Li-ion batteries (LIB) are used in most portable electronics. Among a wide variety of materials, LiCoO2 (LCO) is one of the most used for the cathode of LIB. LCO particles induce oxidative stress in mouse lungs due to their Co content, and have a strong inflammatory potential. In this study, we assessed the mutagenic potential of LCO particles in lung cells in comparison to another particulate material used in LIB, LTO (Li4Ti5O12), which has a low inflammatory potential compared to LCO particles. We assessed the mutagenic potential of LCO and LTO particles in vitro by performing a cytokinesis-block micronucleus (MN) assay with rat lung epithelial cells (RLE), as well as in vivo in alveolar type II epithelial (AT-II) cells. LCO particles induced MN in vitro at non-cytotoxic concentrations and in vivo at non-inflammatory doses, indicating a primary genotoxic mechanism. LTO particles did not induce MN. Electron paramagnetic resonance and terephthalate assays showed that LCO particles produce hydroxyl radicals (•OH). Catalase inhibits this •OH production. In an alkaline comet assay with the oxidative DNA damage repair enzyme human 8-oxoguanine DNA glycosylase 1, LCO particles induced DNA strand breaks and oxidative lesions. The addition of catalase reduced the frequency of MN induced by LCO particles in vitro. We report the mutagenic activity of LCO particles used in LIB in vitro and in vivo. Our data support the role of Co(II) ions released from these particles in their primary genotoxic activity which includes the formation of •OH by a Fenton-like reaction, oxidative DNA lesions and strand breaks, thus leading to chromosomal breaks and the formation of MN. Documenting the genotoxic potential of the other LIB particles, especially those containing Co and/or Ni, is therefore needed to guarantee a safe and sustainable development of LIB.

中文翻译：

---

锂离子电池中使用的LiCoO2颗粒通过其产生羟基自由基的能力，在肺细胞中引起主要的致突变性。

锂离子电池（LIB）用于大多数便携式电子产品。在各种各样的材料中，LiCoO2（LCO）是最常用于LIB阴极的材料之一。LCO颗粒由于其Co含量而在小鼠肺中引起氧化应激，并具有很强的炎症潜能。在这项研究中，我们评估了与LIB中使用的另一种颗粒材料LTO（Li4Ti5O12）相比，LCO颗粒在肺细胞中的诱变潜力，该材料与LCO颗粒相比具有较低的炎症潜力。我们通过对大鼠肺上皮细胞（RLE）以及在肺泡II型上皮细胞（AT-II）体内进行胞质阻滞微核（MN）分析，评估了LCO和LTO颗粒在体外的诱变潜力。LCO颗粒在体外以非细胞毒性浓度诱导MN，在体内以非炎性剂量诱导MN，说明主要的遗传毒性机制。LTO颗粒不诱导MN。电子顺磁共振和对苯二甲酸酯测定表明，LCO颗粒产生羟基自由基（•OH）。过氧化氢酶抑制了•OH的产生。在使用氧化性DNA损伤修复酶的人彗星8氧鸟嘌呤DNA糖基化酶1进行的碱性彗星试验中，LCO颗粒诱导了DNA链断裂和氧化性损伤。过氧化氢酶的添加降低了体外由LCO颗粒诱导的MN的频率。我们报告了体外和体内LIB中使用的LCO颗粒的诱变活性。我们的数据支持了从这些颗粒中释放出的Co（II）离子在其主要的基因毒性活性中的作用，包括通过Fenton样反应形成•OH，氧化性DNA损伤和链断裂，从而导致染色体断裂和环糊精的形成。 MN。