ArticleToxicology and applied pharmacology2018
Low-level arsenic causes proteotoxic stress and not oxidative stress.
Article in Toxicology and applied pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
39 citing papers in PubMed, 55 citations in OpenAlex.
- Heavy metal toxicity as a driver of endoplasmic reticulum stress and dysfunction.The FEBS journal · 2026Review
- Understanding the contribution of toxicant exposures to Alzheimer's disease and related dementias.Current opinion in neurobiology · 2026Review
- N-Acetylcysteine Prevents Arsenic-Induced Apoptosis but Not Supernumerary Motor Neuron Development in Zebrafish Embryos: Assessment of Protein Carbonylation and the p53 Pathway.International journal of molecular sciences · 2026Article
- Arsenic disrupts autophagosome-lysosome fusion in a zinc dependent manner across multiple human skin and lung cells lines.Archives of toxicology · 2026Article
- Arsenic disrupts H3K9me3 and H3K27me3 balance by biasing PRC2.1 and PRC2.2 activity via PALI1 inhibition in carcinogenesis.International journal of biological sciences · 2025Article
- Proteomic-miRNA Biomics Profile Reveals 2D Cultures of Human iPSC-Derived Neural Progenitor Cells More Sensitive than 3D Spheroid System Against the Experimental Exposure to Arsenic.Molecular neurobiology · 2024Article
- Chronic arsenic exposure suppresses proteasomal and autophagic protein degradation.Environmental toxicology and pharmacology · 2024Article
- Arsenic Impairs Wound Healing Processes in Dermal Fibroblasts and Mice.International journal of molecular sciences · 2024Article
- Migrasomal autophagosomes relieve endoplasmic reticulum stress in glioblastoma cells.BMC biology · 2024Article
- Arsenic-induced prostate cancer: an enigma.Medical oncology (Northwood, London, England) · 2024Review
- Altered Regulation of the Glucose Transporter GLUT3 in PRDX1 Null Cells Caused Hypersensitivity to Arsenite.Cells · 2023Article
- Mechanisms of genotoxicity and proteotoxicity induced by the metalloids arsenic and antimony.Cellular and molecular life sciences : CMLS · 2023Review
- NRF2 controls iron homeostasis and ferroptosis through HERC2 and VAMP8.Science advances · 2023Article
- Arsenic and cancer: Evidence and mechanisms.Advances in pharmacology (San Diego, Calif.) · 2023Article
- Signal amplification in the KEAP1-NRF2-ARE antioxidant response pathway.Redox biology · 2022Review
- Mitochondrial ROS, ER Stress, and Nrf2 Crosstalk in the Regulation of Mitochondrial Apoptosis Induced by Arsenite.Antioxidants (Basel, Switzerland) · 2022Review
- Nuclear Organization in Response to Stress: A Special Focus on Nucleoli.Results and problems in cell differentiation · 2022Article
- Connections between endoplasmic reticulum stress-associated unfolded protein response, mitochondria, and autophagy in arsenic-induced carcinogenesis.Seminars in cancer biology · 2021Review
- The intricacies of NRF2 regulation in cancer.Seminars in cancer biology · 2021Review
- Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Prolonged exposure to arsenic has been shown to increase the risk of developing a number of diseases, including cancer and type II diabetes. Arsenic is present throughout the environment in its inorganic forms, and the level of exposure varies greatly by geographical location. The current recommended maximum level of arsenic exposure by the EPA is 10μg/L, but levels>50-1000μg/L have been detected in some parts of Asia, the Middle East, and the Southwestern United States. One of the most important steps in developing treatment options for arsenic-linked pathologies is to understand the cellular pathways affected by low levels of arsenic. Here, we show that acute exposure to non-lethal, low-level arsenite, an environmentally relevant arsenical, inhibits the autophagy pathway. Furthermore, arsenite-induced autophagy inhibition initiates a transient, but moderate ER stress response. Significantly, low-level arsenite exposure does not exhibit an increase in oxidative stress. These findings indicate that compromised autophagy, and not enhanced oxidative stress occurs early during arsenite exposure, and that restoring the autophagy pathway and proper proteostasis could be a viable option for treating arsenic-linked diseases. As such, our study challenges the existing paradigm that oxidative stress is the main underlying cause of pathologies associated with environmental arsenic exposure.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.