Iron overload, notably caused by hereditary hemochromatosis, is an excess storage of iron in various organs that causes tissue damage and may promote tumorigenesis. To manage that disorder, free iron depletion can be induced by iron chelators like deferoxamine that are of increasing interest also in the cancer field since iron stock could be a potent target for managing tumorigenesis. Curcumin, a well-known active substance extracted from the turmeric rhizome, destabilizes endoplasmic reticulum, and secondarily lysosomes, thereby increasing mitophagy/autophagy and subsequent apoptosis. Recent findings show that cells treated with curcumin also exhibit a decrease in ferritin, which is consistent with its chemical structure and iron chelating activity. Here we investigated how curcumin influences the intracellular effects of iron overload via Fe-nitriloacetic acid or ferric ammonium citrate loading in Huh-7 cells and explored the consequences in terms of antioxidant activity, autophagy, and apoptotic signal transduction. In experiments with T51B and RL-34 epithelial cells, we have found evidence that curcumin-iron complexation abolishes both curcumin-induced autophagy and apoptosis, together with the tumorigenic action of iron overload.

中文翻译：

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姜黄素与铁的螯合抑制了姜黄素诱导的自噬和细胞死亡以及铁超负荷赘生物转化。

铁超载，主要是由遗传性血色素沉着症引起的，是铁在各个器官中的过量储存，会导致组织损伤并可能促进肿瘤发生。为了控制该疾病，可以通过铁螯合剂如去铁胺来诱导自由铁耗竭，铁螯合剂在癌症领域也越来越引起人们的关注，因为铁储备可能是管理肿瘤发生的有效靶标。姜黄素是一种从姜黄根茎中提取的众所周知的活性物质，它会破坏内质网和其次是溶酶体的稳定性，从而增加线粒体/自噬和随后的细胞凋亡。最近的发现表明，用姜黄素处理的细胞也表现出铁蛋白的减少，这与其化学结构和铁螯合活性是一致的。在这里，我们研究了姜黄素如何通过Fe-亚硝酸乙酸或柠檬酸铁铵加载到Huh-7细胞中来影响铁超负荷的细胞内效应，并探讨了抗氧化剂活性，自噬和凋亡信号转导的后果。在T51B和RL-34上皮细胞的实验中，我们发现了姜黄素-铁复合物消除了姜黄素诱导的自噬和细胞凋亡以及铁超负荷的致瘤作用的证据。