首页> 外文会议>International Conference on Modelling, Monitoring and Management of AIR Pollution >AIR POLLUTION AND OTHER ENVIRONMENTAL STRESSES: GASEOUS NO_2 EXPOSURE LEADS TO SPECIFIC ALTERATIONS OF PSEUDOMONAS FL UORESCENS
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AIR POLLUTION AND OTHER ENVIRONMENTAL STRESSES: GASEOUS NO_2 EXPOSURE LEADS TO SPECIFIC ALTERATIONS OF PSEUDOMONAS FL UORESCENS

机译:空气污染和其他环境压力:气态NO_2暴露导致假单胞菌的特异性改变

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In the environment, microorganisms are subjected to a wide range of stresses. These stresses can be of natural origin, like temperature variations and ultraviolet exposure, but can also originate from humans like air pollution. The effects of air pollution on humans are more and more studied and reveal increasing concerns for human health, including augmentations of respiratory infections. However, the microbial responses to atmospheric pollution are still largely unknown. In a similar fashion, few studies investigate the effects of UV radiation on microorganisms. As NO_2 is an air pollutant causing nitrosative stress in biological organisms by reacting with various biological molecules, solar UV radiations are also an important environmental source of cell damage. UVB can directly damage DNA and cause erythema, but only represent 6% of the total UV reaching the earth surface. The 94% others are UVA, that cause oxidative stress in the cells. Since oxidative and nitrosative stresses are interlinked, the exposition of airborne bacteria to these two stresses could have synergistic consequences. In this study, the airborne Pseudomonas fluorescens strain MFAF76a was exposed successively to gaseous NO_2 and UV light to assess whether these two environmental stresses have synergistic effects on bacterial physiology. Bacterial growth was assessed by optical density and membrane permeability by flow cytometry. Exposures to successively gaseous NO_2 and UVB light lead to a non-synergistic decrease of bacterial viability. Furthermore, only NO_2 seems to damage the membrane and induces membrane permeabilization. Lipidomic analysis reveals similarities between the lipidic profile of bacteria in their exponential growth phase or for the exposed ones to NO_2 during their stationary growth phase. Furthermore, lipidic alterations show that mechanisms induced by NO_2 differ from those implemented by temperature. In conclusion, this study reveals that bacterial alterations caused by NO_2 are specific, with a strong emphasis on membrane damage.
机译:在环境中,微生物受到广泛的应力。这些应力可以是天然来源的,如温度变化和紫外线暴露,但也可以源自空气污染等人。越来越多地研究了空气污染对人类的影响,并揭示了对人类健康的增加,包括增强呼吸道感染。然而,对大气污染的微生物反应仍然很大程度上是未知的。以类似的方式,很少有研究调查紫外线辐射对微生物的影响。由于NO_2是通过与各种生物分子反应导致生物生物中的氮化应激的空气污染物,太阳紫外线辐射也是细胞损伤的重要环境源。 UVB可以直接损伤DNA并导致红斑,但只占地下紫外线的6%。其他94%的是UVA,其导致细胞中的氧化应激。由于氧化和亚硝化胁迫是相互连接的,因此空气中细菌对这两个应力的阐述可能具有协同的后果。在这项研究中,空气传播的假单胞菌荧光菌株MFAF76A依次暴露于气态NO_2和UV光,以评估这两个环境应力是否对细菌生理学具有协同作用。通过流式细胞术通过光密度和膜渗透来评估细菌生长。暴露于连续的气态NO_2和UVB光导致细菌活力的不协同减少。此外,只有NO_2似乎损伤膜并诱导膜透化物。脂质体分析揭示了在其指数生长期的细菌的脂质概况之间的相似性,或在其固定生长阶段期间暴露于NO_2。此外,脂质改变表明,NO_2诱导的机制不同于温度所实施的机制。总之,本研究表明,NO_2引起的细菌改变是特异性的,强调膜损伤。

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