TY - JOUR
T1 - Oxidative stress and altered antioxidant defenses in children with acute exacerbation of atopic dermatitis
AU - Tsukahara, Hirokazu
AU - Shibata, Rumiko
AU - Ohshima, Yusei
AU - Todoroki, Yukiko
AU - Sato, Shuko
AU - Ohta, Naoko
AU - Hiraoka, Masahiro
AU - Yoshida, Akira
AU - Nishima, Sankei
AU - Mayumi, Mitsufumi
N1 - Funding Information:
We are grateful to Dr. Mitsuhiko Nambu, Tenri Hospital, Nara, and Dr. Masao Morita, Hamamatsu Rosai Hospital, Shizuoka, for including patients under their care in this study. We also thank Ms. Michiyo Toyooka for the excellent technical assistance. This study was supported by a Health Sciences Research Grant from the Ministry of Health, Labor and Welfare, Japan.
PY - 2003/4/18
Y1 - 2003/4/18
N2 - The underlying mechanisms of skin inflammation in atopic dermatitis (AD) are not completely understood. The purpose of the present study was to examine the involvement of oxidative stress and antioxidant defenses in children with acute exacerbation of AD. We studied 13 children who were hospitalized for acute exacerbation of AD with purulent skin infection by Staphylococcal aureus (age, 1.5 to 10.0 years), and 28 age-matched healthy subjects (controls). Urine samples obtained from the patients on admission, on 2nd and 7th-9th hospital days, as well as from the controls were analyzed for 8-hydroxy-2′-deoxyguanosine (8-OHdG) (a marker of oxidative DNA damage), acrolein-lysine adducts (a marker of lipid peroxidation), bilirubin oxidative metabolites (BOM) (a marker of antioxidant activity of bilirubin under oxidative stress) and nitrite/nitrate (NOx-) (a marker of endogenous nitric oxide production). Of these, urinary concentrations of 8-OHdG, acrolein-lysine adducts and BOM, but not NOx-, were significantly higher in AD children on admission than those in control subjects. Response to treatment was associated with significant falls in the concentrations of 8-OHdG and acrolein-lysine adducts. Urinary concentrations of acrolein-lysine adducts, but not 8-OHdG, were still significantly higher in AD patients on the 7th-9th hospital day relative to the control. Urinary BOM remained almost constant and significantly high in AD children during hospitalization. Our findings indicate that oxidative stress and altered antioxidant defenses are involved in the pathophysiology of acute exacerbation of AD, and that suppression of oxidative stress might be a potentially useful strategy for the treatment of AD.
AB - The underlying mechanisms of skin inflammation in atopic dermatitis (AD) are not completely understood. The purpose of the present study was to examine the involvement of oxidative stress and antioxidant defenses in children with acute exacerbation of AD. We studied 13 children who were hospitalized for acute exacerbation of AD with purulent skin infection by Staphylococcal aureus (age, 1.5 to 10.0 years), and 28 age-matched healthy subjects (controls). Urine samples obtained from the patients on admission, on 2nd and 7th-9th hospital days, as well as from the controls were analyzed for 8-hydroxy-2′-deoxyguanosine (8-OHdG) (a marker of oxidative DNA damage), acrolein-lysine adducts (a marker of lipid peroxidation), bilirubin oxidative metabolites (BOM) (a marker of antioxidant activity of bilirubin under oxidative stress) and nitrite/nitrate (NOx-) (a marker of endogenous nitric oxide production). Of these, urinary concentrations of 8-OHdG, acrolein-lysine adducts and BOM, but not NOx-, were significantly higher in AD children on admission than those in control subjects. Response to treatment was associated with significant falls in the concentrations of 8-OHdG and acrolein-lysine adducts. Urinary concentrations of acrolein-lysine adducts, but not 8-OHdG, were still significantly higher in AD patients on the 7th-9th hospital day relative to the control. Urinary BOM remained almost constant and significantly high in AD children during hospitalization. Our findings indicate that oxidative stress and altered antioxidant defenses are involved in the pathophysiology of acute exacerbation of AD, and that suppression of oxidative stress might be a potentially useful strategy for the treatment of AD.
KW - 8-Hydroxy-2′-deoxyguanosine
KW - Acrolein
KW - Acute exacerbation
KW - Atopic dermatitis
KW - Bilirubin oxidative metabolites
KW - Oxidative stress
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U2 - 10.1016/S0024-3205(03)00145-0
DO - 10.1016/S0024-3205(03)00145-0
M3 - Article
C2 - 12650859
AN - SCOPUS:0345700746
VL - 72
SP - 2509
EP - 2516
JO - Life Sciences
JF - Life Sciences
SN - 0024-3205
IS - 22
ER -