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Induction of apoptosis and antiproliferative activity of naringenin in human epidermoid carcinoma cell through ROS generation and cell cycle arrest.

Ahamad MS, Siddiqui S, Jafri A, Ahmad S, Afzal M, Arshad M - PLoS ONE (2014)

Bottom Line: The search for antiproliferative agents that reduce skin carcinoma is a task of great importance.The intracellular ROS generation assay showed statistically significant (p<0.001) dose-related increment in ROS production for naringenin.Cell cycle study showed that naringenin induced cell cycle arrest in G0/G1 phase of cell cycle and caspase-3 analysis revealed a dose dependent increment in caspase-3 activity which led to cell apoptosis.

View Article: PubMed Central - PubMed

Affiliation: Department of Zoology, Shibli National (PG) College, Azamgarh, Uttar Pradesh, India.

ABSTRACT
A natural predominant flavanone naringenin, especially abundant in citrus fruits, has a wide range of pharmacological activities. The search for antiproliferative agents that reduce skin carcinoma is a task of great importance. The objective of this study was to analyze the anti-proliferative and apoptotic mechanism of naringenin using MTT assay, DNA fragmentation, nuclear condensation, change in mitochondrial membrane potential, cell cycle kinetics and caspase-3 as biomarkers and to investigate the ability to induce reactive oxygen species (ROS) initiating apoptotic cascade in human epidermoid carcinoma A431 cells. Results showed that naringenin exposure significantly reduced the cell viability of A431 cells (p<0.01) with a concomitant increase in nuclear condensation and DNA fragmentation in a dose dependent manner. The intracellular ROS generation assay showed statistically significant (p<0.001) dose-related increment in ROS production for naringenin. It also caused naringenin-mediated epidermoid carcinoma apoptosis by inducing mitochondrial depolarization. Cell cycle study showed that naringenin induced cell cycle arrest in G0/G1 phase of cell cycle and caspase-3 analysis revealed a dose dependent increment in caspase-3 activity which led to cell apoptosis. This study confirms the efficacy of naringenin that lead to cell death in epidermoid carcinoma cells via inducing ROS generation, mitochondrial depolarization, nuclear condensation, DNA fragmentation, cell cycle arrest in G0/G1 phase and caspase-3 activation.

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Related in: MedlinePlus

DNA fragmentation analysis.DNA fragmentation of A431cell treated with 100 µM, 200 µM and 300 µM of naringenin. 1st well showing the 3 kb DNA marker. DNA laddering pattern showed that naringenin induces DNA fragmentation in a dose dependent manner.
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pone-0110003-g005: DNA fragmentation analysis.DNA fragmentation of A431cell treated with 100 µM, 200 µM and 300 µM of naringenin. 1st well showing the 3 kb DNA marker. DNA laddering pattern showed that naringenin induces DNA fragmentation in a dose dependent manner.

Mentions: Naringenin was tested to ascertain the DNA damage following exposure of various concentrations of compound to A431 cells. The results obtained from the DNA fragmentation assay (Fig. 5) showed the undamaged DNA in control cells whereas naringenin treated cells represent DNA fragmentation which was increased in a dose dependent manner. Small shearing was observed in the cells treated with 100 µM and 300 µM of naringenin, though maximum fragmentation was observed at 500 µM of naringenin exposure.


Induction of apoptosis and antiproliferative activity of naringenin in human epidermoid carcinoma cell through ROS generation and cell cycle arrest.

Ahamad MS, Siddiqui S, Jafri A, Ahmad S, Afzal M, Arshad M - PLoS ONE (2014)

DNA fragmentation analysis.DNA fragmentation of A431cell treated with 100 µM, 200 µM and 300 µM of naringenin. 1st well showing the 3 kb DNA marker. DNA laddering pattern showed that naringenin induces DNA fragmentation in a dose dependent manner.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4199682&req=5

pone-0110003-g005: DNA fragmentation analysis.DNA fragmentation of A431cell treated with 100 µM, 200 µM and 300 µM of naringenin. 1st well showing the 3 kb DNA marker. DNA laddering pattern showed that naringenin induces DNA fragmentation in a dose dependent manner.
Mentions: Naringenin was tested to ascertain the DNA damage following exposure of various concentrations of compound to A431 cells. The results obtained from the DNA fragmentation assay (Fig. 5) showed the undamaged DNA in control cells whereas naringenin treated cells represent DNA fragmentation which was increased in a dose dependent manner. Small shearing was observed in the cells treated with 100 µM and 300 µM of naringenin, though maximum fragmentation was observed at 500 µM of naringenin exposure.

Bottom Line: The search for antiproliferative agents that reduce skin carcinoma is a task of great importance.The intracellular ROS generation assay showed statistically significant (p<0.001) dose-related increment in ROS production for naringenin.Cell cycle study showed that naringenin induced cell cycle arrest in G0/G1 phase of cell cycle and caspase-3 analysis revealed a dose dependent increment in caspase-3 activity which led to cell apoptosis.

View Article: PubMed Central - PubMed

Affiliation: Department of Zoology, Shibli National (PG) College, Azamgarh, Uttar Pradesh, India.

ABSTRACT
A natural predominant flavanone naringenin, especially abundant in citrus fruits, has a wide range of pharmacological activities. The search for antiproliferative agents that reduce skin carcinoma is a task of great importance. The objective of this study was to analyze the anti-proliferative and apoptotic mechanism of naringenin using MTT assay, DNA fragmentation, nuclear condensation, change in mitochondrial membrane potential, cell cycle kinetics and caspase-3 as biomarkers and to investigate the ability to induce reactive oxygen species (ROS) initiating apoptotic cascade in human epidermoid carcinoma A431 cells. Results showed that naringenin exposure significantly reduced the cell viability of A431 cells (p<0.01) with a concomitant increase in nuclear condensation and DNA fragmentation in a dose dependent manner. The intracellular ROS generation assay showed statistically significant (p<0.001) dose-related increment in ROS production for naringenin. It also caused naringenin-mediated epidermoid carcinoma apoptosis by inducing mitochondrial depolarization. Cell cycle study showed that naringenin induced cell cycle arrest in G0/G1 phase of cell cycle and caspase-3 analysis revealed a dose dependent increment in caspase-3 activity which led to cell apoptosis. This study confirms the efficacy of naringenin that lead to cell death in epidermoid carcinoma cells via inducing ROS generation, mitochondrial depolarization, nuclear condensation, DNA fragmentation, cell cycle arrest in G0/G1 phase and caspase-3 activation.

Show MeSH
Related in: MedlinePlus