Kupffer Cells Degrade 14C-Labeled Few-Layer Graphene to 14CO2 in Liver through Erythrophagocytosis
Kupffer Cells Degrade 14C-Labeled Few-Layer Graphene to 14CO2 in Liver through Erythrophagocytosis
复制标题
库普弗细胞在肝脏中通过噬红细胞作用将 14C 标记的少层石墨烯降解为 14CO2
DOI：
10.1021/acsnano.0c07452
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发表时间：
2021-01-26
期刊：
影响因子：
17.1
通讯作者：
Mao, Liang
中科院分区：
文献类型：
--
作者：
Lu, Kun;Dong, Shipeng;Mao, Liang
石墨烯材料作为药物递送系统在器官和亚器官水平的长期分布和清除仍不清楚。在这里，我们比较了C-14标记的具有不同横向尺寸的少层石墨烯在小鼠中静脉注射长达1年后的命运，并证明了少层石墨烯主要在肝脏中积累，较大的石墨烯可以通过枯否细胞降解为（CO2）-C-14。该机制涉及肝细胞对石墨烯的摄取、较大的石墨烯诱导的红细胞膜扰动以及库普弗细胞增强的红细胞吞噬作用，导致血红蛋白降解为血红素和细胞中铁浓度升高。增加的铁引发了芬顿反应以产生羟基自由基，促进较大的石墨烯降解为（CO2）-C-14。我们的研究结果提出了一种石墨烯转化的机制，这对我们了解石墨烯在体内的肝脏命运有很大贡献。
The distribution and clearance of graphene materials as drug delivery systems at organ and suborgan levels over the long term remain unclear. Here we compared the fate of C-14-labeled few-layer graphene with different lateral sizes in mice after one intravenous injection for up to 1 year and demonstrated that few-layer graphene mainly accumulated in the liver, and larger graphene can be degraded into (CO2)-C-14 by Kupffer cells. The mechanism involves the uptake of graphene by liver cells, larger graphene-induced membrane perturbation of red blood cells, and enhanced erythrophagocytosis by the Kupffer cells, resulting in the degradation of hemoglobin into hemes and a rise in iron concentrations in cells. The increased iron triggered a Fenton reaction to generate the hydroxyl radical, facilitating the degradation of larger graphene into (CO2)-C-14. Our findings propose a mechanism for the transformation of graphene that significantly contributes to our understanding of the hepatic fate of graphene in vivo.