职业接触砷与白细胞减少症风险:毒理学警报。

IF 1.7 4区 医学 Q3 PUBLIC, ENVIRONMENTAL & OCCUPATIONAL HEALTH Toxicology and Industrial Health Pub Date : 2024-12-01 Epub Date: 2024-09-02 DOI:10.1177/07482337241277261
Nadielle Silva Bidu, Diogo Sousa Lemos, Bruno José Dumêt Fernandes
{"title":"职业接触砷与白细胞减少症风险:毒理学警报。","authors":"Nadielle Silva Bidu, Diogo Sousa Lemos, Bruno José Dumêt Fernandes","doi":"10.1177/07482337241277261","DOIUrl":null,"url":null,"abstract":"<p><p>Arsenic and its inorganic compounds affect numerous organs and systemic functions, such as the nervous and hematopoietic systems, liver, kidneys, and skin. Despite a large number of studies on arsenic toxicity, rare reports have investigated the leukopenia incidence in workers exposed to arsenic. In workplaces, the main source of workers' exposure is the contaminated air by the inorganic arsenic in mines, arsenic or copper smelter industries, and chemical factories. Erythropoiesis inhibition is one of the arsenic effects and it is related to regulatory factor GATA-1. This factor is necessary for the normal differentiation of early erythroid progenitors. JAK-STAT is an important intracellular signal transduction pathway responsible for the mediating normal functions of several cytokines related to cell proliferation and hematopoietic systems development and regulation. Arsenic inactivates JAK-STAT by inhibiting JAK tyrosine kinase and using the IFNγ pathway. The intravascular hemolysis starts after the absorption phase when arsenic binds to the globin of hemoglobin in erythrocytes and is transported into the body, which increases the oxidation of sulfhydryl groups in hemoglobin. So, this article intends to highlight the potential leukopenia risk via inhalation for workers exposed to arsenic and suggests a possible mechanism for this leukopenia through the JAK-signal transducer and activator of transcription (STAT) pathway inhibition.</p>","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":null,"pages":null},"PeriodicalIF":1.7000,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Occupational exposure to arsenic and leukopenia risk: Toxicological alert.\",\"authors\":\"Nadielle Silva Bidu, Diogo Sousa Lemos, Bruno José Dumêt Fernandes\",\"doi\":\"10.1177/07482337241277261\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Arsenic and its inorganic compounds affect numerous organs and systemic functions, such as the nervous and hematopoietic systems, liver, kidneys, and skin. Despite a large number of studies on arsenic toxicity, rare reports have investigated the leukopenia incidence in workers exposed to arsenic. In workplaces, the main source of workers' exposure is the contaminated air by the inorganic arsenic in mines, arsenic or copper smelter industries, and chemical factories. Erythropoiesis inhibition is one of the arsenic effects and it is related to regulatory factor GATA-1. This factor is necessary for the normal differentiation of early erythroid progenitors. JAK-STAT is an important intracellular signal transduction pathway responsible for the mediating normal functions of several cytokines related to cell proliferation and hematopoietic systems development and regulation. Arsenic inactivates JAK-STAT by inhibiting JAK tyrosine kinase and using the IFNγ pathway. The intravascular hemolysis starts after the absorption phase when arsenic binds to the globin of hemoglobin in erythrocytes and is transported into the body, which increases the oxidation of sulfhydryl groups in hemoglobin. So, this article intends to highlight the potential leukopenia risk via inhalation for workers exposed to arsenic and suggests a possible mechanism for this leukopenia through the JAK-signal transducer and activator of transcription (STAT) pathway inhibition.</p>\",\"PeriodicalId\":23171,\"journal\":{\"name\":\"Toxicology and Industrial Health\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.7000,\"publicationDate\":\"2024-12-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Toxicology and Industrial Health\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1177/07482337241277261\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/9/2 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q3\",\"JCRName\":\"PUBLIC, ENVIRONMENTAL & OCCUPATIONAL HEALTH\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Toxicology and Industrial Health","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1177/07482337241277261","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/9/2 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"PUBLIC, ENVIRONMENTAL & OCCUPATIONAL HEALTH","Score":null,"Total":0}
引用次数: 0

摘要

砷及其无机化合物会影响许多器官和全身功能,如神经和造血系统、肝脏、肾脏和皮肤。尽管有大量关于砷毒性的研究,但很少有报告调查接触砷的工人出现白细胞减少症的情况。在工作场所,工人接触砷的主要来源是矿场、砷或铜冶炼厂及化工厂受无机砷污染的空气。红细胞生成抑制是砷的影响之一,它与调节因子 GATA-1 有关。该因子是早期红细胞祖细胞正常分化所必需的。JAK-STAT 是一种重要的细胞内信号转导途径,负责介导与细胞增殖和造血系统发育和调节有关的几种细胞因子的正常功能。砷通过抑制 JAK 酪氨酸激酶和利用 IFNγ 途径使 JAK-STAT 失活。当砷与红细胞中的血红蛋白球蛋白结合并被转运到体内,使血红蛋白中的巯基氧化增加时,血管内溶血就开始了。因此,本文旨在强调接触砷的工人通过吸入砷可能导致白细胞减少症的风险,并提出了通过抑制 JAK 信号转导和激活转录(STAT)途径导致白细胞减少症的可能机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Occupational exposure to arsenic and leukopenia risk: Toxicological alert.

Arsenic and its inorganic compounds affect numerous organs and systemic functions, such as the nervous and hematopoietic systems, liver, kidneys, and skin. Despite a large number of studies on arsenic toxicity, rare reports have investigated the leukopenia incidence in workers exposed to arsenic. In workplaces, the main source of workers' exposure is the contaminated air by the inorganic arsenic in mines, arsenic or copper smelter industries, and chemical factories. Erythropoiesis inhibition is one of the arsenic effects and it is related to regulatory factor GATA-1. This factor is necessary for the normal differentiation of early erythroid progenitors. JAK-STAT is an important intracellular signal transduction pathway responsible for the mediating normal functions of several cytokines related to cell proliferation and hematopoietic systems development and regulation. Arsenic inactivates JAK-STAT by inhibiting JAK tyrosine kinase and using the IFNγ pathway. The intravascular hemolysis starts after the absorption phase when arsenic binds to the globin of hemoglobin in erythrocytes and is transported into the body, which increases the oxidation of sulfhydryl groups in hemoglobin. So, this article intends to highlight the potential leukopenia risk via inhalation for workers exposed to arsenic and suggests a possible mechanism for this leukopenia through the JAK-signal transducer and activator of transcription (STAT) pathway inhibition.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
CiteScore
3.50
自引率
5.30%
发文量
72
审稿时长
4 months
期刊介绍: Toxicology & Industrial Health is a journal dedicated to reporting results of basic and applied toxicological research with direct application to industrial/occupational health. Such research includes the fields of genetic and cellular toxicology and risk assessment associated with hazardous wastes and groundwater.
期刊最新文献
Occupational exposure to arsenic and leukopenia risk: Toxicological alert. Perfluorooctane sulfonate causes damage to L-02 cells via Wnt/β-catenin signal path and endoplasmic reticulum stress pathway. The impact of genetic polymorphism for detecting genotoxicity in workers occupationally exposed to formaldehyde: A systematic review. Impact of xylene exposure during organogenesis on foeto-placental efficiency and foetal viability: Exploring its association with oxidative stress-induced inflammation and apoptosis in utero. Environmental exposure to lead and cadmium only minimally affects the redox system of the follicular fluid and the outcome of intracytoplasmic sperm injection.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1