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Cited by 81Bioactive Compounds and Antitumor AgentsCancer and biochemical researchCell death mechanisms and regulation

Albendazole as a promising molecule for tumor control

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Castro, L.S.E.P.W., Kviecinski, M.R., Ourique, F., Parisotto, E.B., Grinevicius, V.M.A.S., Correia, J.F.G., Wilhelm Filho, D., Pedrosa, R.C.·2016·Redox Biology
DOI 10.1016/j.redox.2016.09.013PMC PMC5053114
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Abstract

This work evaluated the antitumor effects of albendazole (ABZ) and its relationship with modulation of oxidative stress and induction of DNA damage. The present results showed that ABZ causes oxidative cleavage on calf-thymus DNA suggesting that this compound can break DNA. ABZ treatment decreased MCF-7 cell viability (EC 50 =44.9 for 24 h) and inhibited MCF-7 colony formation (~67.5% at 5 μM). Intracellular ROS levels increased with ABZ treatment (~123%). The antioxidant NAC is able to revert the cytotoxic effects, ROS generation and loss of mitochondrial membrane potential of MCF-7 cells treated with ABZ. Ehrlich carcinoma growth was inhibited (~32%) and survival time was elongated (~50%) in animals treated with ABZ. Oxidative biomarkers (TBARS and protein carbonyl levels) and activity of antioxidant enzymes (CAT, SOD and GR) increased, and reduced glutathione (GSH) was depleted in animals treated with ABZ, indicating an oxidative stress condition, leading to a DNA damage causing phosphorylation of histone H2A variant, H2AX, and triggering apoptosis signaling, which was confirmed by increasing Bax/Bcl-xL rate, p53 and Bax expression. We propose that ABZ induces oxidative stress promoting DNA fragmentation and triggering apoptosis and inducing cell death, making this drug a promising leader molecule for development of new antitumor drugs.

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  • Albendazole and mebendazole have been repositioned as promising anti-cancer drugs.

    “It is of particular note that albendazole and mebendazole have been repositioned as promising anti-cancer drugs.”

    From Albendazole and Mebendazole as Anti-Parasitic and Anti-Cancer Agents: an Update (2021) · cites this paper as [33]

    The Introduction says there is evidence supporting albendazole repositioning for cancer therapy, and the paper describes it as a promising molecule for antitumor-drug development. It does not make that claim for mebendazole; mebendazole appears in the References in a study of oxidative stress, not cancer repositioning. (LLM, conf=0.88)

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  • In Ehrlich carcinoma model in mice, albendazole induced oxidative stress promoting DNA fragmentation, triggering apoptosis, and inducing cancer cell death.

    “In Ehrlich carcinoma model in mice, albendazole induced oxidative stress promoting DNA fragmentation, triggering apoptosis, and inducing cancer cell death [33].”

    From Albendazole and Mebendazole as Anti-Parasitic and Anti-Cancer Agents: an Update (2021) · cites this paper as [33]

    The Results and discussion report oxidative stress, DNA damage, increased apoptosis, and reduced viable Ehrlich carcinoma cells after albendazole treatment. The proposed causal chain is more tentative: the authors say DNA damage 'could be associated' with increased ROS and was 'probably responsible' for increased apoptotic cell death. The claim presents that mechanism as established. (LLM, conf=0.85)

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References 67 · Cited by 81

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Authors
Castro, L. S. E. P. W., Kviecinski, M. R., Ourique, F., Parisotto, E. B., Grinevicius, V. M. A. S., Correia, J. F. G., Wilhelm Filho, D., & Pedrosa, R. C.
Affiliations
  • Universidade Federal de Santa Catarina (BR)
  • Universidade do Sul de Santa Catarina (BR)
Corresponding author
Pedrosa, R.C.
ORCID
Venue
Redox Biology
Publisher
Elsevier BV
Published
2016-12
Volume
10
Pages
90-99
ISSN
2213-2317 (ISSN-L)
DOI
10.1016/j.redox.2016.09.013
PMC
PMC5053114
OpenAlex
W2521851594
Cited by
81
References
67
Citations by year
2026: 5 · 2025: 6 · 2024: 4 · 2023: 7 · 2022: 9 · 2021: 20 · 2020: 10 · 2019: 8 · 2018: 6 · 2017: 6
FWCI
5.45
Type
journal article
Language
en
Open access
Licence
Locations
  • Redox Biology (publishedVersion, cc-by-nc-nd)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
  • Conselho Nacional de Pesquisa (302404/2011-2, 303234/2015-6)
Topics
  • Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Toxicology › Bioactive Compounds and Antitumor Agents
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cancer and biochemical research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords
albendazole, anticancer activity, oxidative stress, DNA damage, reactive oxygen species, MCF-7 cells, Ehrlich ascites carcinoma, apoptosis, H2AX phosphorylation, glutathione depletion, antioxidant enzymes, N-acetylcysteine, Bax/Bcl-xL ratio, p53, colony formation
MeSH terms
Animals, Antineoplastic Agents, Carcinoma, Ehrlich Tumor, Cell Survival, DNA Damage, Humans, Albendazole, Reactive Oxygen Species, Oxidative Stress, Xenograft Model Antitumor Assays, Cell Proliferation, Mice, Membrane Potential, Mitochondrial, Drug Repositioning, MCF-7 Cells

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