Influence of naringin on ferric iron induced oxidative damage in vitro

Ganesh Chandra Jagetia, Tiyyagura Koti Reddy, V. A. Venkatesha, Rajendra Kedlaya

Research output: Contribution to journalArticle

47 Citations (Scopus)

Abstract

Background: Iron is essential for oxygen transport and a variety of cellular processes like respiration and DNA synthesis. It may become toxic when not handled carefully by cellular proteins and shielded from surrounding media. Naringin treatment may help to overcome the iron-induced toxic effects in vitro. Methods: HepG2 cells were treated with 0.5, 1, 2.5, and 5 mmol/l naringin 1 h before exposure to 0.1, 0.25, 0.5, and 1 mmol/l ferric iron. The effect of iron or naringin or their combination treatment was studied on cell survival, DNA double-strand break induction, DNA oxidation, lipid peroxidation, and various antioxidants. Results: The exposure of cells to iron caused a dose-dependent decline in their clonogenic potential, while naringin pretreatment resulted in a significant elevation in the cell survival. Exposure of cells to iron resulted in a time-dependent elevation in DNA strand breaks and a peak level of DNA strand breaks was observed at 24 h, while naringin pretreatment inhibited the DNA double-strand breaks accompanied by an early repair. Similarly, treatment of HepG2 cells with iron caused increased DNA oxidation that showed reduction when cells were pretreated with naringin. The iron overload caused a significant elevation in the lipid peroxidation accompanied by depletion in glutathione (GSH) concentration, while naringin inhibited lipid peroxidation and arrested the iron-induced depletion in the GSH concentration. Iron treatment also reduced various antioxidant enzymes like glutathione peroxidase (GSHPx), catalase, and superoxide dismutase (SOD). Pretreatment of HepG2 cells with naringin resulted in an elevation in all the antioxidant enzymes. Conclusions: E-nhanced antioxidant status by naringin could compensate the oxidative stress and may facilitate an early recovery from iron-induced genomic insult in vitro.

Original languageEnglish
Pages (from-to)189-197
Number of pages9
JournalClinica Chimica Acta
Volume347
Issue number1-2
DOIs
Publication statusPublished - 01-09-2004
Externally publishedYes

Fingerprint

Iron
DNA
Hep G2 Cells
Antioxidants
Lipid Peroxidation
DNA Breaks
Double-Stranded DNA Breaks
Poisons
Lipids
Cell Survival
In Vitro Techniques
naringin
Cells
Iron Overload
Oxidation
Oxidative stress
Enzymes
Glutathione Peroxidase
Catalase
Superoxide Dismutase

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Clinical Biochemistry
  • Biochemistry, medical

Cite this

Chandra Jagetia, G., Koti Reddy, T., Venkatesha, V. A., & Kedlaya, R. (2004). Influence of naringin on ferric iron induced oxidative damage in vitro. Clinica Chimica Acta, 347(1-2), 189-197. https://doi.org/10.1016/j.cccn.2004.04.022
Chandra Jagetia, Ganesh ; Koti Reddy, Tiyyagura ; Venkatesha, V. A. ; Kedlaya, Rajendra. / Influence of naringin on ferric iron induced oxidative damage in vitro. In: Clinica Chimica Acta. 2004 ; Vol. 347, No. 1-2. pp. 189-197.
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Chandra Jagetia, G, Koti Reddy, T, Venkatesha, VA & Kedlaya, R 2004, 'Influence of naringin on ferric iron induced oxidative damage in vitro', Clinica Chimica Acta, vol. 347, no. 1-2, pp. 189-197. https://doi.org/10.1016/j.cccn.2004.04.022

Influence of naringin on ferric iron induced oxidative damage in vitro. / Chandra Jagetia, Ganesh; Koti Reddy, Tiyyagura; Venkatesha, V. A.; Kedlaya, Rajendra.

In: Clinica Chimica Acta, Vol. 347, No. 1-2, 01.09.2004, p. 189-197.

Research output: Contribution to journalArticle

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N2 - Background: Iron is essential for oxygen transport and a variety of cellular processes like respiration and DNA synthesis. It may become toxic when not handled carefully by cellular proteins and shielded from surrounding media. Naringin treatment may help to overcome the iron-induced toxic effects in vitro. Methods: HepG2 cells were treated with 0.5, 1, 2.5, and 5 mmol/l naringin 1 h before exposure to 0.1, 0.25, 0.5, and 1 mmol/l ferric iron. The effect of iron or naringin or their combination treatment was studied on cell survival, DNA double-strand break induction, DNA oxidation, lipid peroxidation, and various antioxidants. Results: The exposure of cells to iron caused a dose-dependent decline in their clonogenic potential, while naringin pretreatment resulted in a significant elevation in the cell survival. Exposure of cells to iron resulted in a time-dependent elevation in DNA strand breaks and a peak level of DNA strand breaks was observed at 24 h, while naringin pretreatment inhibited the DNA double-strand breaks accompanied by an early repair. Similarly, treatment of HepG2 cells with iron caused increased DNA oxidation that showed reduction when cells were pretreated with naringin. The iron overload caused a significant elevation in the lipid peroxidation accompanied by depletion in glutathione (GSH) concentration, while naringin inhibited lipid peroxidation and arrested the iron-induced depletion in the GSH concentration. Iron treatment also reduced various antioxidant enzymes like glutathione peroxidase (GSHPx), catalase, and superoxide dismutase (SOD). Pretreatment of HepG2 cells with naringin resulted in an elevation in all the antioxidant enzymes. Conclusions: E-nhanced antioxidant status by naringin could compensate the oxidative stress and may facilitate an early recovery from iron-induced genomic insult in vitro.

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Chandra Jagetia G, Koti Reddy T, Venkatesha VA, Kedlaya R. Influence of naringin on ferric iron induced oxidative damage in vitro. Clinica Chimica Acta. 2004 Sep 1;347(1-2):189-197. https://doi.org/10.1016/j.cccn.2004.04.022