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通过计算和实验方法揭示一系列羧酸在肝细胞中的毒性机制。

Uncovering the toxicity mechanisms of a series of carboxylic acids in liver cells through computational and experimental approaches.

机构信息

ProtoQSAR SL., Centro Europeo de Empresas e Innovación (CEEI), Parque Tecnológico de Valencia, Av. Benjamín Franklin, 12, Valencia, Paterna 46980, Spain.

Unidad de Hepatología Experimental, Instituto de Investigación Sanitaria La Fe (IIS La Fe), Av Fernando Abril Martorell 106, Valencia 46026, Spain.

出版信息

Toxicology. 2024 May;504:153764. doi: 10.1016/j.tox.2024.153764. Epub 2024 Feb 28.

Abstract

Hepatotoxicity poses a significant concern in drug design due to the potential liver damage that can be caused by new drugs. Among common manifestations of hepatotoxic damage is lipid accumulation in hepatic tissue, resulting in liver steatosis or phospholipidosis. Carboxylic derivatives are prone to interfere with fatty acid metabolism and cause lipid accumulation in hepatocytes. This study investigates the toxic behaviour of 24 structurally related carboxylic acids in hepatocytes, specifically their ability to cause accumulation of fatty acids and phospholipids. Using high-content screening (HCS) assays, we identified two distinct lipid accumulation patterns. Subsequently, we developed structure-activity relationship (SAR) and quantitative structure-activity relationship (QSAR) models to determine relevant molecular substructures and descriptors contributing to these adverse effects. Additionally, we calculated physicochemical properties associated with lipid accumulation in hepatocytes and examined their correlation with our chemical structure characteristics. To assess the applicability of our findings to a wide range of chemical compounds, we employed two external datasets to evaluate the distribution of our QSAR descriptors. Our study highlights the significance of subtle molecular structural variations in triggering hepatotoxicity, such as the presence of nitrogen or the specific arrangement of substitutions within the carbon chain. By employing our comprehensive approach, we pinpointed specific molecules and elucidated their mechanisms of toxicity, thus offering valuable insights to guide future toxicology investigations.

摘要

肝毒性是药物设计中的一个重大关注点,因为新药可能会导致潜在的肝损伤。肝毒性损伤的常见表现之一是肝组织中的脂质积累,导致肝脂肪变性或磷脂沉积症。羧酸衍生物容易干扰脂肪酸代谢,导致肝细胞内脂质积累。本研究调查了 24 种结构相关羧酸在肝细胞中的毒性行为,特别是它们引起脂肪酸和磷脂积累的能力。我们使用高内涵筛选(HCS)测定法,确定了两种不同的脂质积累模式。随后,我们开发了构效关系(SAR)和定量构效关系(QSAR)模型,以确定导致这些不良反应的相关分子亚结构和描述符。此外,我们计算了与肝细胞内脂质积累相关的物理化学性质,并研究了它们与我们化学结构特征的相关性。为了评估我们的研究结果在广泛的化学化合物中的适用性,我们使用了两个外部数据集来评估我们的 QSAR 描述符的分布。我们的研究强调了触发肝毒性的微小分子结构变化的重要性,例如氮的存在或碳链内取代基的特定排列。通过采用我们全面的方法,我们确定了特定的分子,并阐明了它们的毒性机制,从而为指导未来的毒理学研究提供了有价值的见解。

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