Chu Stephanie, Woodfin Seth, Bayliss Emily, Smith Merritt, Fulp Alan, Mirabelli Ersilia, Moore William
Department of Biology and Chemistry, School of Health Sciences, Liberty University, Lynchburg, VA 24515, USA.
Department of Biomedical Sciences, West Virginia School of Osteopathic Medicine, Lewisburg, WV 24901, USA.
Int J Mol Sci. 2025 Sep 3;26(17):8585. doi: 10.3390/ijms26178585.
One in 36 children were identified with autism in 2020, a 22% increase from 2018 and a 98% increase from 2010. Simultaneously, attention-deficit/hyperactivity disorder (ADHD) diagnoses increased 36% from 2003 to 2016-2019. Despite this surge, their etiologies remain largely unknown. However, numerous studies document higher incidences of mitochondrial abnormalities in affected individuals. Additionally, acetaminophen has been implicated in these disorders in longitudinal studies and murine models. This paper is a compilation of literature aiming to explore a theoretical framework for acetaminophen-induced mitochondrial damage in utero. It focuses on a toxic metabolite of acetaminophen, N-acetyl-p-benzoquinone imine (NAPQ1), and its role in neuroinflammation. Based on our findings, we recommend further research studying fetal mitochondria after maternal acetaminophen usage.
2020年，每36名儿童中就有1名被确诊患有自闭症，较2018年增长了22%，较2010年增长了98%。与此同时，2003年至2016 - 2019年期间，注意力缺陷多动障碍（ADHD）的诊断率增长了36%。尽管发病率激增，但其病因仍 largely未知。然而，大量研究表明，受影响个体中线粒体异常的发生率更高。此外，在纵向研究和小鼠模型中，对乙酰氨基酚与这些疾病有关。本文是一篇文献综述，旨在探讨对乙酰氨基酚在子宫内诱导线粒体损伤的理论框架。它聚焦于对乙酰氨基酚的一种有毒代谢物，N - 乙酰 - 对苯醌亚胺（NAPQ1）及其在神经炎症中的作用。基于我们的研究结果，我们建议进一步研究母亲使用对乙酰氨基酚后胎儿的线粒体情况。
