ArticleArchives of toxicology2025
miR-451a and miR-486-5p: biomarkers for benzene-induced hematotoxicity.
Article in Archives of toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Advances in biomarkers of benzene exposure and toxicity: From mechanistic insights to occupational health applications (Review).Molecular medicine reports · 2026Review
- Transcriptomics and proteomics reveals the potential mechanisms of hydroquinone-inhibited erythroid differentiation in K562 cells.Toxicology research · 2025Article
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Authors and funding
13 authors.
Funding
Abstract
The hematopoietic system is the primary target of benzene exposure. Whether peripheral blood miRNA can serve as sensitive biomarkers for benzene-induced hematopoietic damage has attracted considerable attention. This study focuses on exploring the role of miR-451a and miR-486-5p in benzene-induced erythroid damage and assessing their potential as biomarkers of benzene-induced hematotoxicity. Animal experiments and human studies were conducted to reveal expression patterns of miR-451a and miR-486-5p in bone marrow and peripheral blood after benzene exposure, along with their correlations with erythrocyte indices. In C57BL/6J mice exposed to benzene, the expression levels of miR-451a and miR-486-5p in bone marrow decreased, which also positively correlated with red blood cell count (RBC), hemoglobin (Hb), and hematocrit (HCT). Conversely, in peripheral blood of C57BL/6J mice, the expression levels of the two miRNAs increased and showed a negative correlation with the three erythroid indices. Subsequent validation in bone marrow samples of chronic benzene poisoning patients and peripheral blood of workers from petrochemical plant confirmed significant correlations between miR-451a and miR-486-5p expression levels and red blood cell parameters. Furthermore, receiver operator characteristic (ROC) curve analyses revealed that miR-451a emerged as a potential biomarker for benzene-induced hematotoxicity, exhibiting superior discriminatory power compared to miR-486-5p and conventional erythroid indices. Additionally, in vitro experiments using K562 cells revealed differential regulatory effects of benzene metabolite hydroquinone (HQ) on miR-451a expression based on erythroid differentiation status. These findings emphasized the important role of miR-451a and miR-486-5p in benzene-induced erythrogenesis disruption, offering valuable insights for biomarker development and therapeutic interventions.
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