{"title":"An Overview of Hexavalent Chromium-Induced Necroptosis, Pyroptosis, and Ferroptosis","authors":"Saulesh Kurmangaliyeva, Kristina Baktikulova, Viktoriya Tkachenko, Bibigul Seitkhanova, Nasriddin Shapambayev, Farida Rakhimzhanova, Altyn Almagambetova, Kairat Kurmangaliyev","doi":"10.1007/s12011-024-04376-1","DOIUrl":null,"url":null,"abstract":"<p>Heavy metals are common environmental industrial pollutants. Due to anthropogenic activity, chromium, especially its hexavalent form [Cr(VI)], is a widespread environmental contaminant that poses a threat to human health. In this review paper, we summarize the currently reported molecular mechanisms involved in chromium toxicity with a focus on the induction of pro-inflammatory non-apoptotic cell death pathways such as necroptosis, pyroptosis, and ferroptosis. The review highlights the ability of chromium to induce necroptosis, pyroptosis, and ferroptosis revealing the signaling pathways involved. Cr(VI) can induce RIPK1/RIPK3-dependent necroptosis both in vitro and in vivo. Chromium toxicity is associated with pyroptotic NLRP3 inflammasome/caspase-1/gasdermin D-dependent secretion of IL-1β and IL-18. Furthermore, this review emphasizes the role of redox imbalance and intracellular iron accumulation in Cr(VI)-induced ferroptosis. Of note, the crosstalk between the investigated lethal subroutines in chromium-induced toxicity is primarily mediated by reactive oxygen species (ROS), which are suggested to act as a rheostat determining the cell death pathway in cells exposed to chromium. The current study provides novel insights into the pro-inflammatory effects of chromium, since necroptosis, pyroptosis, and ferroptosis affect inflammation owing to their immunogenic properties linked primarily with damage-associated molecular patterns. Inhibition of these non-apoptotic lethal subroutines can be considered a therapeutic strategy to reduce the toxicity of heavy metals, including chromium.</p>","PeriodicalId":8917,"journal":{"name":"Biological Trace Element Research","volume":"17 1","pages":""},"PeriodicalIF":3.4000,"publicationDate":"2024-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biological Trace Element Research","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1007/s12011-024-04376-1","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Heavy metals are common environmental industrial pollutants. Due to anthropogenic activity, chromium, especially its hexavalent form [Cr(VI)], is a widespread environmental contaminant that poses a threat to human health. In this review paper, we summarize the currently reported molecular mechanisms involved in chromium toxicity with a focus on the induction of pro-inflammatory non-apoptotic cell death pathways such as necroptosis, pyroptosis, and ferroptosis. The review highlights the ability of chromium to induce necroptosis, pyroptosis, and ferroptosis revealing the signaling pathways involved. Cr(VI) can induce RIPK1/RIPK3-dependent necroptosis both in vitro and in vivo. Chromium toxicity is associated with pyroptotic NLRP3 inflammasome/caspase-1/gasdermin D-dependent secretion of IL-1β and IL-18. Furthermore, this review emphasizes the role of redox imbalance and intracellular iron accumulation in Cr(VI)-induced ferroptosis. Of note, the crosstalk between the investigated lethal subroutines in chromium-induced toxicity is primarily mediated by reactive oxygen species (ROS), which are suggested to act as a rheostat determining the cell death pathway in cells exposed to chromium. The current study provides novel insights into the pro-inflammatory effects of chromium, since necroptosis, pyroptosis, and ferroptosis affect inflammation owing to their immunogenic properties linked primarily with damage-associated molecular patterns. Inhibition of these non-apoptotic lethal subroutines can be considered a therapeutic strategy to reduce the toxicity of heavy metals, including chromium.
期刊介绍:
Biological Trace Element Research provides a much-needed central forum for the emergent, interdisciplinary field of research on the biological, environmental, and biomedical roles of trace elements. Rather than confine itself to biochemistry, the journal emphasizes the integrative aspects of trace metal research in all appropriate fields, publishing human and animal nutritional studies devoted to the fundamental chemistry and biochemistry at issue as well as to the elucidation of the relevant aspects of preventive medicine, epidemiology, clinical chemistry, agriculture, endocrinology, animal science, pharmacology, microbiology, toxicology, virology, marine biology, sensory physiology, developmental biology, and related fields.