The Effects of Vitamins E and D Supplementation on Erythrocyte Superoxide Dismutase and Catalase in Atopic Dermatitis

Article excerpt


Background: Atopic dermatitis is a public health problem worldwide. Increment of reactive oxygen species (ROS) production may be one of the contributing factors of tissue damage in atopic dermatitis. The present study was designed to determine the effect of vitamins E and/or D on erythrocyte superoxide dismutase and catalase activities in patients with atopic dermatitis.

Methods: In a randomized, double blind, placebo controlled clinical trial 45 atopic dermatitis patients were divided into four groups. Each group received one of the following supplements for 60 days: group A (n=11) vitamins E and D placebos; group B (n= 12) 1600 international unit (IU) vitamin D3 plus vitamin E placebo; group C (n=11) 600 IU synthetic all-rac-α tocopherol plus vitamin D placebo; group D (n=11) 1600 IU vitamin D3 plus 600 IU synthetic all-rac-α tocopherol. Erythrocyte superoxide dismutase (SOD) and catalase activities, serum 25 (OH) D, plasma α-tocopherol were determined. The data were analyzed by analysis of variance (ANOVA) and paired t-test.

Results: After 60 days vitamin D and E supplementation, erythrocyte SOD activities increased in groups B, C and D (P= 0.002, P= 0.016 and P= 0.015, respectively). Erythrocyte catalase activities increased in groups B and D (P= 0.026 and P= 0.004, respectively). The increment of erythrocyte catalase activity was not significant in group C. There was a positive significant correlation between SOD activity and serum 25 (OH) D (r= 0.378, P= 0.01).

Conclusions: It is concluded that vitamin D is as potent as vitamin E in increasing the activities of erythrocyte SOD and catalase in atopic dermatitis patients.

Keywords: Atopic dermatitis, Vitamin E, Vitamin D, Superoxide dismutase, Catalase


Atopic dermatitis (AD) is a highly pruritic, chronic, and relapsing inflammatory skin disease characterized by typically distributed eczematous skin lesions (1). Atopic dermatitis is a public health problem worldwide. Its lifetime prevalence is 10-20% and 1-3% among children and adults, respectively. Prevalence of AD has increased by two to three folds during the past three decades in industrialized countries. Atopic dermatitis is the most common cause of occupational skin disease in adults (2).

Skin inflammation in AD is characterized by an intense infiltration of lymphocytes and eosinophils. These cells release pro-inflammatory cytokines, superoxide radical, hydrogen peroxide and peroxinitrite (3). Oxidative stress contributes to adverse effects on the skin, in form of erythema, edema, wrinkling, inflammation, hypersensitivity and keratinization abnormality (4). It seems that reactive oxygen species (ROS) are involved in the pathogenesis of allergic inflammation; therefore, increased ROS production may be one of the contributing factors of tissue damage in atopic dermatitis (5-7). Defense mechanisms exist to cope with oxidative stress. These systems are consisted of two main groups; the group of antioxidant enzymes and the group of the non-enzymatic antioxidants. Some of antioxidant enzymes include superoxide dismutase (SOD), catalase, glutathione peroxidase (GPX), and glutathione reductase (GR) (3).

Superoxide dismutase (SOD) is an antioxidant enzyme which catalyses the dismutation of superoxide anion to O2 and H2O2. H2O2 is then deactivated to H2O by catalase (8).

Some non-enzymatic antioxidants include α-tocopherol and β-carotene which are located in the cellular membranes and defend against lipid peroxidation, as well as interacting with free radicals. The increased membrane lipid peroxidation may stimulate immune and inflammatory response (6).

Although considerable effort has been put into studying the antioxidant effects of vitamin E and its protective effects on oxidative damage, the role of vitamin D as a potential antioxidant has not been fully investigated. Vitamin D is well recognized for its action on calcium and phosphorus metabolism, and its beneficial effects on bone metabolism (9). …