Document Detail


Protective effects of memantine and epicatechin on catechol-induced toxicity on Müller cells in vitro.
MedLine Citation:
PMID:  20347921     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
This study evaluates the toxic effects of catechol (a component from cigarette smoke) on Müller cells (MIO-M1) in vitro, and investigates the inhibitors memantine and epicatechin to determine if they can reverse the catechol toxic effects. MIO-M1 cells were exposed to varying concentrations of catechol with or without memantine or epicatechin. Cell viability (CV) was measured by a trypan blue dye-exclusion assay. Caspase-3/7 activity was measured by fluorochrome assay. The production of reactive oxygen/nitrogen species (ROS/RNS) was measured with 2',7'-dichlorodihydrofluorescein diacetate dye assay. Mitochondrial membrane potential (DeltaPsim) was measured using JC-1 assay. Intracellular ATP content was determined by the ATPLite kit. MIO-M1 cells showed significant decrease in cell viability, increased caspase-3/7 activity, elevated ROS/RNS levels, decreased DeltaPsim value, and decreased intracellular ATP content after exposure to catechol 150, 300, and 600 microM compared with control. Pre-treatment with memantine 10 microM or epicatechin 15 microM reversed loss of cell viability in catechol 150 microM-treated cultures (22.3%, p<0.01 and 17.8%, p<0.05), respectively. Similarly, pre-treatment with memantine 10 microM and epicatechin 15 microM prior to catechol resulted in decreased caspase-3/7 activities (77% and 64.2%, p<0.001), decreased ROS/RNS levels (82.3% and 79%, p<0.001), increased DeltaPsim value (76.4% and 72.2%, p<0.001), and increased ATP levels (46.6% and 40.4%, p<0.001) compared to 150 microM catechol-treated cultures. Catechol, a component of smoking, can diminish cell viability and mitochondrial function in MIO-M1 cells in vitro. However, memantine and epicatechin can partially reverse the cytotoxic effect of catechol. Their administration may reduce or prevent Müller cells degeneration in AMD or other retinal degenerative disorders.
Authors:
Saffar Mansoor; Navin Gupta; Georgia Luczy-Bachman; G Astrid Limb; Baruch D Kuppermann; M Cristina Kenney
Publication Detail:
Type:  Journal Article     Date:  2010-03-27
Journal Detail:
Title:  Toxicology     Volume:  271     ISSN:  1879-3185     ISO Abbreviation:  Toxicology     Publication Date:  2010 May 
Date Detail:
Created Date:  2010-05-10     Completed Date:  2010-05-20     Revised Date:  2014-02-19    
Medline Journal Info:
Nlm Unique ID:  0361055     Medline TA:  Toxicology     Country:  Ireland    
Other Details:
Languages:  eng     Pagination:  107-14     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Benzimidazoles / metabolism
Carbocyanines / metabolism
Caspase 3 / analysis,  metabolism
Catechin / pharmacology*
Catechols / toxicity*
Cell Survival / drug effects
Fluoresceins / metabolism
Fluorescent Dyes / metabolism
Humans
Memantine / pharmacology*
Membrane Potential, Mitochondrial / drug effects
Mitochondria / metabolism
Protective Agents / pharmacology*
Reactive Oxygen Species / metabolism
Retina / cytology,  drug effects*,  metabolism
Grant Support
ID/Acronym/Agency:
G0900002//Medical Research Council
Chemical
Reg. No./Substance:
0/2',7'-dichlorodihydrofluorescein diacetate; 0/Benzimidazoles; 0/Carbocyanines; 0/Catechols; 0/Fluoresceins; 0/Fluorescent Dyes; 0/Protective Agents; 0/Reactive Oxygen Species; 21527-78-6/5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolocarbocyanine; 8R1V1STN48/Catechin; EC 3.4.22.-/Caspase 3; LF3AJ089DQ/catechol; W8O17SJF3T/Memantine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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