ArticleEnvironmental health perspectives2021
Assessing the Association of Mitochondrial Function and Inflammasome Activation in Murine Macrophages Exposed to Select Mitotoxic Tri-Organotin Compounds.
Article in Environmental health perspectives, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Tributyltin Alters Hepatic Immune Microenvironment to ProMote Liver Fibrosis Progression in Rats.Toxics · 2026Article
- Innovative Insights into Interleukin-Mediated Macrophage Polarization: Metabolic Reprogramming and Inflammatory Pathway Crosstalk in Chronic Kidney Disease and Therapeutic Implications-A Narrative Review.International journal of general medicine · 2026Review
- Modified mRNA-Based Therapeutic Strategies for Myocardial Ischemia-Reperfusion Injury.International journal of molecular sciences · 2025Review
- Environmental Health and Toxicology: Immunomodulation Promoted by Endocrine-Disrupting Chemical Tributyltin.Toxics · 2023Review
- Article
- Role of mitochondrial stress and the NLRP3 inflammasome in lung diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- Imaging Inflammasome Activation in Microglia.Current protocols · 2022Article
- Reframing the Question: Does Mitochondrial Damage Set the Stage for Future Inflammation?Environmental health perspectives · 2021Article
- Microglia in Neurodegenerative Events-An Initiator or a Significant Other?International journal of molecular sciences · 2021Review
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundMitochondrial function is implicated as a target of environmental toxicants and found in disease or injury models, contributing to acute and chronic inflammation. One mechanism by which mitochondrial damage can propagate inflammation is via activation of the nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) family, pyrin domain-containing receptor (NLRP)3 inflammasome, a protein complex that processes mature interleukin
objectiveThe objective was to evaluate whether mitochondrial toxicants recruit inflammasome activation and
methodMurine macrophages (RAW 264.7) exposed to tri-organotins (triethyltin bromide (TETBr), trimethyltin hydroxide (TMTOH), triphenyltin hydroxide (TPTOH), bis(tributyltin)oxide) [Bis(TBT)Ox] were examined for pro-inflammatory cytokine induction. TMTOH and TETBr were examined in RAW 264.7 and bone marrow-derived macrophages for mitochondrial bioenergetics, reactive oxygen species (ROS) production, and inflammasome activation via visualization of aggregate formation, caspase-1 flow cytometry,
resultsTETBr and TMTOH induced inflammasome aggregate formation and
conclusionSelect mitotoxic tri-organotins disrupted murine macrophage transcriptional response to LPS, yet triggered inflammasome activation. The differential response pattern suggested unique functional changes in the inflammatory response that may translate to suppressed host defense or prolong inflammation. We posit a framework to examine immune cell effects of environmental mitotoxic compounds for adverse health outcomes. https://doi.org/10.1289/EHP8314.
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