Cutaneous and ocular toxicology · 2013
Serum paraoxonase activity and oxidative status in subjects with alopecia areata.
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Bilgili Serap Gunes, Ozkol Halil, Karadag Ayse Serap, Ozkol Hatice Uce, Seker Ayse, Calka Omer, Aslan Mehmet
Аннотация
INTRODUCTION: Previous studies have suggested that oxidative stress may play an important role in the pathogenesis of alopecia areata (AA) but these reports are limited and conflicting.
OBJECTIVES: The aim of this study was to investigate serum paraoxonase-1 (PON1) activity and oxidative status in subjects with AA.
MATERIALS AND METHODS: Thirty-nine subjects with AA and 39 healthy controls were enrolled. Serum PON1 activity, total antioxidant capacity (TAC), total oxidant status (TOS) and oxidative stress index (OSI) were determined.
RESULTS: Serum TAC levels and PON1 activity were significantly lower in the subjects with AA than controls (p = 0.038, p = 0.001, respectively), whereas TOS levels and OSI were significantly higher (both, p = 0.001) in the subjects with AA.
CONCLUSIONS: Our results suggest that reduced PON1 activity may be related to increased oxidant and decreased antioxidant levels. These data indicated that oxidant/antioxidant imbalance may play a role in the etiopathogenesis of AA.
OBJECTIVES: The aim of this study was to investigate serum paraoxonase-1 (PON1) activity and oxidative status in subjects with AA.
MATERIALS AND METHODS: Thirty-nine subjects with AA and 39 healthy controls were enrolled. Serum PON1 activity, total antioxidant capacity (TAC), total oxidant status (TOS) and oxidative stress index (OSI) were determined.
RESULTS: Serum TAC levels and PON1 activity were significantly lower in the subjects with AA than controls (p = 0.038, p = 0.001, respectively), whereas TOS levels and OSI were significantly higher (both, p = 0.001) in the subjects with AA.
CONCLUSIONS: Our results suggest that reduced PON1 activity may be related to increased oxidant and decreased antioxidant levels. These data indicated that oxidant/antioxidant imbalance may play a role in the etiopathogenesis of AA.