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Differentiating racial differences in oxidative stress levels: in vitro and in vivo
Author(s) -
Feairheller Deborah L,
Park JoonYoung,
Sturgeon Kathleen M,
Kim Boa,
Williamson Sheara T,
Diaz Keith M,
Brown Michael D
Publication year - 2010
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.24.1_supplement.lb592
Subject(s) - oxidative stress , superoxide dismutase , umbilical vein , nitric oxide , in vivo , antioxidant , chemistry , medicine , in vitro , oxidative phosphorylation , reactive oxygen species , endothelial dysfunction , endocrinology , andrology , biochemistry , biology , genetics
Black (B) ethnicity has become a strong independent risk factor for cardiovascular disease, endothelial dysfunction, and enhanced oxidative stress. Identifying the racial differences in specific origins of oxidative stress is paramount to guiding future mechanistic research. We examined racial differences in oxidative stress markers, in healthy B (N=9) and White (W) (N=9) young adults (21± .4 yrs) as well as in B (N=4) and W (N=4) Human Umbilical Vein Endothelial Cells (HUVECs). A heightened oxidative stress level in B was confirmed. In unstimulated culture, B HUVECs had significantly lower superoxide dismutase activity (SOD) indicating active O 2 − scavenging. We also found enhanced nitric oxide (NO) levels in B HUVECs suggesting overproduction of NO in response to increased O 2 − . Finally, B HUVECs had higher levels of total antioxidant capacity (TAC), a measure of all antioxidants including those that quench ONOO − . Likewise in humans, we found higher oxidative stress in B adults through significantly higher plasma levels of protein carbonyls, TAC, and SOD. B adults also had lower plasma NO levels relative to W, which is consistent with previous research demonstrating higher ADMA and lower NO levels in young B males. In conclusion, based on these preliminary findings, our future mechanistic research will focus on expression of SOD and NOS isoforms to identify where the racial differences exist in activation of these oxidative stress markers. NIH/NHLBI RO1 HL085497 & NIH/NIA KO1 AG019640