Evidence map›Paper›PMID 22732187›Full record

ArticleFree radical biology & medicine2012

Lutein and zeaxanthin supplementation reduces photooxidative damage and modulates the expression of inflammation-related genes in retinal pigment epithelial cells.

Qingning Bian, Shasha Gao, Jilin Zhou, Jian Qin, Allen Taylor, Elizabeth J Johnson, Guangwen Tang, Janet R Sparrow, Dennis Gierhart, Fu Shang

Abstract read
In one paragraph

Article in Free radical biology & medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed, 4 pooled it
12.8field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

95 citing papers in PubMed, 4 syntheses or guidelines pooled it, 232 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. A dose-response meta-analysis of dietary lutein and zeaxanthin intake in relation to risk of age-related cataract.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2014
    Pooled it
  5. Macular peeling-induced retinal damage: clinical and histopathological evaluation after using different dyes.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2018
    Trial
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  12. Freeze-Dried Extracts ofPreventive nutrition and food science · 2026
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35 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 2 countries.

Qingning BianJean Mayer USDA Human Nutrition Research Center on Aging, Tufts University, Boston, MA 02111, USA.
Shasha Gao
Jilin Zhou
Jian Qin
Allen Taylor
Elizabeth J Johnson
Guangwen Tang
Janet R Sparrow
Dennis Gierhart
Fu Shang
Jean Mayer Human Nutrition Research Center on Aging · USTufts University · USColumbia University · US

Funding

Instrumentation, Fabrication, and Design CoreP30EY019007 · NEI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Xin Zhang · 2010 to 2026
$12.9M
IMPACT OF LIPOFUSCIN IN RETINAL PIGMENT EPITHELIAL CELLSR01EY012951 · NEI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI SPARROW, JANET RUTHE · 2000 to 2024
$8.9M
Ubiquitin Function In Eye LensR01EY013250 · NEI · TUFTS UNIVERSITY BOSTON · PI TAYLOR, ALLEN · 2001 to 2012
$4.0M
Role of ubiqutin in quality control of lens proteinsR01EY011717 · NEI · TUFTS UNIVERSITY BOSTON · PI SHANG, FU · 2003 to 2010
$1.8M
Mechanistically linking AMD, glycemic index and protein homeostasisR01EY021212 · NEI · TUFTS UNIVERSITY BOSTON · PI TAYLOR, ALLEN · 2011 to 2013
$1.2M
UBIQUITIN DEPENDENT PATHWAY AND LENS EPITHELIUMR29EY011717 · NEI · TUFTS UNIVERSITY BOSTON · PI SHANG, FU · 1998 to 2002
$381k
NEI NIH HHS EY011717NEI NIH HHS P30 EY019007NEI NIH HHS R01 EY011717NEI NIH HHS R01 EY012951NEI NIH HHS R01 EY013250NEI NIH HHS R01 EY021212NEI NIH HHS R29 EY011717
6 · The paper itself

Abstract

Oxidative damage and inflammation are related to the pathogenesis of age-related macular degeneration (AMD). Epidemiologic studies suggest that insufficient dietary lutein and zeaxanthin intake or lower serum zeaxanthin levels are associated with increased risk for AMD. The objective of this work is to test the protective effects of lutein and zeaxanthin against photooxidative damage to retinal pigment epithelial cells (RPE) and oxidation-induced changes in expression of inflammation-related genes. To mimic lipofuscin-mediated photooxidation in vivo, we used ARPE-19 cells that accumulated A2E, a lipofuscin fluorophore and photosensitizer, as a model system to investigate the effects of lutein and zeaxanthin supplementation. The data show that supplementation with lutein or zeaxanthin in the medium resulted in accumulation of lutein or zeaxanthin in the RPE cells. The concentrations of lutein and zeaxanthin in the cells were 2- to 14-fold of that detected in the medium, indicating that ARPE-19 cells actively take up lutein or zeaxanthin. As compared with untreated cells, exposure of A2E-containing RPE to blue light resulted in a 40-60% decrease in proteasome activity, a 50-80% decrease in expression of CFH and MCP-1, and an~20-fold increase in expression of IL-8. The photooxidation-induced changes in expression of MCP-1, IL-8, and CFH were similar to those caused by chemical inhibition of the proteasome, suggesting that inactivation of the proteasome is involved in the photooxidation-induced alteration in expression of these inflammation-related genes. Incubation of the A2E-containing RPE with lutein or zeaxanthin prior to blue light exposure significantly attenuated the photooxidation-induced inactivation of the proteasome and photooxidation-induced changes in expression of MCP-1, IL-8, and CFH. Together, these data indicate that lutein or zeaxanthin modulates inflammatory responses in cultured RPE in response to photooxidation. Protecting the proteasome from oxidative inactivation appears to be one of the mechanisms by which lutein and zeaxanthin modulate the inflammatory response. Similar mechanisms may explain salutary effects of lutein and zeaxanthin in reducing the risk for AMD.

Indexed as

Ultraviolet RaysCells, CulturedChemokine CCL2Complement Factor HCulture MediaDietary SupplementsDown-RegulationGene ExpressionHumansInflammation MediatorsInterleukin-6Interleukin-8LuteinMacular DegenerationOxidation-ReductionOxidative StressCCL2 protein, humanChemokine CCL2Complement Factor HCulture MediaCXCL8 protein, humanIL6 protein, humanInflammation MediatorsInterleukin-6Interleukin-8LuteinProteasome Endopeptidase ComplexRadiation-Protective AgentsXanthophyllsZeaxanthins

Identifiers

PMID22732187
PMCPMC3744865
OpenAlexW2026085655

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.