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锂离子电池中使用的 LiCoO 颗粒通过其产生羟基自由基的能力诱导肺细胞产生原发性致突变性。

LiCoO particles used in Li-ion batteries induce primary mutagenicity in lung cells via their capacity to generate hydroxyl radicals.

机构信息

Louvain centre for Toxicology and Applied Pharmacology, Institut de Recherche Expérimentale et Clinique, Université catholique de Louvain, Avenue Hippocrate 57, box B1.57.06, 1200, Brussels, Belgium.

Laboratory of Toxicology, Unit of Environment and Health, Department of Public Health and Primary Care, Katholieke Universiteit Leuven, Herestraat 49 - O&N1 - Room: 07.702, box 706, 3000, Leuven, Belgium.

出版信息

Part Fibre Toxicol. 2020 Jan 29;17(1):6. doi: 10.1186/s12989-020-0338-9.

DOI:10.1186/s12989-020-0338-9
PMID:31996255
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6990559/
Abstract

BACKGROUND

Li-ion batteries (LIB) are used in most portable electronics. Among a wide variety of materials, LiCoO (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 (LiTiO), which has a low inflammatory potential compared to LCO particles.

RESULTS

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.

CONCLUSIONS

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.

摘要

背景

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,LiCoO(LCO)是 LIB 阴极最常用的材料之一。由于其 Co 含量,LCO 颗粒会在小鼠肺部引起氧化应激,并且具有很强的炎症潜力。在这项研究中,我们评估了 LCO 颗粒在肺细胞中的致突变潜力,与另一种用于 LIB 的颗粒材料 LTO(LiTiO)进行了比较,LTO 颗粒与 LCO 颗粒相比具有较低的炎症潜力。

结果

我们通过使用大鼠肺上皮细胞(RLE)进行细胞有丝分裂阻断微核(MN)测定,以及在肺泡 II 型上皮(AT-II)细胞中进行体内试验,评估了 LCO 和 LTO 颗粒的致突变潜力。LCO 颗粒在非细胞毒性浓度下在体外和非炎症剂量下在体内诱导 MN,表明存在原发性遗传毒性机制。LTO 颗粒不会诱导 MN。电子顺磁共振和对苯二甲酸酯测定表明,LCO 颗粒会产生羟基自由基(•OH)。过氧化氢酶抑制这种•OH 的产生。在碱性彗星试验中,使用氧化 DNA 损伤修复酶人 8-氧鸟嘌呤 DNA 糖基化酶 1,LCO 颗粒诱导 DNA 链断裂和氧化损伤。添加过氧化氢酶可减少 LCO 颗粒在体外诱导的 MN 频率。

结论

我们报告了 LIB 中使用的 LCO 颗粒在体外和体内的致突变活性。我们的数据支持这些颗粒释放的 Co(II)离子在其原发性遗传毒性活性中的作用,包括通过类 Fenton 反应形成•OH、氧化 DNA 损伤和链断裂,从而导致染色体断裂和 MN 的形成。因此,需要记录其他 LIB 颗粒的遗传毒性潜力,特别是那些含有 Co 和/或 Ni 的颗粒,以保证 LIB 的安全和可持续发展。

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