Developmental toxicity induced by PM2.5 through endoplasmic reticulum stress and autophagy pathway in zebrafish embryos

Zhang, Yun; Li, Saiyu; Li, Juanjuan; Han, Liwen; He, Qiuxia; Wang, Rongchun; Wang, Ximin; Liu, Kechun

doi:10.1016/j.chemosphere.2018.01.092

Cited by 61 publications

(28 citation statements)

References 39 publications

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“…Hence, our study suggests a paradigm by which hypothalamic ER stress response induced by benzene exposure can mediate peripheral metabolic imbalance associated with T2D and related problems. These findings complement the recent research which has proposed that exposure to PM2.5 induces inflammation via the activation of the IRE1α -XBP1 and ATF6 pathways in zebrafish and mice hepatocytes [62]. Chronic benzene exposure robustly activates hypothalamic ER stress response and, stimulates glial inflammatory reaction highlighting the susceptibility of the hypothalamus to stress and inflammation that lead to changes in metabolic status.…”

Section: Discussionsupporting

confidence: 88%

Acarbose Protects From Central and Peripheral Metabolic Imbalance Induced by Benzene Exposure

Debarba

Mulka

Lima

et al. 2020

Preprint

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Abbreviations:CNS, central nervous system; ARC, arcuate nucleus of the hypothalamus; DMH, dorsomedial hypothalamic nucleus; LHA, lateral hypothalamus; PVH, paraventricular hypothalamic nucleus; AbstractBenzene is a well-known human carcinogen that is one of the major components of air pollution. Sources of benzene in ambient air include cigarette smoke, e-cigarettes vaping and evaporation of benzene containing petrol processes. While carcinogenic effects of benzene exposure have been well studied, less is known about metabolic effects of benzene exposure.We show that chronic exposure to benzene at low levels induces severe metabolic imbalance in a sex-specific manner, which is associated with hypothalamic inflammation and endoplasmic reticulum (ER) stress. Benzene exposure rapidly activates hypothalamic ER stress and neuroinflammatory responses in male mice, while pharmacological inhibition of ER stress response by inhibiting IRE1α-XBP1 pathway significantly alleviates benzene-induced glial inflammatory responses. Additionally, feeding mice with Acarbose, a clinically available anti-diabetes drug, protected against benzene induced central and peripheral metabolic imbalance. Acarbose imitates the slowing of dietary carbohydrate digestion, suggesting that choosing a diet with a low glycemic index might be a potential strategy for reducing the negative metabolic effect of chronic exposure to benzene for smokers or for people living/working in urban environments with high concentrations of exposure to automobile exhausts.

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Section: Discussionsupporting

confidence: 88%

Acarbose Protects From Central and Peripheral Metabolic Imbalance Induced by Benzene Exposure

Debarba

Mulka

Lima

et al. 2020

Preprint

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“…Autophagy is a physiological process whereby eukaryotic cells undergo self-digestion, which allows the degradation and recycling of unnecessary intracellular proteins and dysfunctional organelles via the autophagosome and lysosomes (Deng et al, 2013;Deng et al, 2014;Su et al, 2017). The formation of the autophagosome involves the action of multiple autophagy-related genes (Atgs), such as Beclin-1(Atg6), and microtubule-associated proteins light chain 3 (LC3) (Deng et al, 2013;Zhang et al, 2018b). Sequestosome1/P62 (SQSTM1) is a regulatory autophagy protein originally identi ed as a binding protein for nonreceptor-type tyrosine kinase P56 Lck (Ichimura et al, 2013;Zhou et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

PM2.5 exposure induced renal injury via the activation of the autophagic pathway in the rat and HK-2 cell

Huang

Zhou

Liu

et al. 2020

Preprint

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Abstract Background: Exposure to airborne fine particulate matter (PM2.5) has been declared to be harmful to human kidney. However, whether activation of the autophagic pathway plays key roles in the nephrotoxicity caused by PM2.5 exposure is still poorly understood. The aim of this study was to explore the mechanism of kidney damage after PM2.5 exposure in vivo and in vitro.Results: In the present study, statistically significant alterations in water intake, urine flow rate and mean blood pressure were observed between the concentrated PM2.5 (PM2.5) group and the filtered air (FA) group. Exposed animals showed severe edema of renal tubular epithelial cells, capillary congestion, reduction of the glomerular urinary space and early pro-fibrotic state. Moreover, significant increases in the levels of early kidney damage markers were observed in the exposed rats and these animals exhibited more apoptosis rate in kidney cells. In addition, PM2.5 exposure activated the autophagic pathway, as evidenced by LC3-I to LC3-II conversion, activation of P62 and beclin-1. All of these effects are in concurrence with the presence of more autophagosomes both in vivo and in vitro after PM2.5 exposure. Conclusions: Taken together, our findings indicated that PM2.5-induced renal function impairment via the activation of the autophagic pathway in renal tubular epithelial cells.

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“…One study performed in rats used 9 and 24 mg/kg PM exposure via intratracheal instillation for seven weeks (Wei et al, 2018). Another study exposed zebrafish embryos with up to 900 mg/ml PM2.5 in water for 120 h (Zhang Y. et al, 2018). In the current study, 0, 0.05, 0.2, 0.5, 2, and 5 mg/kg PM2.5 were exposed to fertile chicken eggs as a one-time air cell injection, which is comparable to previous studies.…”

Section: Discussionmentioning

confidence: 99%

Particulate Matter 2.5 Induced Developmental Cardiotoxicity in Chicken Embryo and Hatchling

et al. 2020

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Particulate matter poses health risk to developing organisms. To investigate particulate matters with a diameter smaller than 2.5 um (PM2.5)-induced developmental cardiotoxicity, fertile chicken eggs were exposed to PM2.5 via air cell injection at doses of 0.05, 0.2, 0.5, 2, and 5 mg/egg kg. Morphological changes in the embryonic day four (ED4) and hatchling hearts were assessed with histological techniques. Heart rates of hatchling chickens were measured with electrocardiography. The protein expression levels of nuclear factor kappa-light-chain-enhancer of activated B cells p65 (NF-kb p65), inducible nitric oxide synthase (iNOS), and matrix metallopeptidase 9 (MMP9) were assessed with immunohistochemistry or western blotting in hatchling hearts. PM2.5 exposure elevated areas of heart in ED4 embryo, increased heart rate, and thickened right ventricular wall thickness in hatchling chickens. Immunohistochemistry revealed enhanced NF-kb p65 expression in hatchling hearts. Western blotting results indicated that both iNOS and MMP9 expression were enhanced by lower doses of PM2.5 exposure (0.2 and 0.5 mg/kg) but not 2 mg/kg. In summary, developmental exposure to PM2.5 induced developmental cardiotoxicity in chicken embryo and hatchling chickens, which is associated with NF-kb p65, iNOS, and MMP9.

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Developmental toxicity induced by PM2.5 through endoplasmic reticulum stress and autophagy pathway in zebrafish embryos

Cited by 61 publications

References 39 publications

Acarbose Protects From Central and Peripheral Metabolic Imbalance Induced by Benzene Exposure

Acarbose Protects From Central and Peripheral Metabolic Imbalance Induced by Benzene Exposure

PM2.5 exposure induced renal injury via the activation of the autophagic pathway in the rat and HK-2 cell

Particulate Matter 2.5 Induced Developmental Cardiotoxicity in Chicken Embryo and Hatchling

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