Saxena Manoj, Loza-Rosas Sergio A, Gaur Kavita, Sharma Shweta, Pérez Otero Sofia C, Tinoco Arthur D
Department of Chemistry, University of Puerto Rico Río Piedras, San Juan, PR 00931.
Department of Environmental Sciences, University of Puerto Rico Río Piedras, San Juan, PR 00931.
Coord Chem Rev. 2018 May 15;363:109-125. doi: 10.1016/j.ccr.2018.03.006. Epub 2018 Mar 20.
Despite its natural abundance and widespread use as food, paint additive, and in bone implants, no specific biological function of titanium is known in the human body. High concentrations of Ti(IV) could result in cellular toxicity, however, the absence of Ti toxicity in the blood of patients with titanium bone implants indicates the presence of one or more biological mechanisms to mitigate toxicity. Similar to Fe(III), Ti(IV) in blood binds to the iron transport protein serum transferrin (sTf), which gives credence to the possibility of its cellular uptake mechanism by transferrin-directed endocytosis. However, once inside the cell, how sTf bound Ti(IV) is released into the cytoplasm, utilized, or stored remain largely unknown. To explain the molecular mechanisms involved in Ti use in cells we have drawn parallels with those for Fe(III). Based on its chemical similarities with Fe(III), we compare the biological coordination chemistry of Fe(III) and Ti(IV) and hypothesize that Ti(IV) can bind to similar intracellular biomolecules. The comparable ligand affinity profiles suggest that at high Ti(IV) concentrations, Ti(IV) could compete with Fe(III) to bind to biomolecules and would inhibit Fe bioavailability. At the typical Ti concentrations in the body, Ti might exist as a labile pool of Ti(IV) in cells, similar to Fe. Ti could exhibit different types of properties that would determine its cellular functions. We predict some of these functions to mimic those of Fe in the cell and others to be specific to Ti. Bone and cellular speciation and localization studies hint toward various intracellular targets of Ti like phosphoproteins, DNA, ribonucleotide reductase, and ferritin. However, to decipher the exact mechanisms of how Ti might mediate these roles, development of innovative and more sensitive methods are required to track this difficult to trace metal in vivo.
尽管钛在自然界中储量丰富,且广泛用作食品、涂料添加剂以及骨植入物,但人们对其在人体中的具体生物学功能仍一无所知。高浓度的Ti(IV)可能导致细胞毒性,然而,植入钛骨的患者血液中不存在钛毒性,这表明存在一种或多种减轻毒性的生物学机制。与Fe(III)类似,血液中的Ti(IV)与铁转运蛋白血清转铁蛋白(sTf)结合,这使得通过转铁蛋白介导的内吞作用进行细胞摄取的可能性变得可信。然而,一旦进入细胞,与sTf结合的Ti(IV)如何释放到细胞质中、被利用或储存,在很大程度上仍然未知。为了解释细胞中钛利用所涉及的分子机制,我们将其与Fe(III)的机制进行了类比。基于其与Fe(III)的化学相似性,我们比较了Fe(III)和Ti(IV)的生物配位化学,并假设Ti(IV)可以与类似的细胞内生物分子结合。可比的配体亲和力谱表明,在高Ti(IV)浓度下,Ti(IV)可能与Fe(III)竞争结合生物分子,并抑制铁的生物利用度。在人体典型的钛浓度下,钛可能以类似于铁的不稳定Ti(IV)池的形式存在于细胞中。钛可能表现出不同类型的特性,这些特性将决定其细胞功能。我们预测其中一些功能会模仿细胞中铁的功能,而其他功能则是钛特有的。骨骼和细胞形态及定位研究表明钛在细胞内有各种靶点,如磷蛋白、DNA、核糖核苷酸还原酶和铁蛋白。然而,要破译钛如何介导这些作用的确切机制,需要开发创新且更灵敏的方法来在体内追踪这种难以追踪的金属。