Zearalenone, a mycotoxin produced by fungi of the genus Fusarium, widely exists in animal feed and human food. The structure of zearalenone is similar to estrogen, so it mainly has estrogenic effects on various organisms. Products contaminated with zearalenone can pose risks to animals and humans. Therefore, it is imperative to carry out toxicological research on zearalenone and evaluate its risk to human health. This paper briefly introduces the production, physical, and chemical properties of zearalenone and the research progress of its toxicity kinetics, focusing on its genetic toxicity, reproductive toxicity, hepatotoxicity, immunotoxicity, carcinogenicity, endocrine interference, and its impact on intestinal health. Finally, the progress of the risk assessment of human exposure is summarized to provide a reference for the follow-up study of zearalenone.
Loss-of-function mutations in the gene that encodes TYRO protein kinase-binding protein (TYROBP) cause Nasu-Hakola disease, a heritable disease resembling Alzheimer’s disease (AD). Methylation of N6 methyl-adenosine (m6A) in mRNA plays essential roles in learning and memory. Aberrant m6A methylation has been detected in AD patients and animal models. In the present study, Tyrobp–/– mice showed learning and memory deficits in the Morris water maze, which worsened with age. Tyrobp–/– mice also showed elevated levels of total tau, Ser202/Thr205-phosphorylated tau and amyloid β in the hippocampus and cerebrocortex, which worsened with aging. The m6A methyltransferase components METTL3, METTL14, and WTAP were downregulated in Tyrobp–/– mice, while expression of demethylases that remove the m6A modification (e.g., FTO and ALKBH5) were unaltered. Methylated RNA immunoprecipitation sequencing identified 498 m6A peaks that were upregulated in Tyrobp–/– mice, and 312 m6A peaks that were downregulated. Bioinformatic analysis suggested that most of these m6A peaks occur in sequences near stop codons and 3′-untranslated regions. These findings suggest an association between m6A RNA methylation and pathological TYROBP deficiency.
Background Alzheimer's disease (AD) is the leading cause of dementia, yet its underlying causes remain unknown. Increasing evidence supports a role for epigenetic modifications in AD pathogenesis. N6-methyladenosine (m6A), the most common RNA modification, is critical for learning and memory, and its abnormal presence has been observed in the brains of AD patients and animal models. Methods To compare levels of m6A in RNA as well as expression of the responsible enzymes in peripheral blood mononuclear cells (PBMCs) between AD patients and healthy controls. 42 AD patients and 42 age-matched healthy controls were prospectively enrolled from the Affiliated Hospital of Jining Medical University. m6A levels in RNA were quantified and expressions of m6A-related proteins and mRNA were examined. Genome-wide profiling of m6A-tagged transcripts was performed by m6A-modified RNA immunoprecipitation sequencing and RNA sequencing. Results Lower levels of m6A in PBMCs RNA in AD patients compared to controls, as well as downregulation of m6A methyltransferase and demethylase components. Dysregulation of m6A was associated with upregulation of m6A at 230 loci and downregulation at 163 loci, resulting in altered expression of disease-related genes. Conclusion Dysregulation of m6A in RNA may play a role in AD pathogenesis and may provide new avenues for diagnosis and treatment.
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