Oxidative damage to macromolecules in atopic dermatitis patients

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

Research output: Contribution to journalArticle

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), plasma MDA levels were significantly increased in atopic dermatitis patients compared to controls (1.45 and 0.80 μ M/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.

Original languageEnglish
Pages (from-to)456-461
Number of pages6
JournalKorean Journal of Dermatology
Volume53
Issue number6
Publication statusPublished - 2015 Jul 1

Fingerprint

Atopic Dermatitis
Reactive Oxygen Species
DNA Damage
Lymphocytes
Oxidative Stress
Antioxidants
Lipid Peroxidation
Control Groups
Malondialdehyde
Comet Assay
Granulocytes
Reverse Transcription
Oxidation-Reduction
Flow Cytometry
Urine
Lipids
Polymerase Chain Reaction

Keywords

  • Atopic dermatitis
  • Oxidative stress
  • Reactive oxygen species (ROS)

ASJC Scopus subject areas

  • Dermatology

Cite this

Lee, E. I., Oh, E. H., Song, H. J., Choi, W. J., Baek, J. O., Lee, J. R., & Roh, J. Y. (2015). Oxidative damage to macromolecules in atopic dermatitis patients. Korean Journal of Dermatology, 53(6), 456-461.

Oxidative damage to macromolecules in atopic dermatitis patients. / Lee, Eun Il; Oh, Eun Ha; Song, Hae Jun; Choi, Won Jun; Baek, Jin Ok; Lee, Jong Rok; Roh, Joo Young.

In: Korean Journal of Dermatology, Vol. 53, No. 6, 01.07.2015, p. 456-461.

Research output: Contribution to journalArticle

Lee, EI, Oh, EH, Song, HJ, Choi, WJ, Baek, JO, Lee, JR & Roh, JY 2015, 'Oxidative damage to macromolecules in atopic dermatitis patients', Korean Journal of Dermatology, vol. 53, no. 6, pp. 456-461.
Lee, Eun Il ; Oh, Eun Ha ; Song, Hae Jun ; Choi, Won Jun ; Baek, Jin Ok ; Lee, Jong Rok ; Roh, Joo Young. / Oxidative damage to macromolecules in atopic dermatitis patients. In: Korean Journal of Dermatology. 2015 ; Vol. 53, No. 6. pp. 456-461.
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AB - 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), plasma MDA levels were significantly increased in atopic dermatitis patients compared to controls (1.45 and 0.80 μ M/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.

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