线粒体呼吸对缺铁性贫血的反应：外周血单个核细胞和肝脏的比较

Mitochondrial respiration in response to iron deficiency anemia. Comparison of peripheral blood mononuclear cells and liver.

Keywords: anemia, iron deficiency, peripheral blood mononuclear cells, liver, mitochondrial function, OXPHOS, mitochondrial respiration, surrogate 

关键词：贫血，缺铁，外周血单个核细胞，肝脏，线粒体功能，OXPHOS，线粒体呼吸，替代物
作者：Fischer Christine, Valente de Souza Lara, Komlódi Timea, Garcia-Souza Luiz F, Volani Chiara, Tymoszuk Piotr, Demetz Egon, Seifert Markus, Auer Kristina, Hilbe Richard, Brigo Natascha, Petzer Verena, Asshoff Malte, Gnaiger Erich, Weiss Guenter 
出版期刊：《Metabolites》 2022/3/21

Abstract：

Iron is an essential component for metabolic processes, including oxygen transport within hemoglobin, tricarboxylic acid (TCA) cycle activity, and mitochondrial energy transformation. Iron deficiency can thus lead to metabolic dysfunction and eventually result in iron deficiency anemia (IDA), which affects approximately 1.5 billion people worldwide.Using a rat model of IDA induced by phlebotomy, we studied the effects of IDA on mitochondrial respiration in peripheral blood mononuclear cells (PBMCs) and the liver. Furthermore, we evaluated whether the mitochondrial function evaluated by high-resolution respirometry in PBMCs reflects corresponding alterations in the liver. Surprisingly, mitochondrial respiratory capacity was increased in PBMCs from rats with IDA compared to the controls. In contrast,mitochondrial respiration remained unaffected in livers from IDA rats. Of note, citrate synthase activity indicated an increased mitochondrial density in PBMCs, whereas it remained unchanged in the liver, partly explaining the different responses of mitochondrial respiration in PBMCs and the liver. Taken together, these results indicate that mitochondrial function determined in PBMCs cannot serve as a valid surrogate for respiration in the liver. Metabolic adaptions to iron deficiency resulted in different metabolic reprogramming in the blood cells and liver tissue.

文章摘要：

铁是代谢过程的重要组成部分，包括血红蛋白内的氧转运、三羧酸 (TCA) 循环活动和线粒体能量转换。因此，缺铁会导致代谢功能障碍，并最终导致缺铁性贫血 (IDA)，影响全球约 15 亿人。 使用放血诱导的 IDA 大鼠模型，我们研究了 IDA 对外周血单个核细胞 (PBMC) 和肝脏线粒体呼吸的影响。此外，我们评估了通过高分辨率呼吸测量法评估的 PBMC 中的线粒体功能是否反映了肝脏的相应改变。令人惊讶的是，与对照组相比，IDA 大鼠的 PBMC 中线粒体呼吸能力增加。相比之下，IDA 大鼠的肝脏中的线粒体呼吸仍然不受影响。值得注意的是，柠檬酸合酶活性表明 PBMCs 中线粒体密度增加，而在肝脏中保持不变，部分解释了 PBMCs 和肝脏中线粒体呼吸的不同反应。总之，这些结果表明在 PBMC 中确定的线粒体功能不能作为肝脏呼吸的有效替代物。对缺铁的代谢适应导致血细胞和肝组织中不同的代谢重编程。

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