Oxidative Damage to Macromolecules in Atopic Dermatitis Patients

Lee, Eunil; Oh, Eun Ha; Song, Hae Jun; Choi, Won Jun; Baek, Jin Ok; Lee, Jong Rok; Roh, Joo Young

Abstract

BACKGROUND
Excessive exposure to reactive oxygen species (ROS) or decreased antioxidants leads to damage of proteins, lipids, and DNA. Previous studies suggest that oxidative stress may be important in the pathogenesis of atopic dermatitis.
OBJECTIVE
To investigate whether oxidative stress is increased in atopic dermatitis patients compared to a normal control group, we examined DNA damage, lipid peroxidation, ROS production and antioxidant expression.
METHODS
Patients with atopic dermatitis (n=16; mean Scoring Atopic Dermatitis [SCORAD] index=53.06) were investigated compared to a normal control group (n=25). To examine DNA damage in the cellular level, we performed comet assays on lymphocytes and granulocytes taken from patients and control group. To measure lipid peroxidation products, urine and plasma malondialdehyde (MDA) levels were analyzed. To examine intracellular redox in lymphocytes, ROS were measured using flow cytometry. Expression of superoxide dismutase (SOD) 1, 2 antioxidants were analyzed using reverse transcription polymerase chain reaction (RT-PCR).
RESULTS
Atopic dermatitis patients showed severe DNA damage compared to the control group in both lymphocytes (1.89 and 1.51, respectively, p<0.05) and granulocytes (2.07 and 1.58, respectively, p<0.05). While urine MDA levels were not significantly different between groups (1.64 and 1.13 microM/g respectively, p>0.05), plasma MDA levels were significantly increased in atopic dermatitis patients compared to controls (1.45 and 0.80 microM/g respectively, p<0.005). ROS production by activated lymphocytes was increased in atopic dermatitis patients compared to controls. SOD 1, 2 were expressed in all atopic dermatitis patients without significant increase compared to controls.
CONCLUSION
Increased DNA damage, lipid peroxidation and ROS production in lymphocytes as indices of oxidative stress were observed in moderate to severe atopic dermatitis patients compared to normal control. Although precise mechanism of oxidative stress on the pathogenesis of atopic dermatitis is not defined yet, decreasing ROS exposure or augmenting antioxidant defenses may be alternative therapeutic approaches for atopic dermatitis.