materials

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Buprofezin is known for its broad-spectrum action and environmental safety. The popularity of buprofezin has raised concerns about its potentially adverse effects on human health and risk to the environment. In this study, we first identified the liver as one of the major organs in which buprofezin accumulated, and we detected a severe oxidative stress response. Next, we demonstrated that sublethal concentrations of buprofezin promoted the conversion of energy metabolism from the aerobic tricarboxylic acid (TCA) cycle and oxidative phosphorylation to anaerobic glycolysis. Importantly, reactive oxygen species (ROS) generation partially accounted for the shunting of the energy metabolism through the buprofezin-mediated inhibition of cytochrome c oxidase activity. ROS directly perturbed the activities of several key TCA cycle enzymes, stimulated glycolysis, and indirectly disturbed the activity of the respiratory chain complex by altering mitochondrial DNA (mtDNA). These findings clarify the potential mechanisms of buprofezin toxicity and provide biomarkers for buprofezin-mediated hepatotoxicity at sublethal concentrations.

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Acute nitrogen dioxide inhalation induces mitochondrial dysfunction in rat brain

Cited by 68 publications

References 51 publications

Toxicological Responses of Wistar Rats Exposed to Controlled Emissions of Carbon Monoxide and Nitrogen Dioxide

Toxicological Responses of Wistar Rats Exposed to Controlled Emissions of Carbon Monoxide and Nitrogen Dioxide

The impact of ambient air pollution on suicide mortality: a case-crossover study in Guangzhou, China

Potential hepatic toxicity of buprofezin at sublethal concentrations: ROS-mediated conversion of energy metabolism

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