Document Detail

Role of antioxidants in the survival of normal and vitiliginous avian melanocytes.
MedLine Citation:
PMID:  10644011     Owner:  NLM     Status:  MEDLINE    
Mutant feather melanocytes from Barred Plymouth Rock (BPR) and White Leghorn (WL) chickens are currently being used as avian models of vitiligo. Feather melanocytes in BPR and WL chickens die prematurely in vivo due to low (50-66%) antioxidant glutathione and superoxide dismutase levels when compared to the wild type Jungle Fowl (JF) melanocytes. Excess superoxide anions, generated by xanthine:xanthine oxidase (X:XO), caused a 15-20% increase in mortality after 1 and 2 hrs. in all three genotypes of in vitro melanocytes as compared to control values that received no X:XO. Overall, the JF wild type melanocytes had the lowest mortality rate, WL melanocytes had the highest mortality rate and the BPR melanocytes had an intermediate mortality rate. Superoxide anion and hydroxyl radical production in the WL feather were double the production in the JF wild type feather. The production of reactive oxygen species in BPR was intermediate to the other two genotypes. In an effort to mimic the low antioxidant levels of the BPR and WL feathers in the JF feather, JF in vitro feather melanocytes were treated with buthionine sulfoximine (BSO), a glutathione synthesis inhibitor. With BSO added to the medium, the JF mortality rates increased by 20-25%, reaching the mortality levels of the mutant BPR melanocytes. The addition of iron to the JF melanocyte X:XO medium increased their mortality rate by 20%, probably via the Fenton reaction. Thus, antioxidants play an extremely important role in both the viability of normal avian melanocytes and the premature death of the vitiliginous avian melanocytes. A working hypothesis, supported in part by the current results, is that the premature death of the mutant melanocytes could be precipitated in the poorly vascularized feather by low antioxidant protection due to both low turnover of tissue fluids which contain SOD and to genetically determined low levels of internal antioxidant protection in these melanocytes. This same mechanistic hypothesis could apply as "a" cause of premature melanocyte cell death in human vitiligo wherein the vitiliginous melanocytes may have a genetic defect in their antioxidant protection system and blood flow to an area may be restricted.
R R Bowers; B Nguyen; S Buckner; Y Gonzalez; F Ruiz
Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Cellular and molecular biology (Noisy-le-Grand, France)     Volume:  45     ISSN:  0145-5680     ISO Abbreviation:  Cell. Mol. Biol. (Noisy-le-grand)     Publication Date:  1999 Nov 
Date Detail:
Created Date:  2000-03-15     Completed Date:  2000-03-15     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  9216789     Medline TA:  Cell Mol Biol (Noisy-le-grand)     Country:  FRANCE    
Other Details:
Languages:  eng     Pagination:  1065-74     Citation Subset:  IM    
Department of Biology and Microbiology, California State University, Los Angeles, 90032, USA.
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MeSH Terms
Antioxidants / metabolism*
Buthionine Sulfoximine / pharmacology
Cell Survival
Chickens / genetics
Disease Models, Animal
Feathers / cytology*,  metabolism
Ferrous Compounds / pharmacology
Glutathione / physiology*
Hydroxyl Radical / metabolism
Melanocytes / cytology*,  metabolism
Models, Biological
Oxidative Stress
Pigmentation / genetics
Reactive Oxygen Species / metabolism
Superoxide Dismutase / physiology*
Superoxides / metabolism
Vitiligo / genetics,  pathology*
Grant Support
2S06RR08101-21/RR/NCRR NIH HHS
Reg. No./Substance:
0/Antioxidants; 0/Ferrous Compounds; 0/Reactive Oxygen Species; 11062-77-4/Superoxides; 3352-57-6/Hydroxyl Radical; 5072-26-4/Buthionine Sulfoximine; 70-18-8/Glutathione; 7758-94-3/ferrous chloride; EC Dismutase

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