Metabolic dysregulations underlying the pulmonary toxicity of atmospheric fine particulate matter: focus on energy-producing pathways and lipid metabolism

Silva, Tatiana D.; Alves, Célia; Oliveira, Helena Coutinho Franco de; Duarte, Iola F.

doi:10.1007/s11869-022-01236-6

Cited by 6 publications

(1 citation statement)

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“…Commonly reported effects include diminished cell viability, induction of oxidative stress, inflammatory responses, and DNA damage [26][27][28][29][30]. Moreover, changes in cell metabolism have started to emerge as an important biological endpoint of PM exposure, mainly because (i) metabolic alterations tend to manifest at relatively low PM exposure concentrations, often preceding the detection of other traditional toxicity indicators; (ii) the dysregulation of metabolic processes induced by PM exposure may have significant implications for the pathobiology of various lung diseases [31]. However, our comprehension of how PM precisely modulates distinct metabolic pathways in diverse cell types remains limited.…”

Section: Introductionmentioning

confidence: 99%

Biological Impact of Organic Extracts from Urban-Air Particulate Matter: An In Vitro Study of Cytotoxic and Metabolic Effects in Lung Cells

Silva,

Alves,

Oliveira

et al. 2023

IJMS

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Atmospheric particulate matter (PM) with diameters below 10 µm (PM10) may enter the lungs through inhalation and are linked to various negative health consequences. Emergent evidence emphasizes the significance of cell metabolism as a sensitive target of PM exposure. However, the current understanding of the relationship between PM composition, conventional toxicity measures, and the rewiring of intracellular metabolic processes remains limited. In this work, PM10 sampled at a residential area (urban background, UB) and a traffic-impacted location (roadside, RS) of a Portuguese city was comprehensively characterized in terms of polycyclic aromatic hydrocarbons and plasticizers. Epithelial lung cells (A549) were then exposed for 72 h to PM10 organic extracts and different biological outcomes were assessed. UB and RS PM10 extracts dose-dependently decreased cell viability, induced reactive oxygen species (ROS), decreased mitochondrial membrane potential, caused cell cycle arrest at the G0/G1 phase, and modulated the intracellular metabolic profile. Interestingly, the RS sample, richer in particularly toxic PAHs and plasticizers, had a greater metabolic impact than the UB extract. Changes comprised significant increases in glutathione, reflecting activation of antioxidant defences to counterbalance ROS production, together with increases in lactate, NAD+, and ATP, which suggest stimulation of glycolytic energy production, possibly to compensate for reduced mitochondrial activity. Furthermore, a number of other metabolic variations hinted at changes in membrane turnover and TCA cycle dynamics, which represent novel clues on potential PM10 biological effects.

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