Polystyrene microplastics up-regulates liver glutamine and glutamate synthesis and promotes autophagy-dependent ferroptosis and apoptosis in the cerebellum through the liver-brain axis

Yin, Kai; Wang, Dongxu; Zhao, Hongjing; Wang, Yu; Zhang, Yue; Liu, Yachen; Li, Baoying; Xing, Mingwei

doi:10.1016/j.envpol.2022.119449

Cited by 73 publications

(32 citation statements)

References 88 publications

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“…The downregulation of Beclin-1 attenuated viral-induced inflammation in HIV-1-infected microglial cells [ 60 ]. These results indicate that autophagy is involved in the regulation of neurotoxicity induced by PS-NPs, which is also in accordance with the study conducted by Yin et al, showing that microplastics triggered autophagy-dependent ferroptosis and apoptosis in chicken brains [ 22 ].…”

Section: Resultssupporting

confidence: 92%

“…The accumulated PS-NPs in mouse brains resulted in neurobehavior alteration and cognitive impairment [ 20 ]. Penetration by PS-NPs through the blood–brain barrier (BBB) is mainly due to increased BBB permeability [ 21 ], which could potentially result from the reduced expression of tight junction proteins [ 22 ]. Mechanism research conducted by Barboza et al indicated that the neurotoxicity induced by PS-NPs in European seabass was mediated by the induction of oxidative stress, the promotion of lipid oxidation, and the inhibition of acetylcholinesterase (AChE) activity [ 23 ].…”

Section: Introductionmentioning

confidence: 99%

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PS-NPs Induced Neurotoxic Effects in SHSY-5Y Cells via Autophagy Activation and Mitochondrial Dysfunction

Tang

Chen

et al. 2022

Brain Sciences

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Polystyrene nanoparticles (PS-NPs) are organic pollutants that are widely detected in the environment and organisms, posing potential threats to both ecosystems and human health. PS-NPs have been proven to penetrate the blood–brain barrier and increase the incidence of neurodegenerative diseases. However, information relating to the pathogenic molecular mechanism is still unclear. This study investigated the neurotoxicity and regulatory mechanisms of PS-NPs in human neuroblastoma SHSY-5Y cells. The results show that PS-NPs caused obvious mitochondrial damages, as evidenced by inhibited cell proliferation, increased lactate dehydrogenase release, stimulated oxidative stress responses, elevated Ca2+ level and apoptosis, and reduced mitochondrial membrane potential and adenosine triphosphate levels. The increased release of cytochrome c and the overexpression of apoptosis-related proteins apoptotic protease activating factor-1 (Apaf-1), cysteinyl aspartate specific proteinase-3 (caspase-3), and caspase-9 indicate the activation of the mitochondrial apoptosis pathway. In addition, the upregulation of autophagy markers light chain 3-II (LC3-II), Beclin-1, and autophagy-related protein (Atg) 5/12/16L suggests that PS-NPs could promote autophagy in SHSY-5Y cells. The RNA interference of Beclin-1 confirms the regulatory role of autophagy in PS-NP-induced neurotoxicity. The administration of antioxidant N-acetylcysteine (NAC) significantly attenuated the cytotoxicity and autophagy activation induced by PS-NP exposure. Generally, PS-NPs could induce neurotoxicity in SHSY-5Y cells via autophagy activation and mitochondria dysfunction, which was modulated by mitochondrial oxidative stress. Mitochondrial damages caused by oxidative stress could potentially be involved in the pathological mechanisms for PS-NP-induced neurodegenerative diseases.

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Section: Resultssupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

PS-NPs Induced Neurotoxic Effects in SHSY-5Y Cells via Autophagy Activation and Mitochondrial Dysfunction

Tang

Chen

et al. 2022

Brain Sciences

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“…PS-MPs were also found to activate the expression of autophagy-related proteins in chicken cerebellum and avian heart, respectively, in chickens [ 153 ] and birds [ 154 ].…”

Section: Potential Mechanisms Of Mps/nps Toxicity On the Livermentioning

confidence: 99%

Nanoplastics and Microplastics May Be Damaging Our Livers

Yin

Qian

et al. 2022

Toxics

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Plastics in the environment can be degraded and even broken into pieces under the action of natural factors, and the degraded products with a particle size of less than 5 mm are called microplastics (MPs). MPs exist in a variety of environmental media that come into contact with the human body. It can enter the body through environmental media and food chains. At present, there are many studies investigating the damage of MPs to marine organisms and mammals. The liver is the largest metabolizing organ and plays an important role in the metabolism of MPs in the body. However, there is no available systematic review on the toxic effects of MPs on the liver. This paper summarizes the adverse effects and mechanisms of MPs on the liver, by searching the literature and highlighting the studies that have been published to date, and provides a scenario for the liver toxicity caused by MPs.

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“…According to previous studies, inhaled particles could pass the air–blood barrier and then translocate to other organs, e . g ., heart, brain, and even knee joint. ,, Thus, the target cells of FPM vary in diverse studies and the reported mechanisms are different. For example, the FPM could sensitize lung epithelial cells to apoptosis via the NF-κB pathway and induce apoptosis on endothelial cells through the COX-2/PGES/PGE2 pathway.…”

Section: Discussionmentioning

confidence: 99%

Cell Death Pathways: The Variable Mechanisms Underlying Fine Particulate Matter-Induced Cytotoxicity

Chen

et al. 2023

ACS Nanosci. Au

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Recently, the advent of health risks due to the cytotoxicity of fine particulate matter (FPM) is concerning. Numerous studies have reported abundant data elucidating the FPM-induced cell death pathways. However, several challenges and knowledge gaps are still confronted nowadays. On one hand, the undefined components of FPM (such as heavy metals, polycyclic aromatic hydrocarbons, and pathogens) are all responsible for detrimental effects, thus rendering it difficult to delineate the specific roles of these copollutants. On the other hand, owing to the crosstalk and interplay among different cell death signaling pathways, precisely determining the threats and risks posed by FPM is difficult. Herein, we recapitulate the current knowledge gaps present in the recent studies regarding FPM-induced cell death, and propose future research directions for policy-making to prevent FPM-induced diseases and improve knowledge concerning the adverse outcome pathways and public health risks of FPM.

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Polystyrene microplastics up-regulates liver glutamine and glutamate synthesis and promotes autophagy-dependent ferroptosis and apoptosis in the cerebellum through the liver-brain axis

Cited by 73 publications

References 88 publications

PS-NPs Induced Neurotoxic Effects in SHSY-5Y Cells via Autophagy Activation and Mitochondrial Dysfunction

PS-NPs Induced Neurotoxic Effects in SHSY-5Y Cells via Autophagy Activation and Mitochondrial Dysfunction

Nanoplastics and Microplastics May Be Damaging Our Livers

Cell Death Pathways: The Variable Mechanisms Underlying Fine Particulate Matter-Induced Cytotoxicity

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