Selenylated Imidazo[1,2-a]pyridine Induces Cell Senescence and Oxidative Stress in Chronic Myeloid Leukemia Cells

Imidazo[1,2-a]pyridines (IPs) have been studied regarding drug development. The objective of this work was to evaluate the antileukemic capacity of IP derivatives by screening their ability as a pro-oxidant. IP derivatives were synthesized and oral bioavailability and toxicity were analyzed in silic...

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Published in:Molecules (Basel, Switzerland) Vol. 28; no. 2; p. 893
Main Authors: Burkner, Gabriella Teles, Dias, Dhébora Albuquerque, Souza, Kamylla Fernanda Souza de, Araújo, Anna Júlia Papa de, Basilio, Denise Caroline Luiz Soares, Jacobsen, Fernanda Tondello, Moraes, Ana Carolina Rabello de, Silva-Filho, Saulo Euclides, Cavalcante, Marcos Filipe de Oliveira, Moraes, Cassio Augusto de Oliveira, Saba, Sumbal, Macedo, Maria Lígia Rodrigues, Paredes-Gamero, Edgar Julian, Rafique, Jamal, Parisotto, Eduardo Benedetti
Format: Journal Article
Language:English
Published: Switzerland MDPI AG 01.01.2023
MDPI
Subjects:
Antineoplastic Agents - pharmacology
Apoptosis
Bioavailability
Breast cancer
Cancer therapies
Cell cycle
Cell growth
Cell Proliferation
Cellular Senescence
Chemotherapy
chronic myeloid leukemia
DNA damage
Drug development
Humans
imidazo[1,2-a]pyridines
K562 Cells
Kinases
Leukemia
Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy
Leukemia, Myeloid
Oxidative Stress
Pyridines - pharmacology
selenide
Senescence
Toxicity
senescence
leukemia
chronic myeloid leukemia
imidazo[1,2-a]pyridines
selenide
oxidative stress
ISSN:1420-3049, 1420-3049
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Abstract Imidazo[1,2-a]pyridines (IPs) have been studied regarding drug development. The objective of this work was to evaluate the antileukemic capacity of IP derivatives by screening their ability as a pro-oxidant. IP derivatives were synthesized and oral bioavailability and toxicity were analyzed in silico. Redox screening was performed on human Kasumi, KG-1, K562, and Jurkat leukemia cells. The IP derivative and the most responsive leukemic cell were selected for cytotoxicity, cell proliferation, cell senescence, and oxidative stress assays. The predictive toxicity analysis showed a possible effect on the reproductive system, but without mutagenic, carcinogenic, or irritability effects. MRK-107 against K562 cells was the compound that showed the best redox profile. MRK-107 did not induce cell death in K562 and monocyte cells. However, this compound was able to decrease cell proliferation and increase cell senescence after 48 and 72 h. Furthermore, MRK-107 induced oxidative stress in K562 cells after 72 h, increasing lipid peroxidation and decreasing reduced glutathione (GSH) contents. This study demonstrated that MRK-107-induced senescence with the involvement of oxidative stress is a possible mechanism of action, addressing this compound as a potential antitumor drug against chronic myeloid leukemia.
AbstractList Imidazo[1,2-a]pyridines (IPs) have been studied regarding drug development. The objective of this work was to evaluate the antileukemic capacity of IP derivatives by screening their ability as a pro-oxidant. IP derivatives were synthesized and oral bioavailability and toxicity were analyzed in silico. Redox screening was performed on human Kasumi, KG-1, K562, and Jurkat leukemia cells. The IP derivative and the most responsive leukemic cell were selected for cytotoxicity, cell proliferation, cell senescence, and oxidative stress assays. The predictive toxicity analysis showed a possible effect on the reproductive system, but without mutagenic, carcinogenic, or irritability effects. MRK-107 against K562 cells was the compound that showed the best redox profile. MRK-107 did not induce cell death in K562 and monocyte cells. However, this compound was able to decrease cell proliferation and increase cell senescence after 48 and 72 h. Furthermore, MRK-107 induced oxidative stress in K562 cells after 72 h, increasing lipid peroxidation and decreasing reduced glutathione (GSH) contents. This study demonstrated that MRK-107-induced senescence with the involvement of oxidative stress is a possible mechanism of action, addressing this compound as a potential antitumor drug against chronic myeloid leukemia.
