Involvement of Nrf2 Signaling in Lead-induced Toxicity
- Authors: Arabnezhad M.1, Haghani F.2, Ghaffarian-Bahraman A.3, Jafarzadeh E.4, Mohammadi H.5, Yadegari J.6, Farkhondeh T.7, Aschner M.8, Darroudi M.9, Marouzi S.10, Samarghandian S.11
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Affiliations:
- Department of Toxicology and Pharmacology, Faculty of Pharmacy, Kerman University of Medical Sciences
- Department of Pharmaceutical Biotechnology, Faculty of Pharmacy, Kerman University of Medical Sciences
- Occupational Environment Research Center, Rafsanjan University of Medical Sciences
- Department of Toxicology and Pharmacology, Faculty of Pharmacy,, Tehran University of Medical Sciences (TUMS)
- Department of Pharmacology and Toxicology, Faculty of Pharmacy, Lorestan University of Medical Sciences
- Department of Pharmacognosy, Faculty of Pharmacy, Lorestan University of Medical Sciences
- Department of Toxicology and Pharmacology, School of Pharmacy,, Birjand University of Medical Sciences
- Department of Molecular Pharmacology, Albert Einstein College of Medicine
- Nuclear Medicine Research Center, Mashhad University of Medical Sciences,
- Department of Basic Medical Sciences, Neyshabur University of Medical Sciences
- Healthy Ageing Research Centre, Neyshabur University of Medical Sciences
- Issue: Vol 31, No 23 (2024)
- Pages: 3529-3549
- Section: Anti-Infectives and Infectious Diseases
- URL: https://jdigitaldiagnostics.com/0929-8673/article/view/645221
- DOI: https://doi.org/10.2174/0929867330666230522143341
- ID: 645221
Cite item
Full Text
Abstract
Nuclear factor erythroid 2-related factor 2 (Nrf2) is used as one of the main protective factors against various pathological processes, as it regulates cells resistant to oxidation. Several studies have extensively explored the relationship between environmental exposure to heavy metals, particularly lead (Pb), and the development of various human diseases. These metals have been reported to be able to, directly and indirectly, induce the production of reactive oxygen species (ROS) and cause oxidative stress in various organs. Since Nrf2 signaling is important in maintaining redox status, it has a dual role depending on the specific biological context. On the one hand, Nrf2 provides a protective mechanism against metal-induced toxicity; on the other hand, it can induce metalinduced carcinogenesis upon prolonged exposure and activation. Therefore, the aim of this review was to summarize the latest knowledge on the functional interrelation between toxic metals, such as Pb and Nrf2 signaling.
Keywords
About the authors
Mohammad-Reza Arabnezhad
Department of Toxicology and Pharmacology, Faculty of Pharmacy, Kerman University of Medical Sciences
Email: info@benthamscience.net
Fatemeh Haghani
Department of Pharmaceutical Biotechnology, Faculty of Pharmacy, Kerman University of Medical Sciences
Email: info@benthamscience.net
Ali Ghaffarian-Bahraman
Occupational Environment Research Center, Rafsanjan University of Medical Sciences
Email: info@benthamscience.net
Emad Jafarzadeh
Department of Toxicology and Pharmacology, Faculty of Pharmacy,, Tehran University of Medical Sciences (TUMS)
Email: info@benthamscience.net
Hamidreza Mohammadi
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Lorestan University of Medical Sciences
Email: info@benthamscience.net
Javad Yadegari
Department of Pharmacognosy, Faculty of Pharmacy, Lorestan University of Medical Sciences
Email: info@benthamscience.net
Tahereh Farkhondeh
Department of Toxicology and Pharmacology, School of Pharmacy,, Birjand University of Medical Sciences
Email: info@benthamscience.net
Michael Aschner
Department of Molecular Pharmacology, Albert Einstein College of Medicine
Email: info@benthamscience.net
Majid Darroudi
Nuclear Medicine Research Center, Mashhad University of Medical Sciences,
Email: info@benthamscience.net
Somayeh Marouzi
Department of Basic Medical Sciences, Neyshabur University of Medical Sciences
Email: info@benthamscience.net
Saeed Samarghandian
Healthy Ageing Research Centre, Neyshabur University of Medical Sciences
Author for correspondence.
Email: info@benthamscience.net
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