Hormesis of methylmercury-human serum albumin conjugate on N9 microglia via ERK/MAPKs and STAT3 signaling pathways

Tan, Qiaozhu; Zhang, Ming; Geng, Lujing; Xia, Zhijun; Usman, Muhammad; Du, Yuzhi; Wei, Lixin; Bi, Haibo

doi:10.1016/j.taap.2018.10.017

Cited by 15 publications

(22 citation statements)

References 54 publications

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“…Other studies showed an increase in mRNA and protein levels of interleukin-1 beta (IL-1β) [125,138]. Additionally, mRNA and protein levels of the tumor necrosis factor (TNF) seem also to increase in microglia following a MeHg stimulus [125,134,138]. In line with these findings, Iwai-Shimada and colleagues detected an increase in TNF mRNA levels in the cerebrum and cerebellum which, despite not being confirmed, may be of microglial origin [144].…”

Section: Microgliamentioning

confidence: 87%

“…Another alteration related to MeHg-induced oxidative stress is the increased mitochondrial depolarization and the reduction of aconitase activity and cytoplasmic content in microglia [124]. Interestingly, exposure to a low concentration (2ng/mL) of MeHg for 48 h was able to induce an increase in microglial cells viability, contrarily to what is observed with higher MeHg concentrations [125].…”

Section: Microgliamentioning

confidence: 92%

“…Nonetheless, MeHg seems to induce changes in this cytokine. Other studies showed an increase in mRNA and protein levels of interleukin-1 beta (IL-1β) [125,138]. Additionally, mRNA and protein levels of the tumor necrosis factor (TNF) seem also to increase in microglia following a MeHg stimulus [125,134,138].…”

Section: Microgliamentioning

confidence: 99%

“…In vitro experiments reveal a decrease in microglial viability which is time-and concentrationdependent. Additionally, the biological model of microglia used in the experiments may determine the magnitude of the effect of MeHg in cell viability [122][123][124][125][126][127][128][129]. However, some researchers indicate the absence of microglial death and clustering surrounding apoptotic cells in aggregating brain cell cultures [130].…”

Section: Microgliamentioning

confidence: 99%

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Cellular and Molecular Mechanisms Mediating Methylmercury Neurotoxicity and Neuroinflammation

Novo

Martins

Raposo

et al. 2021

IJMS

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Methylmercury (MeHg) toxicity is a major environmental concern. In the aquatic reservoir, MeHg bioaccumulates along the food chain until it is consumed by riverine populations. There has been much interest in the neurotoxicity of MeHg due to recent environmental disasters. Studies have also addressed the implications of long-term MeHg exposure for humans. The central nervous system is particularly susceptible to the deleterious effects of MeHg, as evidenced by clinical symptoms and histopathological changes in poisoned humans. In vitro and in vivo studies have been crucial in deciphering the molecular mechanisms underlying MeHg-induced neurotoxicity. A collection of cellular and molecular alterations including cytokine release, oxidative stress, mitochondrial dysfunction, Ca2+ and glutamate dyshomeostasis, and cell death mechanisms are important consequences of brain cells exposure to MeHg. The purpose of this review is to organize an overview of the mercury cycle and MeHg poisoning events and to summarize data from cellular, animal, and human studies focusing on MeHg effects in neurons and glial cells. This review proposes an up-to-date compendium that will serve as a starting point for further studies and a consultation reference of published studies.

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Section: Microgliamentioning

confidence: 87%

Section: Microgliamentioning

confidence: 92%

Section: Microgliamentioning

confidence: 99%

Section: Microgliamentioning

confidence: 99%

See 2 more Smart Citations

Cellular and Molecular Mechanisms Mediating Methylmercury Neurotoxicity and Neuroinflammation

Novo

Martins

Raposo

et al. 2021

IJMS

View full text Add to dashboard Cite

show abstract

“…Here relevant human cell types have to be exposed from very low (10 −21 M) to high (10 −6 M) concentrations of MeHg + . For instance, non-differentiated or differentiated neurons or glial cells have to be incubated with MeHg + and physiologically relevant MeHg-S conjugates (cysteine, GSH, albumin or hemoglobin, as an example see Tan et al, 2019) for different periods. MeHg + toxicity will have to be determined by proteomics, specifically by the -SHand -SeH-omics, epigenomics, metabolomics, and transcriptomics.…”

mentioning

confidence: 99%

Transcriptomic and Proteomic Tools in the Study of Hg Toxicity: What Is Missing?

et al. 2020

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Unbalanced ER‐mitochondrial calcium homeostasis promotes mitochondrial dysfunction and associated apoptotic pathways activation in methylmercury exposed rat cortical neurons

Pan

Wei

et al. 2022

J Biochem & Molecular Tox

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Methylmercury (MeHg) is a cumulative environmental pollutant that can easily cross the blood–brain barrier and cause damage to the brain, mainly targeting the central nervous system. The purpose of this study is to investigate the role of calcium ion (Ca2+) homeostasis between the endoplasmic reticulum (ER) and mitochondria in MeHg‐induced neurotoxicity. Rat primary cortical neurons exposed to MeHg (0.25–1 μm) underwent dose‐dependent cell damage, accompanied by increased Ca2+ release from the ER and elevated levels of free Ca2+ in cytoplasm and mitochondria. MeHg also increased the protein and messenger RNA expressions of the inositol 1,4,5‐triphosphate receptor, ryanodine receptor 2, and mitochondrial calcium uniporter. Ca2+ channel inhibitors 2‐aminoethyl diphenylborinate and procaine reduced the release of Ca2+ from ER, while RR and 4,4′‐diisothiocyanatostilbene‐2,2′‐disulfonate inhibited Ca2+ uptake from mitochondria. In addition, pretreatment with Ca2+ chelator BAPTA‐AM effectively restored mitochondrial membrane potential levels, inhibited over opening of mitochondrial permeability transition pore, and maintained mitochondrial function stability. Meanwhile, the expression of mitochondrial apoptosis‐related proteins recovered to some extent, along with the reduction of the early apoptosis ratio. These results suggest that Ca2+ homeostasis plays an essential role in mitochondrial damage and apoptosis induced by MeHg, which may be one of the important mechanisms of MeHg‐induced neurotoxicity.

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Hormesis of methylmercury-human serum albumin conjugate on N9 microglia via ERK/MAPKs and STAT3 signaling pathways

Cited by 15 publications

References 54 publications

Cellular and Molecular Mechanisms Mediating Methylmercury Neurotoxicity and Neuroinflammation

Cellular and Molecular Mechanisms Mediating Methylmercury Neurotoxicity and Neuroinflammation

Transcriptomic and Proteomic Tools in the Study of Hg Toxicity: What Is Missing?

Unbalanced ER‐mitochondrial calcium homeostasis promotes mitochondrial dysfunction and associated apoptotic pathways activation in methylmercury exposed rat cortical neurons

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