Venediktova Natalya, Khmil Natalya, Pavlik Lyubov, Mikheeva Irina, Mironova Galina
Institute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Pushchino, Russia.
Cell Biochem Biophys. 2025 Jul 22. doi: 10.1007/s12013-025-01838-8.
The aim of the study was to examine how the administration of uridine influences the mitochondrial function in hepatocytes in a rat model of hyperthyroidism (HT) induced by thyroxine treatment. Excess thyroid hormones (TH) increased the mitochondrial oxygen consumption, enhanced biogenesis, and altered the expression of proteins regulating the mitochondrial fusion and fission. Hyperthyroid rats had a mixed population of mitochondria, including swollen and damaged organelles. Although uridine did not affect the level of serum TH, it restored the normal body weight. The administration of uridine used for therapeutic purposes improved the main parameters of respiration and oxidative phosphorylation, prevented destructive changes in the morphology of liver mitochondria, and influenced the biogenesis and dynamics of these organelles. Overall, the results obtained indicate that uridine has a protective effect against functional and some structural destructions in rat liver mitochondria induced by HT.
本研究的目的是探讨在甲状腺素诱导的甲状腺功能亢进（HT）大鼠模型中，尿苷的给药如何影响肝细胞中的线粒体功能。过量的甲状腺激素（TH）增加了线粒体的氧消耗，增强了生物合成，并改变了调节线粒体融合和裂变的蛋白质表达。甲状腺功能亢进的大鼠有混合的线粒体群体，包括肿胀和受损的细胞器。虽然尿苷不影响血清TH水平，但它恢复了正常体重。用于治疗目的的尿苷给药改善了呼吸和氧化磷酸化的主要参数，防止了肝线粒体形态的破坏性变化，并影响了这些细胞器的生物合成和动态变化。总体而言，所得结果表明尿苷对HT诱导的大鼠肝线粒体的功能和一些结构破坏具有保护作用。
