Genotoxic effects of carotenoid breakdown products in human retinal pigment epithelial cells

Nilesh M. Kalariya, Kota Ramana, Satish Srivastava, Frederik J G M Van Kuijk

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

Purpose: To investigate the genotoxic effects of lutein (LBP) and β -carotene breakdown products (β -apo-8-carotenal, BA8C) and the preventive role of GSH in human retinal pigment epithelial cells (ARPE-19). Methods: LBP- and BA8C-induced DNA damage in human retinal pigment epithelial cells (ARPE-19) was determined by comet assay. The DNA damage was quantified by the image analysis system using Comet Score™ software. ARPE-19 cell viability was determined by CellTiter 96 AQueous one-solution cell proliferation assay kit. Intracellular GSH levels were measured by Ellman's reagent. Results: Incubation of serum-starved ARPE-19 cells with LBP and BA8C caused significant DNA damage in a dose- and time-dependent manner. The DNA damage and cell death incurred by LBP and BA8C were significantly prevented by N-acetylcysteine (NAC) but not by α -tocopherol ascorbic acid (T AA). Furthermore, BSO-induced GSH depletion in ARPE-19 cells caused a significant elevation in LBP- and BA8C-induced DNA damage, whereas increased GSH levels in ARPE-19 cells prevented it. Conclusions: Our results suggest that breakdown products of dietary carotenoids could be genotoxic in ARPE-19 cells. LBP-induced genotoxic effects could worsen oxidative stress. The intracellular GSH pool in ARPE-19 cells might play a critical role in carotenoid breakdown products-induced genotoxicity.

Original languageEnglish (US)
Pages (from-to)737-747
Number of pages11
JournalCurrent Eye Research
Volume34
Issue number9
DOIs
StatePublished - 2009

Fingerprint

Retinal Pigments
Carotenoids
DNA Damage
Epithelial Cells
Dithionitrobenzoic Acid
Lutein
Comet Assay
Tocopherols
Acetylcysteine
Ascorbic Acid
Cell Survival
Oxidative Stress
Cell Death
Software
Cell Proliferation
Serum

Keywords

  • Age-related macular degeneration
  • Antioxidants
  • Carotenoid breakdown products
  • Carotenoids
  • DNA damage
  • Lutein breakdown products

ASJC Scopus subject areas

  • Ophthalmology
  • Sensory Systems
  • Cellular and Molecular Neuroscience

Cite this

Genotoxic effects of carotenoid breakdown products in human retinal pigment epithelial cells. / Kalariya, Nilesh M.; Ramana, Kota; Srivastava, Satish; Van Kuijk, Frederik J G M.

In: Current Eye Research, Vol. 34, No. 9, 2009, p. 737-747.

Research output: Contribution to journalArticle

Kalariya, Nilesh M. ; Ramana, Kota ; Srivastava, Satish ; Van Kuijk, Frederik J G M. / Genotoxic effects of carotenoid breakdown products in human retinal pigment epithelial cells. In: Current Eye Research. 2009 ; Vol. 34, No. 9. pp. 737-747.
@article{f3ec96649a1e49a9972df8d3c481375f,
title = "Genotoxic effects of carotenoid breakdown products in human retinal pigment epithelial cells",
abstract = "Purpose: To investigate the genotoxic effects of lutein (LBP) and β -carotene breakdown products (β -apo-8-carotenal, BA8C) and the preventive role of GSH in human retinal pigment epithelial cells (ARPE-19). Methods: LBP- and BA8C-induced DNA damage in human retinal pigment epithelial cells (ARPE-19) was determined by comet assay. The DNA damage was quantified by the image analysis system using Comet Score™ software. ARPE-19 cell viability was determined by CellTiter 96 AQueous one-solution cell proliferation assay kit. Intracellular GSH levels were measured by Ellman's reagent. Results: Incubation of serum-starved ARPE-19 cells with LBP and BA8C caused significant DNA damage in a dose- and time-dependent manner. The DNA damage and cell death incurred by LBP and BA8C were significantly prevented by N-acetylcysteine (NAC) but not by α -tocopherol ascorbic acid (T AA). Furthermore, BSO-induced GSH depletion in ARPE-19 cells caused a significant elevation in LBP- and BA8C-induced DNA damage, whereas increased GSH levels in ARPE-19 cells prevented it. Conclusions: Our results suggest that breakdown products of dietary carotenoids could be genotoxic in ARPE-19 cells. LBP-induced genotoxic effects could worsen oxidative stress. The intracellular GSH pool in ARPE-19 cells might play a critical role in carotenoid breakdown products-induced genotoxicity.",
keywords = "Age-related macular degeneration, Antioxidants, Carotenoid breakdown products, Carotenoids, DNA damage, Lutein breakdown products",
author = "Kalariya, {Nilesh M.} and Kota Ramana and Satish Srivastava and {Van Kuijk}, {Frederik J G M}",
year = "2009",
doi = "10.1080/02713680903046855",
language = "English (US)",
volume = "34",
pages = "737--747",
journal = "Current Eye Research",
issn = "0271-3683",
publisher = "Informa Healthcare",
number = "9",

