期刊
CLINICAL ENDOCRINOLOGY
卷 81, 期 3, 页码 458-466出版社
WILEY
DOI: 10.1111/cen.12449
关键词
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资金
- National Center for Advancing Translational Sciences of the National Institutes of Health [UL1 TR000454]
- National Institutes of Health [K23 AR054334, T32 DK007298-32S1, P20 HL113451, K24 DK096574]
Objective Redox status and inflammation are important in the pathophysiology of numerous chronic diseases. Epidemiological studies have linked vitamin D status to a number of chronic diseases. We aimed to examine the relationships between serum 25-hydroxyvitamin D [25(OH)D] and circulating thiol/disulphide redox status and biomarkers of inflammation. Design This was a cross-sectional study of N = 693 adults (449 females, 244 males) in an apparently healthy, working cohort in Atlanta, GA. Plasma glutathione (GSH), cysteine (Cys) and their associated disulphides were determined with high-performance liquid chromatography, and their redox potentials (E-h GSSG and E-h CySS) were calculated using the Nernst equation. Serum inflammatory markers included interleukin-6 (IL-6), interleukin-8 (IL-8) and tumour necrosis factor-alpha, assayed on a multiplex platform, and C-reactive protein (CRP), assayed commercially. Relationships were assessed with multiple linear regression analyses. Results Serum 25(OH)D was positively associated with plasma GSH (beta +/- SE: 0.002 +/- 0.0004) and negatively associated with plasma E-h GSSG (beta +/- SE: -0.06 +/- 0.01) and Cys (beta +/- SE: -0.01 +/- 0.003) (P < 0.001 for all); statistical significance remained after adjusting for age, gender, race, percentage body fat and traditional cardiovascular risk factors (P = 0.01-0.02). The inverse relationship between serum 25(OH) D and CRP was confounded by percentage body fat, and full adjustment for covariates attenuated serum 25(OH) D relationships with other inflammatory markers to nonstatistical significance. Conclusions Serum 25(OH) D concentrations were independently associated with major plasma thiol/disulphide redox systems, suggesting that vitamin D status may be involved in redox-mediated pathophysiology.
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