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Vitamin D status is linked with plasma glutathione and cysteine thiol/disulfide redox status in adults (260.4)
Author(s) -
Alvarez Jessica,
Chowdhury Ritam,
Jones Dean,
Martin Greg,
Brigham Kenneth,
Bigo Jose,
Ziegler Thomas,
Tangpricha Vin
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.260.4
Subject(s) - glutathione , glutathione disulfide , cysteine , cystine , thiol , redox , chemistry , inflammation , medicine , vitamin c , pathophysiology , endocrinology , oxidative stress , vitamin d and neurology , biochemistry , enzyme , organic chemistry
Objective: Redox status and inflammation are important in the pathophysiology of numerous chronic diseases. Epidemiological studies have linked vitamin D nutriture to a number of chronic diseases. We examined the relationships between serum 25‐hydroxyvitamin D (25(OH)D) concentrations and circulating biomarkers of redox and inflammation. Methods: We studied a community‐based cohort of working adults in Atlanta, GA (N=693). Plasma thiol/disulfide redox status was determined by HPLC [glutathione (GSH), glutathione disulfide (GSSG), cysteine (Cys), cystine (CySS), and their calculated redox potentials (Eh), calculated by the Nernst equation]. Pro‐inflammatory biomarkers included IL‐6, IL‐8, TNF‐α, and C‐reactive protein. Relationships were assessed by multiple linear regression. Results: Serum 25(OH)D levels were positively associated with plasma GSH levels, a more reducing GSH/GSSG EhCys, and inversely with Cys levels (P<0.001). These associations were not influenced by subject age, gender, race, % body fat, and cardiovascular risk factors (P<0.02). Serum 25(OH)D was not independently associated with any inflammatory marker. Conclusion: Serum 25(OH)D levels were independently associated with major plasma thiol/disulfide redox systems, suggesting that vitamin D status may be involved in redox‐mediated pathophysiology. Grant Funding Source : Supported by NIH (T32DK007298, UL1TR000454, K23AR054334, and K24RR023356).