Imidazo[1,2 ]pyridines (IPs) have been studied regarding drug development. The objective of this work was to evaluate the antileukemic capacity of IP derivatives by screening their ability as a pro-oxidant. IP derivatives were synthesized and oral bioavailability and toxicity were analyzed in silico. Redox screening was performed on human Kasumi, KG-1, K562, and Jurkat leukemia cells. The IP derivative and the most responsive leukemic cell were selected for cytotoxicity, cell proliferation, cell senescence, and oxidative stress assays. The predictive toxicity analysis showed a possible effect on the reproductive system, but without mutagenic, carcinogenic, or irritability effects. MRK-107 against K562 cells was the compound that showed the best redox profile. MRK-107 did not induce cell death in K562 and monocyte cells. However, this compound was able to decrease cell proliferation and increase cell senescence after 48 and 72 h. Furthermore, MRK-107 induced oxidative stress in K562 cells after 72 h, increasing lipid peroxidation and decreasing reduced glutathione (GSH) contents. This study demonstrated that MRK-107-induced senescence with the involvement of oxidative stress is a possible mechanism of action, addressing this compound as a potential antitumor drug against chronic myeloid leukemia.
Author Dias, Dhébora Albuquerque
Macedo, Maria Lígia Rodrigues
Rafique, Jamal
Araújo, Anna Júlia Papa de
Paredes-Gamero, Edgar Julian
Burkner, Gabriella Teles
Parisotto, Eduardo Benedetti
Jacobsen, Fernanda Tondello
Basilio, Denise Caroline Luiz Soares
Saba, Sumbal
Cavalcante, Marcos Filipe de Oliveira
Moraes, Ana Carolina Rabello de
Moraes, Cassio Augusto de Oliveira
Souza, Kamylla Fernanda Souza de
Silva-Filho, Saulo Euclides
AuthorAffiliation 1 Pharmaceutical Sciences, Food and Nutrition College, Federal University of Mato Grosso do Sul (UFMS), Campo Grande 79070-900, Brazil
5 Institute of Chemistry (INQUI), Federal University of Mato Grosso do Sul (UFMS), Campo Grande 79074-460, Brazil
2 Department of Biochemistry, Federal University of São Paulo, São Paulo 4044-020, Brazil
3 Department of Clinical Analysis, Center for Health Sciences, Federal University of Santa Catarina, Florianópolis 88040-970, Brazil
4 Institute of Chemistry (IQ), Federal University of Goiás (UFG), Goiania 74690-900, Brazil
AuthorAffiliation_xml – name: 4 Institute of Chemistry (IQ), Federal University of Goiás (UFG), Goiania 74690-900, Brazil
– name: 1 Pharmaceutical Sciences, Food and Nutrition College, Federal University of Mato Grosso do Sul (UFMS), Campo Grande 79070-900, Brazil
– name: 2 Department of Biochemistry, Federal University of São Paulo, São Paulo 4044-020, Brazil
– name: 3 Department of Clinical Analysis, Center for Health Sciences, Federal University of Santa Catarina, Florianópolis 88040-970, Brazil
– name: 5 Institute of Chemistry (INQUI), Federal University of Mato Grosso do Sul (UFMS), Campo Grande 79074-460, Brazil
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Issue 2
Keywords senescence
leukemia
chronic myeloid leukemia
imidazo[1,2-a]pyridines
selenide
oxidative stress
Language English
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Snippet Imidazo[1,2-a]pyridines (IPs) have been studied regarding drug development. The objective of this work was to evaluate the antileukemic capacity of IP...
Imidazo[1,2 ]pyridines (IPs) have been studied regarding drug development. The objective of this work was to evaluate the antileukemic capacity of IP...
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SubjectTerms Antineoplastic Agents - pharmacology
Apoptosis
Bioavailability
Breast cancer
Cancer therapies
Cell cycle
Cell growth
Cell Proliferation
Cellular Senescence
Chemotherapy
chronic myeloid leukemia
DNA damage
Drug development
Humans
imidazo[1,2-a]pyridines
K562 Cells
Kinases
Leukemia
Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy
Leukemia, Myeloid
Oxidative Stress
Pyridines - pharmacology
selenide
Senescence
Toxicity
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Title Selenylated Imidazo[1,2-a]pyridine Induces Cell Senescence and Oxidative Stress in Chronic Myeloid Leukemia Cells
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Volume 28
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