硫代乙酰胺处理的肝细胞中由氨、谷氨酰胺和丙氨酸生成尿素的数据以及线粒体水通道蛋白8的表达。

Data of ureagenesis from ammonia, glutamine and alanine, and mitochondrial aquaporin-8 expression in thioacetamide-treated hepatocytes.

作者信息

Capiglioni Alejo M, Alvarez María de Luján, Marinelli Raúl A

机构信息

Instituto de Fisiología Experimental, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Facultad de Ciencias Bioquímicas y Farmacéuticas, Universidad Nacional de Rosario, Rosario, Argentina. Suipacha 570, 2000 Rosario, Santa Fe, Argentina.

出版信息

Data Brief. 2020 Apr 30;30:105632. doi: 10.1016/j.dib.2020.105632. eCollection 2020 Jun.

DOI:10.1016/j.dib.2020.105632

PMID:32395591

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7210421/

Abstract

We present data about the synthesis of urea from different substrates, i.e., free ammonia, glutamine and alanine in primary cultured rat hepatocytes treated or untreated with the model hepatotoxic agent thioacetamide (TAA). We also provide data about the expression of mitochondrial aquaporin-8 (mtAQP8), a hepatocyte channel protein which facilitates ammonia diffusion into mitochondria to supply the urea cycle. Ammonia-derived ureagenesis was significantly inhibited by about 30% while that from the both amino acids resulted unaffected in TAA-treated hepatocytes. Protein expression of mtAQP8 was decreased by about 80% after TAA treatment. These data can be useful for the understanding of the mechanisms of drug-induced hepatic dysfunction.

摘要

我们展示了在经或未经模型肝毒性剂硫代乙酰胺（TAA）处理的原代培养大鼠肝细胞中，由不同底物（即游离氨、谷氨酰胺和丙氨酸）合成尿素的数据。我们还提供了线粒体水通道蛋白8（mtAQP8）的表达数据，mtAQP8是一种肝细胞通道蛋白，可促进氨扩散到线粒体中以供应尿素循环。在TAA处理的肝细胞中，氨衍生的尿素生成显著受抑制约30%，而来自这两种氨基酸的尿素生成未受影响。TAA处理后，mtAQP8的蛋白表达下降了约80%。这些数据有助于理解药物性肝损伤的机制。