N-Acetyl-L-cysteine attenuates titanium dioxide nanoparticle (TiO2 NP)-induced autophagy in male germ cells

IF 4.2 3区环境科学与生态学 Q2 ENVIRONMENTAL SCIENCES

Environmental toxicology and pharmacology Pub Date : 2024-05-16 DOI:10.1016/j.etap.2024.104466

Beom-Jin Shin , Bang-Jin Kim , Eun-Ji Paeng , Jack Tyler Rifkin , Sung-Hwan Moon , Seung Hee Shin , Buom-Yong Ryu

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引用次数: 0

Abstract

Titanium dioxide nanoparticles (TiO₂ NPs) are widely used in consumer products, raising concerns about their impact on human health. This study investigates the effects of TiO₂ NPs on male germ cells while focusing on cell proliferation inhibition and underlying mechanisms. This was done by utilizing mouse GC-1 spermatogonia cells, an immortalized spermatogonia cell line. TiO₂ NPs induced a concentration-dependent proliferation inhibition with increased reactive oxygen species (ROS) generation. Notably, TiO₂ NPs induced autophagy and decreased ERK phosphorylation. Treatment with the ROS inhibitor N-Acetyl-l-cysteine (NAC) alleviated TiO₂ NPs-induced autophagy, restored ERK phosphorylation, and promoted cell proliferation. These findings call attention to the reproductive risks posed by TiO₂ NPs while also highlighting NAC as a possible protective agent against reproductive toxins.

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N-乙酰-L-半胱氨酸可减轻二氧化钛纳米粒子（TiO2 NP）诱导的雄性生殖细胞自噬作用

二氧化钛纳米粒子（TiO2 NPs）被广泛应用于消费品中，引起了人们对其对人体健康影响的关注。本研究调查了二氧化钛纳米粒子对男性生殖细胞的影响，重点是细胞增殖抑制和潜在机制。研究利用了小鼠GC-1精原细胞（一种永生的精原细胞系）。TiO2 NPs诱导了浓度依赖性增殖抑制，同时增加了活性氧（ROS）的生成。值得注意的是，TiO2氧化物诱导自噬并降低ERK磷酸化。用ROS抑制剂N-乙酰-L-半胱氨酸处理可缓解TiO2 NPs诱导的自噬，恢复ERK磷酸化，促进细胞增殖。这些发现引起了人们对TiO2 NPs所带来的生殖风险的关注，同时也突出了NAC作为一种可能的生殖毒素保护剂的作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Environmental toxicology and pharmacology 医学-毒理学

CiteScore

7.00

自引率

4.70%

发文量

185

审稿时长

34 days

期刊介绍： Environmental Toxicology and Pharmacology publishes the results of studies concerning toxic and pharmacological effects of (human and veterinary) drugs and of environmental contaminants in animals and man. Areas of special interest are: molecular mechanisms of toxicity, biotransformation and toxicokinetics (including toxicokinetic modelling), molecular, biochemical and physiological mechanisms explaining differences in sensitivity between species and individuals, the characterisation of pathophysiological models and mechanisms involved in the development of effects and the identification of biological markers that can be used to study exposure and effects in man and animals. In addition to full length papers, short communications, full-length reviews and mini-reviews, Environmental Toxicology and Pharmacology will publish in depth assessments of special problem areas. The latter publications may exceed the length of a full length paper three to fourfold. A basic requirement is that the assessments are made under the auspices of international groups of leading experts in the fields concerned. The information examined may either consist of data that were already published, or of new data that were obtained within the framework of collaborative research programmes. Provision is also made for the acceptance of minireviews on (classes of) compounds, toxicities or mechanisms, debating recent advances in rapidly developing fields that fall within the scope of the journal.