Protective effect of lycopene on oxidative stress-induced cell death of pancreatic acinar cells

Jeong Yeon Seo, Atsushi Masamune, Tooru Shimosegawa, Hye Young Kim

Research output: Chapter in Book/Report/Conference proceedingConference contribution

21 Citations (Scopus)

Abstract

Previously we showed that the underlying mechanism of oxidative stress-induced apoptosis is nuclear loss of DNA repair protein Ku70 and Ku80, which are involved in the DNA repair process of double-strand breaks. Lycopene acts as an antioxidant and a singlet oxygen quencher. In the present study, we aim to investigate whether lycopene protects oxidative stress-induced cell death of pancreatic acinar AR42J cells by preventing the loss of Ku70 in the nucleus. The cells received oxidative stress caused by glucose oxidase acting on β-D-glucose (glucose/glucose oxidase) and were cultured in the absence or presence of various concentrations of lycopene. Viable cell numbers, the levels of H2O2 in the medium, level of Ku70 protein, and Ku-DNA-binding activity were determined. As a result, glucose/glucose oxidase induced the decrease in cell viability, increase in H2O2 production, decrease in Ku70 levels in whole-cell extracts and nuclear extracts, and decrease in Ku-DNA-binding activity of AR42J cells. Lycopene inhibited glucose/glucose oxidase-induced cell death by preventing nuclear loss of Ku70 and a decrease in Ku-DNA-binding activity of AR42J cells. In conclusion, lycopene may be beneficial for the treatment of oxidative stress-induced cell death by preventing loss of DNA repair protein Ku70.

Original languageEnglish
Title of host publicationNatural Compounds and Their Role in Apoptotic Cell Signaling Pathways
PublisherBlackwell Publishing Inc.
Pages570-575
Number of pages6
ISBN (Print)9781573317375
DOIs
Publication statusPublished - 2009 Jan 1

Publication series

NameAnnals of the New York Academy of Sciences
Volume1171
ISSN (Print)0077-8923
ISSN (Electronic)1749-6632

Fingerprint

Oxidative stress
Acinar Cells
Cell death
Glucose Oxidase
Oxidative Stress
Cell Death
DNA Repair
DNA
Glucose
Repair
Cells
Singlet Oxygen
DNA-Binding Proteins
Proteins
Cell Extracts
Cell Survival
Cell Count
Antioxidants
lycopene
Apoptosis

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

Cite this

Seo, J. Y., Masamune, A., Shimosegawa, T., & Kim, H. Y. (2009). Protective effect of lycopene on oxidative stress-induced cell death of pancreatic acinar cells. In Natural Compounds and Their Role in Apoptotic Cell Signaling Pathways (pp. 570-575). (Annals of the New York Academy of Sciences; Vol. 1171). Blackwell Publishing Inc.. https://doi.org/10.1111/j.1749-6632.2009.04712.x
Seo, Jeong Yeon ; Masamune, Atsushi ; Shimosegawa, Tooru ; Kim, Hye Young. / Protective effect of lycopene on oxidative stress-induced cell death of pancreatic acinar cells. Natural Compounds and Their Role in Apoptotic Cell Signaling Pathways. Blackwell Publishing Inc., 2009. pp. 570-575 (Annals of the New York Academy of Sciences).
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Seo, JY, Masamune, A, Shimosegawa, T & Kim, HY 2009, Protective effect of lycopene on oxidative stress-induced cell death of pancreatic acinar cells. in Natural Compounds and Their Role in Apoptotic Cell Signaling Pathways. Annals of the New York Academy of Sciences, vol. 1171, Blackwell Publishing Inc., pp. 570-575. https://doi.org/10.1111/j.1749-6632.2009.04712.x

Protective effect of lycopene on oxidative stress-induced cell death of pancreatic acinar cells. / Seo, Jeong Yeon; Masamune, Atsushi; Shimosegawa, Tooru; Kim, Hye Young.

Natural Compounds and Their Role in Apoptotic Cell Signaling Pathways. Blackwell Publishing Inc., 2009. p. 570-575 (Annals of the New York Academy of Sciences; Vol. 1171).

Research output: Chapter in Book/Report/Conference proceedingConference contribution

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T1 - Protective effect of lycopene on oxidative stress-induced cell death of pancreatic acinar cells

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AU - Shimosegawa, Tooru

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PY - 2009/1/1

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N2 - Previously we showed that the underlying mechanism of oxidative stress-induced apoptosis is nuclear loss of DNA repair protein Ku70 and Ku80, which are involved in the DNA repair process of double-strand breaks. Lycopene acts as an antioxidant and a singlet oxygen quencher. In the present study, we aim to investigate whether lycopene protects oxidative stress-induced cell death of pancreatic acinar AR42J cells by preventing the loss of Ku70 in the nucleus. The cells received oxidative stress caused by glucose oxidase acting on β-D-glucose (glucose/glucose oxidase) and were cultured in the absence or presence of various concentrations of lycopene. Viable cell numbers, the levels of H2O2 in the medium, level of Ku70 protein, and Ku-DNA-binding activity were determined. As a result, glucose/glucose oxidase induced the decrease in cell viability, increase in H2O2 production, decrease in Ku70 levels in whole-cell extracts and nuclear extracts, and decrease in Ku-DNA-binding activity of AR42J cells. Lycopene inhibited glucose/glucose oxidase-induced cell death by preventing nuclear loss of Ku70 and a decrease in Ku-DNA-binding activity of AR42J cells. In conclusion, lycopene may be beneficial for the treatment of oxidative stress-induced cell death by preventing loss of DNA repair protein Ku70.

AB - Previously we showed that the underlying mechanism of oxidative stress-induced apoptosis is nuclear loss of DNA repair protein Ku70 and Ku80, which are involved in the DNA repair process of double-strand breaks. Lycopene acts as an antioxidant and a singlet oxygen quencher. In the present study, we aim to investigate whether lycopene protects oxidative stress-induced cell death of pancreatic acinar AR42J cells by preventing the loss of Ku70 in the nucleus. The cells received oxidative stress caused by glucose oxidase acting on β-D-glucose (glucose/glucose oxidase) and were cultured in the absence or presence of various concentrations of lycopene. Viable cell numbers, the levels of H2O2 in the medium, level of Ku70 protein, and Ku-DNA-binding activity were determined. As a result, glucose/glucose oxidase induced the decrease in cell viability, increase in H2O2 production, decrease in Ku70 levels in whole-cell extracts and nuclear extracts, and decrease in Ku-DNA-binding activity of AR42J cells. Lycopene inhibited glucose/glucose oxidase-induced cell death by preventing nuclear loss of Ku70 and a decrease in Ku-DNA-binding activity of AR42J cells. In conclusion, lycopene may be beneficial for the treatment of oxidative stress-induced cell death by preventing loss of DNA repair protein Ku70.

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M3 - Conference contribution

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T3 - Annals of the New York Academy of Sciences

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PB - Blackwell Publishing Inc.

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Seo JY, Masamune A, Shimosegawa T, Kim HY. Protective effect of lycopene on oxidative stress-induced cell death of pancreatic acinar cells. In Natural Compounds and Their Role in Apoptotic Cell Signaling Pathways. Blackwell Publishing Inc. 2009. p. 570-575. (Annals of the New York Academy of Sciences). https://doi.org/10.1111/j.1749-6632.2009.04712.x