ArticleEnvironmental toxicology and pharmacology2022
Hematological effects of glyphosate in mice revealed by traditional toxicology and transcriptome sequencing.
Article in Environmental toxicology and pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 10 citations in OpenAlex.
- Modulation of P2X7-driven purinergic signaling and NLRP3 inflammasome activation underlies the hepatoprotective effects of coenzyme Q10 against glyphosate-based herbicide exposure.Purinergic signalling · 2026Article
- Coenzyme Q10 protects against glyphosate-based herbicide-induced testicular and sperm toxicity by modulating Nrf2/Keap1/HO-1 and TLR4/NF-κB pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Glyphosate exposure exacerbates neuroinflammation and Alzheimer's disease-like pathology despite a 6-month recovery period in mice.Journal of neuroinflammation · 2024Article
- Clarification of the molecular mechanisms underlying glyphosate-induced major depressive disorder: a network toxicology approach.Annals of general psychiatry · 2024Article
- Effects of glyphosate exposure on the miRNA expression profile and construction of the miRNA-mRNA regulatory network in mouse bone marrow cells.Functional & integrative genomics · 2022Article
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11 authors at 1 institution in 1 country.
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Abstract
The herbicide glyphosate is being used worldwide. Hematological toxicity caused by glyphosate exposure has been reported, but the underlying mechanisms remain unclear. In this study, classical toxicology methods and RNA sequencing were performed to explore the molecular mechanisms related to glyphosate hematotoxicity. We found that 500 mg/kg b.w. glyphosate-based herbicide (GBH) significantly decreased leukocyte, neutrophil, lymphocyte and monocyte counts, as well as inhibited colony-forming abilities of CFU-GM, CFU-G and CFU-GEMM. RNA sequencing identified 82 and 48 differentially expressed genes (DEGs) in BM cells after treatment with 250 mg/kg and 500 mg/kg GBH, respectively. Meanwhile, GO and KEGG analyses revealed that the MAPK signaling pathway, hematopoietic cell lineage and cytokine-cytokine receptor interactions were vital pathways involved in GBH-induced toxicity in BM cells. Notably, Nr4a, Fos, Thbs1 and tnfrsf19 contributed to the hematotoxicity of GBH by regulating hematopoietic stem cell functions. In summary, our efforts enhance the understanding of the glyphosate hematotoxic responses and facilitate future studies on its corresponding mechanisms.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.