Cytotoxicity induced by fine particulate matter (PM2.5) via mitochondria-mediated apoptosis pathway in human cardiomyocytes

Yang, Xiaozhe; Lin, Feng; Zhang, Yannan; Hu, Hejing; Shi, Yanfeng; Liang, Shuang; Zhao, Tong; Fu, Yang; Duan, Junchao; Sun, Zhiwei

doi:10.1016/j.ecoenv.2018.05.092

Cited by 95 publications

(37 citation statements)

References 45 publications

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“…Due to the toxic effects, PM 2.5 can lead to the induction of apoptotic events by activating both the extrinsic pathway (caspase-8 and caspase-3 activation) and the intrinsic pathway (caspase-9 and caspase-3 activation) [27,50]. The activation of intrinsic pathway is mainly linked to mitochondrial damage and loss of mitochondrial membrane potential [21]. In this study, mitochondrial membrane breach and cristae disorder were observed, along with the loss of MMP after PM 2.5 exposure.…”

Section: Discussionmentioning

confidence: 99%

“…In general, the harmful effects of reactive oxygen species on cells are mainly composed of DNA damage, lipid peroxidation and protein oxidation [20]. Overproduction of ROS induced by PM 2.5 exposure has been associated with cell homeostasis imbalance, mitochondrial damage and apoptosis [21,22]. Activation of apoptosis pathways, consisting of receptor-mediated (extrinsic) and mitochondrial (intrinsic) pathways, is a key step in apoptosis [23,24].…”

Section: Introductionmentioning

confidence: 99%

“…During this process, early apoptosis is characterized by a decline in mitochondrial membrane potential (MMP) and by activation of Bcl-2 family members [26]. The cytotoxic effects of PM 2.5 exposure that result in apoptosis of various cell types have been widely documented [21,27]. However, there has been no report on the toxicity of PM 2.5 to human proximal tubule epithelial cells via activation of antioxidant and apoptosis signaling pathways.…”

Section: Introductionmentioning

confidence: 99%

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The activation of antioxidant and apoptosis pathways involved in damage of human proximal tubule epithelial cells by PM2.5 exposure

et al. 2020

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Background: Exposure to airborne fine particulate matter (PM 2.5 ) has been reported to be harmful to the human kidney. However, whether the activation of oxidative stress and cell apoptosis plays key roles in the nephrotoxicity caused by PM 2.5 exposure is still poorly understood. The aim of this study was to explore the mechanism of cytotoxicity after PM 2.5 exposure in human proximal tubule epithelial cells (HK-2 cells).Results: PM 2.5 exposure resulted in a significant decrease in cell viability, with an increase in LDH release and the early kidney damage marker kidney injury molecule-1 (KIM-1) expression in a dose-dependent manner and timedependent manner. PM 2.5 exposure induced reactive oxygen species (ROS) generation and markedly elevated apoptosis in HK-2 cells. In addition, PM 2.5 exposure resulted in the activation of antioxidant pathway, as evidenced by the increased expressions of Nrf2, HO-1 and NQO1 and decreased expression of Keap1. Moreover, PM 2.5 exposure also induced the activation of apoptotic pathway, as evidenced by the increased expressions of pro-apoptotic proteins Bax, caspase-3 and caspase-8 and decreased expression of antiapoptotic protein Bcl-2. Conclusions:Our results demonstrated that both antioxidant pathway and apoptotic pathway played critical roles in the damage mediated by PM 2.5 in HK-2 cells. This study would give us a strategy to prevent the impairment of renal function by PM 2.5 induced through repression of oxidative stress and apoptosis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The activation of antioxidant and apoptosis pathways involved in damage of human proximal tubule epithelial cells by PM2.5 exposure

et al. 2020

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“…Biomarkers have an additional role related to environmental health research; validation of the causal relationship between air pollution exposure and health outcomes by revealing of a plausible biologic mechanism. Studies have examined the effect of pollutants on biomarkers expression in different human tissues such as adipose tissue [29], cardiomyocytes [30], lung epithelial cells [31], and blood [28]. For instance, the Multi-Ethnic Study of Atherosclerosis (MESA) showed that the PM 2.5 exposure was correlated with an increase in blood concentration of C-reactive protein (CRP), fibrinogen and E-selectin [142], markers related to the atherogenic process [143][144][145], suggesting a plausible biological mechanism by which air pollution could contribute to the development of cardiovascular diseases.…”

Section: Human Biomonitoringmentioning

confidence: 99%

“…(1) The use of electronic medical records that might provide inaccurate data and frequently lack information on the onset and the duration of events [12][13][14]; (2) Seeking medical attention is frequently influenced by patients' self-perception regardless of their clinical state [15][16][17]. Subclinical events, i.e., events without clinical symptoms presentation, are not routinely recorded while can be clinically important [18][19][20][21][22][23][24][25][26]; (3) The need to obtain human tissue samples for measuring of biological indicators that can reveal a plausible biological mechanism is limited due to a small sample size prospective studies plagued by high costs [27][28][29][30][31].…”

