Toxicological effects of particulate matter (PM2.5) on rats: Bioaccumulation, antioxidant alterations, lipid damage, and ABC transporter activity

Ribeiro, Joaquim de Paula; Kalb, Ana Cristina; Campos, Paula Peixoto; Cruz, Alex Rubén Huamán De La; Martinez, Pablo Elías; Gioda, Adriana; Souza, Maurício de; Gioda, Carolina Rosa

doi:10.1016/j.chemosphere.2016.07.094

Cited by 36 publications

(16 citation statements)

References 48 publications

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“…The chemical composition of airborne PM2.5, particularly metals, could affect bioaccumulation and oxidative damage induced by PM2.5. [ 42 ] As shown earlier by using RNA‐Seq analysis, PM2.5 markedly increased oxidative stress in ovaries. We decided to examine whether the chemical components of PM2.5 was involved in PM2.5‐induced oxidative stress, human ovarian granulosa KGN cells were treated with 100 or 200 µg mL −1 of water‐soluble fraction of PM2.5 (W‐PM) or dimethyl sulfoxide (DMSO)‐soluble fraction of PM2.5 (D‐PM) for 24 or 48 h, respectively.…”

Section: Resultsmentioning

confidence: 65%

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Ovarian Dysfunction Induced by Chronic Whole‐Body PM2.5 Exposure

Zhou

Chen

et al. 2020

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Fine particulate matter (PM2.5) pollution arouses public health concerns over the world. Increasing epidemiologic evidence suggests that exposure to ambient airborne PM2.5 increases the risk of female infertility. However, relatively few studies have systematically explored the harmful effect of chronic PM2.5 exposure on ovarian function and the underlying mechanisms. In this study, female C57BL/6J mice are exposed to filtered air or urban airborne PM2.5 for 4 months through a whole‐body exposure system. It is found that PM2.5 exposure significantly caused the alteration of estrus cycles, reproductivity, hormone levels, and ovarian reserve. The granulosa cell apoptosis via the mitochondria dependent pathway contributes to the follicle atresia. With RNA‐sequencing technique, the differentially expressed genes induced by PM2.5 exposure are mainly enriched in ovarian steroidogenesis, reactive oxygen species and oxidative phosphorylation pathways. Furthermore, it is found that increased PM2.5 profoundly exacerbated ovarian oxidative stress and inflammation in mice through the NF‐κB/IL‐6 signaling pathway. Notably, dietary polydatin (PD) supplement has protective effect in mice against PM2.5‐induced ovarian dysfunction.These striking findings demonstrate that PM2.5 and/or air pollution is a critical factor for ovarian dysfunction through mitochondria‐dependent and NF‐κB/IL‐6‐mediated pathway, and PD may serve as a pharmaceutic candidate for air pollution‐associated ovarian dysfunction.

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Section: Resultsmentioning

confidence: 65%

“…These results are consistent with an earlier report demonstrating that the chemical composition of airborne PM2.5 could affect bioaccumulation and oxidative stress induced by PM2.5. [ 42 ]…”

Section: Discussionmentioning

confidence: 99%

Ovarian Dysfunction Induced by Chronic Whole‐Body PM2.5 Exposure

Zhou

Chen

et al. 2020

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“…Consequently, these proteins played a significant function in the translocation of 4‐CP and in the maintenance of normal activity of microbes (Jeong et al, ). Certainly, the activity of ABC transporter tended to reduce after exposure to toxicants (Ribeiro et al, ). However, the unfortunate truth was that due to the existence of these ABC transporters in human body, drugs targeting cancer faced enhanced efflux, leading to failure of cancer chemotherapy (Li et al, ).…”

Section: Resultsmentioning

confidence: 99%

Effects of hydraulic retention time and proteins on sludge toxicity for 4‐chlorophenol wastewater treatment in sequencing batch reactors

Zhao

Chen

et al. 2018

Water & Environment J

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Due to the higher uncertainty of environmental risk for pollutants’ treatment by activated sludge, 10 mg/L influent 4‐chlorophenol (4‐CP) treated via a sequencing batch reactor (SBR) was used as acclimated SBR. Another SBR was used as control SBR without 4‐CP. The effects of hydraulic retention time (HRT) and proteins on sludge toxicity for 4‐CP treatment were analysed, and compared to the control SBR. Results showed that the sludge toxicity in acclimated SBR was significantly higher than that of the control SBR. Shortening HRT from 12 to 8 hours was beneficial to degrade 4‐CP and lower sludge toxicity. The identified highly expressed protein of ABC transporter co‐existed in control and acclimated SBRs, while other proteins of TonB‐dependent receptor, heat shock 70 kDa protein and superoxide dismutase in acclimated sludge were overexpressed relative to the control sludge, which played an important function in degrading 4‐CP, resisting 4‐CP toxicity and eliminating sludge toxicity.

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“…Previous studies showed that the primary composition of these particles, metallic elements, induce inflammatory response. Trace metals were the most toxic substances in ambient PM (Ribeiro et al 2016). Due to the lack of a constant actual PM 2.5 , these studies have lacked repeatability.…”

Section: Discussionmentioning

confidence: 99%

Toxicological Effects of Artificial Fine Particulate Matter in Rats through Induction of Oxidative Stress and Inflammation

Hong

Zeng

Zhuang

et al. 2021

Tohoku J. Exp. Med.

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Airborne fine particulate matter with an aerodynamic diameter equal to or smaller than 2.5 μm (abbreviated as PM 2.5 ) increases the risk of nasal lesions, but the underlying molecular mechanism has not been fully elucidated. In the atmosphere, the composition of PM 2.5 collected varies in physical and chemical properties, which affects its damage to human health. Thus, we constructed artificial PM 2.5 particles based on actual PM 2.5 and investigated the in vivo effects of artificial PM 2.5 exposure on the oxidative stress, inflammatory response, and nasal mucosa morphology of rats. The results showed that artificial PM 2.5 is comparable in composition ratio, size, and morphology to actual PM 2.5 . This in vivo study indicated that artificial PM 2.5 exposure reduces total superoxide dismutase and glutathione peroxidase activities, elevates malondialdehyde content in the nasal mucosa, and induces increased levels of pro-inflammatory mediators, including interleukin-1, interleukin-6 and tumor necrosis factor-α. Our data shows that artificial PM 2.5 particles could be used for experimental study of PM 2.5 toxicology, ensuring that the physical and chemical properties of experimental PM 2.5 are relatively constant and allowing for repeatability of this research. Oxidative damage and inflammatory response may be the toxic mechanisms that cause nasal lesions after exposure to artificial PM 2.5 .

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Toxicological effects of particulate matter (PM2.5) on rats: Bioaccumulation, antioxidant alterations, lipid damage, and ABC transporter activity

Cited by 36 publications

References 48 publications

Ovarian Dysfunction Induced by Chronic Whole‐Body PM2.5 Exposure

Ovarian Dysfunction Induced by Chronic Whole‐Body PM2.5 Exposure

Effects of hydraulic retention time and proteins on sludge toxicity for 4‐chlorophenol wastewater treatment in sequencing batch reactors

Toxicological Effects of Artificial Fine Particulate Matter in Rats through Induction of Oxidative Stress and Inflammation

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