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金属氧化物吸入所致发热——焊接烟尘的免疫毒理学方面

Metal-oxide inhalation induced fever - Immuntoxicological aspects of welding fumes.

作者信息

Szűcs-Somlyó Éva, Lehel József, Májlinger Kornél, Lőrincz Márta, Kővágó Csaba

机构信息

University of Veterinary Medicine, Department of Epidemiology and Infectious Diseases, Budapest, Hungary.

University of Veterinary Medicine, Department of Food Hygiene, Budapest, Hungary.

出版信息

Food Chem Toxicol. 2023 May;175:113722. doi: 10.1016/j.fct.2023.113722. Epub 2023 Mar 11.

Abstract

Metal fume fever is a well-known occupational disease that arises from prolonged exposure to subtoxic levels of zinc oxide-containing fumes or dust. This review article aims to identify and examine the possible immunotoxicological effects of inhaled zinc oxide nanoparticles. The current most widely accepted pathomechanism for the development of the disease involves the formation of reactive oxygen species following the entry of zinc oxide particles into the alveolus resulting the release of pro-inflammatory cytokines by activation of the Nuclear Factor Kappa B transcriptional signal, thus evoking the symptoms. The role of metallothionein in inducing tolerance is believed to be a key factor in mitigating the development of metal fume fever. The other, poorly proven hypothetical route is that zinc-oxide particles bind to an undefined protein in the body as haptens to form an antigen and act as an allergen. After activation of the immune system, primary antibodies and immune complexes are developed and type 1. hypersensitivity reaction occurs, that can cause asthmatic dyspnoea, urticaria and angioedema. The development of tolerance is explained by the formation of secondary antibodies against primary antibodies. Oxidative stress and immunological processes cannot be completely separated from each other, as they can induce each other.

摘要

金属烟雾热是一种众所周知的职业病,它源于长期接触亚毒性水平的含氧化锌烟雾或粉尘。这篇综述文章旨在识别和研究吸入氧化锌纳米颗粒可能产生的免疫毒理学效应。目前关于该疾病发展最广泛接受的发病机制涉及氧化锌颗粒进入肺泡后产生活性氧,通过激活核因子κB转录信号导致促炎细胞因子释放,从而引发症状。金属硫蛋白在诱导耐受性方面的作用被认为是减轻金属烟雾热发展的关键因素。另一种未经充分证实的假说途径是,氧化锌颗粒作为半抗原与体内一种未明确的蛋白质结合形成抗原并充当过敏原。免疫系统激活后,产生一级抗体和免疫复合物,发生Ⅰ型超敏反应,可导致哮喘性呼吸困难、荨麻疹和血管性水肿。耐受性的形成是通过针对一级抗体产生二级抗体来解释的。氧化应激和免疫过程不能完全相互分离,因为它们可以相互诱导。

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