Introduction: Cyanide is a well-known toxin that disrupts aerobic cellular function by binding to ferric ions in mitochondrial cytochrome oxidase a3. This interaction inhibits ATP production, disrupts oxidative phosphorylation, and leads to cellular hypoxia, ultimately impairing cell function. In response to hypoxic or asphyxic conditions, cells rapidly activate hypoxia-inducible factors (HIFs). Previous studies have identified around 50 microRNAs linked to HIF activation, collectively known as “hypoxamiRs”. This study aims to investigate the relationship between cyanide poisoning and hypoxamiR responses by focusing on two specific hypoxamiRs, miR-200b and miR-429, which have been identified as HIF activators during acute hypoxic states. Methods: Postmortem blood samples were collected from five cyanide poisoning cases and five non-asphyxia control cases. Total RNA (10 ng) was used to synthesize complementary DNA (cDNA) via the MultiScribe™ Reverse Transcriptase. The expression levels of miR-200b and miR-429 were quantified using the TaqMan™ MicroRNA Assay and measured on the QuantStudio™ 5 Real-Time PCR System. The data was analyzed by using the comparative C(T) method. Results: The results indicated an increase in miRNA-429 expression in 4 out of 5 cyanide poisoning cases. In contrast, miR 200b exhibited a decreasing trend, suggesting potential downregulation. Conclusion: Overall, hypoxamiRs, particularly miRNA-429 and miR-200b, could provide valuable insights into the prognosis of cyanide poisoning, highlighting the need for further research to validate their roles as potential biomarkers.
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Pagparpat Varrathyarom
Nattachai Thangsiriskul
Wikanda Worrapitirungsi
Prehospital and Disaster Medicine
Chulalongkorn University
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Varrathyarom et al. (Sun,) studied this question.
www.synapsesocial.com/papers/69c37adcb34aaaeb1a67cc7d — DOI: https://doi.org/10.1017/s1049023x26108218