}

TY - JOUR

T1 - Genotoxic effects of carotenoid breakdown products in human retinal pigment epithelial cells

AU - Kalariya, Nilesh M.

AU - Ramana, Kota

AU - Srivastava, Satish

AU - Van Kuijk, Frederik J G M

PY - 2009

Y1 - 2009

N2 - Purpose: To investigate the genotoxic effects of lutein (LBP) and β -carotene breakdown products (β -apo-8-carotenal, BA8C) and the preventive role of GSH in human retinal pigment epithelial cells (ARPE-19). Methods: LBP- and BA8C-induced DNA damage in human retinal pigment epithelial cells (ARPE-19) was determined by comet assay. The DNA damage was quantified by the image analysis system using Comet Score™ software. ARPE-19 cell viability was determined by CellTiter 96 AQueous one-solution cell proliferation assay kit. Intracellular GSH levels were measured by Ellman's reagent. Results: Incubation of serum-starved ARPE-19 cells with LBP and BA8C caused significant DNA damage in a dose- and time-dependent manner. The DNA damage and cell death incurred by LBP and BA8C were significantly prevented by N-acetylcysteine (NAC) but not by α -tocopherol ascorbic acid (T AA). Furthermore, BSO-induced GSH depletion in ARPE-19 cells caused a significant elevation in LBP- and BA8C-induced DNA damage, whereas increased GSH levels in ARPE-19 cells prevented it. Conclusions: Our results suggest that breakdown products of dietary carotenoids could be genotoxic in ARPE-19 cells. LBP-induced genotoxic effects could worsen oxidative stress. The intracellular GSH pool in ARPE-19 cells might play a critical role in carotenoid breakdown products-induced genotoxicity.

AB - Purpose: To investigate the genotoxic effects of lutein (LBP) and β -carotene breakdown products (β -apo-8-carotenal, BA8C) and the preventive role of GSH in human retinal pigment epithelial cells (ARPE-19). Methods: LBP- and BA8C-induced DNA damage in human retinal pigment epithelial cells (ARPE-19) was determined by comet assay. The DNA damage was quantified by the image analysis system using Comet Score™ software. ARPE-19 cell viability was determined by CellTiter 96 AQueous one-solution cell proliferation assay kit. Intracellular GSH levels were measured by Ellman's reagent. Results: Incubation of serum-starved ARPE-19 cells with LBP and BA8C caused significant DNA damage in a dose- and time-dependent manner. The DNA damage and cell death incurred by LBP and BA8C were significantly prevented by N-acetylcysteine (NAC) but not by α -tocopherol ascorbic acid (T AA). Furthermore, BSO-induced GSH depletion in ARPE-19 cells caused a significant elevation in LBP- and BA8C-induced DNA damage, whereas increased GSH levels in ARPE-19 cells prevented it. Conclusions: Our results suggest that breakdown products of dietary carotenoids could be genotoxic in ARPE-19 cells. LBP-induced genotoxic effects could worsen oxidative stress. The intracellular GSH pool in ARPE-19 cells might play a critical role in carotenoid breakdown products-induced genotoxicity.

KW - Age-related macular degeneration

KW - Antioxidants

KW - Carotenoid breakdown products

KW - Carotenoids

KW - DNA damage

KW - Lutein breakdown products

UR - http://www.scopus.com/inward/record.url?scp=70350663221&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=70350663221&partnerID=8YFLogxK

U2 - 10.1080/02713680903046855

DO - 10.1080/02713680903046855

M3 - Article

VL - 34

SP - 737

EP - 747

JO - Current Eye Research

JF - Current Eye Research

SN - 0271-3683

IS - 9

ER -