Cited by 89Cell death mechanisms and regulationRedox biology and oxidative stressDrug-Induced Hepatotoxicity and Protection

Cell toxicity mechanism and biomarker

Open access
Zhang, Yong·2018·Clinical and Translational Medicine

Abstract

Cell toxicity may result in organ dysfunction and cause severe health problem. Recent studies revealed many toxicants may induced the over production of Nitric oxide, reactive oxygen species and the subsequent oxidative stress, cause cell toxicity. Mitochondrion dysfunction maybe the subsequent consequence of oxidative stress and has been recognized as another contributing factor in cell toxicity. Besides, oxidative products induced by some toxicants may also produce the compounds that damage cell DNA, leading to toxicity. Especially, the significance of nanoparticle induced cell toxicity was disclosed recently and attract more concern. The mechanism mainly includes inflammation, oxidative stress and DNA damage. On the other side, some biomarkers of cell toxicity including autophagy, cytokines, miRNA has been identified. The understanding of these phenomenon may enable us to clarify the cell toxicity mechanism then contribute to cell toxicity protection, disease treatment and drug side effect prevention.

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Crossref · 10.1186/s40169-018-0212-7

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  • Leaked chemicals can elevate reactive oxygen species levels, inducing oxidative stress that may damage cellular DNA, proteins, and lipids.

    “Moreover, these chemicals can elevate reactive oxygen species levels, inducing oxidative stress by increasing the concentration of reactive oxygen species (ROS) that may damage cellular DNA, proteins, and lipids (Zhang, 2018).”

    From Comparative analysis of energy transfer mechanisms for neural implants (2024) · cites this paper as Zhang, 2018

    The 'ROS and oxidative stress' section says toxic agents can increase ROS production and cause subsequent oxidative stress. The 'DNA damage' section discusses DNA damage alongside oxidative stress, but the copy does not establish the claimed ROS-mediated damage to proteins and lipids or specifically address leaked chemicals. (LLM, conf=0.86)

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Authors
Zhang, Y.
Affiliations
Shanghai Medical College of Fudan University (CN)
Corresponding author
Zhang, Yong
Venue
Clinical and Translational Medicine
Publisher
Wiley
Published
2018-10-29
Volume
7
Issue
1
Pages
34-34
ISSN
2001-1326 (ISSN-L)
OpenAlex
W2898771680
Cited by
89
References
59
Citations by year
2026: 8 · 2025: 15 · 2024: 13 · 2023: 11 · 2022: 11 · 2021: 15 · 2020: 9 · 2019: 6 · 2018: 1
FWCI
0.76
Type
journal article
Language
en
Open access
Locations
  • Clinical and Translational Medicine (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Shanghai Leading Academic Discipline Project (B115)
  • National Natural Science Foundation of China (31400713)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
Keywords
cytotoxicity, toxicity mechanisms, oxidative stress, reactive oxygen species, nitric oxide, mitochondrial dysfunction, DNA damage, nanoparticle toxicity, inflammation, biomarkers, autophagy, cytokines, microRNA

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