Reactive Oxygen Species-Mediated Apoptosis and Cytotoxicity of Newly Synthesized Pyridazin-3-Ones In P815 (Murin Mastocytoma) Cell Line.


Journal

Drug research
ISSN: 2194-9387
Titre abrégé: Drug Res (Stuttg)
Pays: Germany
ID NLM: 101602406

Informations de publication

Date de publication:
Oct 2019
Historique:
pubmed: 30 6 2019
medline: 19 2 2020
entrez: 29 6 2019
Statut: ppublish

Résumé

In cancer cells, the intracellular antioxidant capacity and the redox homeostasis are mainly maintained by the glutathione- and thioredoxin-dependent systems which are considered as promising targets for anticancer drugs. Pyridazinones constitute an interesting source of heterocyclic compounds for drug discovery. The present investigation focused on studying the in-vitro antitumor activity of newly synthesized Pyridazin-3(2h)-ones derivatives against P815 (Murin mastocytoma) cell line. The in-vitro cytotoxic activities were investigated toward the P815 cell line using tetrazolium-based MTT assay. Lipid peroxidation and the specific activities of antioxidant enzymes were also determined. The newly compounds had a selective dose-dependent cytotoxic effect without affecting normal cells (PBMCs). Apoptosis was further confirmed through the characteristic apoptotic morphological changes and DNA fragmentation. Two compounds (6F: and 7H: ) were highly cytotoxic and were submitted to extend biological testing to determine the likely mechanisms of their cytotoxicity. Results showed that these molecules may induce cytotoxicity via disturbing the redox homeostasis. Importantly, the anticancer activity of 6F: and 7H: could be due to the intracellular reactive oxygen species hypergeneration through significant loss of glutathione reductase and thioredoxin reductase activities. This eventually leads to oxidative stress-mediated P815 cell apoptosis. Furthermore, the co-administration of 6F: or 7H: with Methotrexate exhibited a synergistic cytotoxic effect. considering their significant anticancer activity and chemosensitivity, 6F: and 7H: may improve the therapeutic efficacy of the current treatment for cancer.

Sections du résumé

BACKGROUND BACKGROUND
In cancer cells, the intracellular antioxidant capacity and the redox homeostasis are mainly maintained by the glutathione- and thioredoxin-dependent systems which are considered as promising targets for anticancer drugs. Pyridazinones constitute an interesting source of heterocyclic compounds for drug discovery. The present investigation focused on studying the in-vitro antitumor activity of newly synthesized Pyridazin-3(2h)-ones derivatives against P815 (Murin mastocytoma) cell line.
METHODS METHODS
The in-vitro cytotoxic activities were investigated toward the P815 cell line using tetrazolium-based MTT assay. Lipid peroxidation and the specific activities of antioxidant enzymes were also determined.
RESULTS RESULTS
The newly compounds had a selective dose-dependent cytotoxic effect without affecting normal cells (PBMCs). Apoptosis was further confirmed through the characteristic apoptotic morphological changes and DNA fragmentation. Two compounds (6F: and 7H: ) were highly cytotoxic and were submitted to extend biological testing to determine the likely mechanisms of their cytotoxicity. Results showed that these molecules may induce cytotoxicity via disturbing the redox homeostasis. Importantly, the anticancer activity of 6F: and 7H: could be due to the intracellular reactive oxygen species hypergeneration through significant loss of glutathione reductase and thioredoxin reductase activities. This eventually leads to oxidative stress-mediated P815 cell apoptosis. Furthermore, the co-administration of 6F: or 7H: with Methotrexate exhibited a synergistic cytotoxic effect.
CONCLUSIONS CONCLUSIONS
considering their significant anticancer activity and chemosensitivity, 6F: and 7H: may improve the therapeutic efficacy of the current treatment for cancer.

Identifiants

pubmed: 31252433
doi: 10.1055/a-0762-3775
doi:

Substances chimiques

Antineoplastic Agents 0
Pyridazines 0
Reactive Oxygen Species 0
Glutathione Reductase EC 1.8.1.7
Thioredoxin-Disulfide Reductase EC 1.8.1.9

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

528-536

Informations de copyright

© Georg Thieme Verlag KG Stuttgart · New York.

Déclaration de conflit d'intérêts

No conflict of interest has been declared by the authors.

Auteurs

Najat Bouchmaa (N)

Laboratory of Medicinal Chemistry, Faculty of Medicine and Pharmacy, Mohammed V University, Rabat, Morocco.
Team of Experimental Oncology and Natural Substances, Cellular and Molecular Immuno-pharmacology, Faculty of Science and Technology, Sultan Moulay Slimane University, Beni-Mellal, Morocco.

Reda Ben Mrid (RB)

Laboratory of Biochemistry and Molecular Genetics, Faculty of Science and Technology, Abdelmalek Essaâdi University, Tangier, Morocco.

Youness Boukharsa (Y)

Laboratory of Medicinal Chemistry, Faculty of Medicine and Pharmacy, Mohammed V University, Rabat, Morocco.

Youssef Bouargalne (Y)

Laboratory of Biochemistry and Molecular Genetics, Faculty of Science and Technology, Abdelmalek Essaâdi University, Tangier, Morocco.

Abderrazak Idir (A)

Team of Experimental Oncology and Natural Substances, Cellular and Molecular Immuno-pharmacology, Faculty of Science and Technology, Sultan Moulay Slimane University, Beni-Mellal, Morocco.

Jamal Taoufik (J)

Laboratory of Medicinal Chemistry, Faculty of Medicine and Pharmacy, Mohammed V University, Rabat, Morocco.

Mʼhammed Ansar (M)

Laboratory of Medicinal Chemistry, Faculty of Medicine and Pharmacy, Mohammed V University, Rabat, Morocco.

Abdelmajid Zyad (A)

Team of Experimental Oncology and Natural Substances, Cellular and Molecular Immuno-pharmacology, Faculty of Science and Technology, Sultan Moulay Slimane University, Beni-Mellal, Morocco.

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Classifications MeSH