Section: Introductionmentioning

confidence: 99%

Novel Approaches to Air Pollution Exposure and Clinical Outcomes Assessment in Environmental Health Studies

et al. 2020

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An accurate assessment of pollutants’ exposure and precise evaluation of the clinical outcomes pose two major challenges to the contemporary environmental health research. The common methods for exposure assessment are based on residential addresses and are prone to many biases. Pollution levels are defined based on monitoring stations that are sparsely distributed and frequently distanced far from residential addresses. In addition, the degree of an association between outdoor and indoor air pollution levels is not fully elucidated, making the exposure assessment all the more inaccurate. Clinical outcomes’ assessment, on the other hand, mostly relies on the access to medical records from hospital admissions and outpatients’ visits in clinics. This method differentiates by health care seeking behavior and is therefore, problematic in evaluation of an onset, duration, and severity of an outcome. In the current paper, we review a number of novel solutions aimed to mitigate the aforementioned biases. First, a hybrid satellite-based modeling approach provides daily continuous spatiotemporal estimations with improved spatial resolution of 1 × 1 km2 and 200 × 200 m2 grid, and thus allows a more accurate exposure assessment. Utilizing low-cost air pollution sensors allowing a direct measurement of indoor air pollution levels can further validate these models. Furthermore, the real temporal-spatial activity can be assessed by GPS tracking devices within the individuals’ smartphones. A widespread use of smart devices can help with obtaining objective measurements of some of the clinical outcomes such as vital signs and glucose levels. Finally, human biomonitoring can be efficiently done at a population level, providing accurate estimates of in-vivo absorbed pollutants and allowing for the evaluation of body responses, by biomarkers examination. We suggest that the adoption of these novel methods will change the research paradigm heavily relying on ecological methodology and support development of the new clinical practices preventing adverse environmental effects on human health.

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Myricetin protects against H₂O₂‐induced oxidative damage and apoptosis in bovine mammary epithelial cells

Kan

Liu

Chen

et al. 2020

Journal Cellular Physiology

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High‐producing dairy cows are prone to oxidative stress due to their high secretion and strong metabolism, and excessive oxidative stress may cause the apoptosis of bovine mammary epithelial cells (bMECs). Myricetin (Myr) has been shown to have a wide range of pharmaceutical activities. The aim of this study was to evaluate the effect of Myr on hydrogen peroxide (H2O2)‐induced oxidative stress and apoptosis in bMECs and to clarify the underlying mechanism. bMECs were pretreated with or without Myr and then stimulated with H2O2. The results showed that Myr significantly increased the total antioxidant capacity and superoxide dismutase levels and decreased the malondialdehyde (MDA) and reactive oxygen species (ROS) levels in a model of oxidative stress induced by H2O2 in bMECs. Mechanistic studies found that Myr inhibited H2O2‐induced oxidative stress in bMECs through the adenosine monophosphate‐activated protein kinase/nuclear factor erythroid‐2 related factor 2 (AMPK/NRF2) signaling pathway. Additional research found that Myr could also inhibit H2O2‐induced apoptosis in bMECs through NRF2. These data suggest that Myr effectively alleviated oxidative stress and apoptosis in H2O2‐induced bMECs through the activation of the AMPK/NRF2 signaling pathway.

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Cytotoxicity induced by fine particulate matter (PM2.5) via mitochondria-mediated apoptosis pathway in human cardiomyocytes

Cited by 95 publications

References 45 publications

The activation of antioxidant and apoptosis pathways involved in damage of human proximal tubule epithelial cells by PM2.5 exposure

The activation of antioxidant and apoptosis pathways involved in damage of human proximal tubule epithelial cells by PM2.5 exposure

Novel Approaches to Air Pollution Exposure and Clinical Outcomes Assessment in Environmental Health Studies

Myricetin protects against H₂O₂‐induced oxidative damage and apoptosis in bovine mammary epithelial cells

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Cytotoxicity induced by fine particulate matter (PM2.5) via mitochondria-mediated apoptosis pathway in human cardiomyocytes

Cited by 95 publications

References 45 publications

The activation of antioxidant and apoptosis pathways involved in damage of human proximal tubule epithelial cells by PM2.5 exposure

The activation of antioxidant and apoptosis pathways involved in damage of human proximal tubule epithelial cells by PM2.5 exposure

Novel Approaches to Air Pollution Exposure and Clinical Outcomes Assessment in Environmental Health Studies

Myricetin protects against H2O2‐induced oxidative damage and apoptosis in bovine mammary epithelial cells

Contact Info

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Myricetin protects against H₂O₂‐induced oxidative damage and apoptosis in bovine mammary epithelial cells