Disparate antioxidant enzyme activities in cultured human cutaneous fibroblasts, keratinocytes, and melanocytes

Antioxidant enzyme activities of cultured human foreskin fibroblasts, keratinocytes, and melanocytes from healthy black and Caucasian donors were measured and compared. Fibroblasts had more (p less than 0.05) peroxidase, catalase, glutathione peroxidase, and superoxide dismutase activity than keratinocytes. Keratinocytes had more (p less than 0.05) peroxidase, catalase, glutathione peroxidase, and superoxide dismutase activity than melanocytes. No differences in antioxidant enzyme activities were observed between the cells of any type taken from black or Caucasian people. Antioxidant enzyme activities may affect resistance to damage by oxidants induced by ultraviolet radiation and inflammation.     

Lipid peroxidation and antioxidant defence system in patients with active or inactive Behçet's disease

To evaluate plasma lipid peroxidation and enzymatic and non-enzymatic antioxidant systems in patients with Beh?et's disease, plasma malondialdehyde levels and total antioxidant status, erythrocyte superoxide dismutase and whole blood glutathione peroxidase activities were studied in 15 patients with active disease and in 30 with inactive disease, and compared with 20 age-matched healthy control subjects. Plasma malondialdehyde levels were significantly higher in patients with active Beh?et's disease than in patients with inactive disease, who had significantly higher levels than control subjects. The plasma total antioxidant status of both groups of patients was significantly lower than that of controls. Furthermore, whole blood glutathione peroxidase activity was significantly lower in patients with active versus inactive Beh?et's disease. There were no significant differences in erythrocyte superoxide dismutase levels between the groups. In conclusion, there is an increase in oxidative stress in Beh?et's disease. Despite this stress, the antioxidant system is deficient and inadequate, especially in patients who are in an active phase of the disease.     

Solar simulated irradiation modulates gene expression and activity of antioxidant enzymes in cultured human dermal fibroblasts

Exposure of skin to solar irradiation generates reactive oxygen species that damage DNA, membranes, mitochondria and proteins. To protect against such damage, skin cells have evolved antioxidant enzymes including glutathione peroxidase (GSH-Px), copper and zinc-dependent superoxide dismutase (SOD1), the mitochondrial manganese-dependent superoxide dismutase (SOD2), and catalase. This report examines the effect of a single low or moderate dose exposure to solar-simulating combined UVB and UVA irradiation on the gene expression and activities of these antioxidant enzymes in cultured normal human fibroblasts. We find that both doses initially decrease GSH-Px, SOD2 and catalase activities, but within 5 days after irradiation the activities of the enzymes return to pre-irradiation level (catalase) or are induced slightly (SOD1, GSH-Px) or substantially (SOD2) above the basal level. For SOD1, SOD2 and catalase, the higher dose also detectably modulates the mRNA level of these enzymes. Our results indicate that the effects of a single physiologic solar simulated irradiation dose persist for at least several days and suggest that skin cells prepare for subsequent exposure to damaging irradiation by upregulating this antioxidant defense system, in particular the mitochondrial SOD2. Our findings are consistent with the existence of a broad-based SOS-like response in irradiated human skin.     

Parameters related to oxygen free radicals in human skin: a study comparing healthy epidermis and skin cancer tissue

In vitro studies with tumor cells have demonstrated that oxygen free radicals are involved in the development of skin cancers and that variations in the body's defense mechanisms can modify the course of the disease. To assess the validity of this hypothesis in spontaneous tumors, we determined glutathione S-transferase, superoxide dismutase, reduced and oxidized glutathione, and thiobarbituric acid reactive substances in healthy whole skin (n = 95), dermis (n = 73), and epidermis (n = 69). The values were compared with those obtained in three types of skin cancer: basal cell carcinoma (n = 16), squamous cell carcinoma (n = 6), and melanoma (n = 33). In healthy skin, glutathione S-transferase, superoxide dismutase, reduced glutathione, and oxidized glutathione were higher in epidermis than in dermis, whereas thiobarbituric acid reactive substances were higher in dermis than in epidermis; whole skin had intermediate values. These results suggest that there is an induction of some anti-oxygen free radicals mechanisms in epidermis as a result of increased oxygen free radicals production. Glutathione S-transferase and thiobarbituric acid reactive substances were higher in all types of tumor than in healthy epidermis but oxidized glutathione was lower. Reduced glutathione and superoxide dismutase activity were lower in basal cell carcinoma and squamous cell carcinoma samples. Glutathione S-transferase increased, whereas superoxide dismutase and thiobarbituric acid reactive substances decreased in melanoma samples in direct relation to the Clark levels. Higher glutathione S-transferase activity, particularly in the most invasive forms of melanoma, indicates that this type of cancer is more malignant. Similarly, a decrease in superoxide dismutase activity can also encourage progression of the tumor. These results are in accord with those from tumor cell cultures and could suggest new strategies (gene therapy) for managing skin cancer.     

Roxithromycin decreases ultraviolet B irradiation-induced reactive oxygen intermediates production and apoptosis of keratinocytes

BACKGROUND: In addition to their antimicrobial action, roxithromycin (RXM), a new 14-membrane macrolide antibiotics, have immunomodulatory, anti-inflammatory and anti-oxidative activity. Ultraviolet B (UVB) irradiation induces reactive oxygen intermediates and apoptosis of keratinocytes. OBJECTIVE: To examine the anti-apoptotic and anti-oxidative effect of RXM on UVB-irradiated keratinocytes. METHODS: UVB-induced apoptosis was determined by cell death assay using crystal violet staining, and DNA fragmentation assay. Superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), and calatase activities were measured in UVB-irradiated SV40-trasnformed human keratinocytes (SVHK cells). Detection of superoxide was performed histologically using hydroethidine and colorimetric quantitative assay using ferrous irons. H(2)O(2) was measured by colorimetrical assay. RESULTS: RXM suppressed UVB-induced apoptosis of SVHK cells. UVB-irradiated SVHK cells showed decreased SOD, GPx, GR, and catalase activities. RXM pretreatment suppressed the decrease in these enzyme activities with the maximal effect detected at 10microM of RXM. The effect was associated with suppression of UVB-induced superoxide and H(2)O(2) production. CONCLUSION: The present study demonstrated that RXM has anti-apoptotic and anti-oxidative effects against UVB-irradiated keratinocytes.     

Tiron protects against UVB-induced senescence-like characteristics in human dermal fibroblasts by the inhibition of superoxide anion production and glutathione depletion

Background/Objectives: Free radicals and reactive oxygen species (ROS), which are generated by UV irradiation, may induce an irreversible growth arrest similar to senescence. Tiron, 4,5-dihydroxy-1,3-benzene disulfonic acid, is a widely used antioxidant to rescue ROS-evoked cell death. The aim of the article was to explore the effects of tiron on skin photoaging and associated mechanisms. Methods: The effects of tiron on cell proliferation were determined using 3-(4,5-dimethylthiazol-2-Yl)-2,5-diphenyltetrazolium bromide. Senescent cells were determined by morphology and senescence-associated β-galactosidase activity analysis. Intracellular hydrogen peroxide, superoxide anion and glutathione concentration were analysed by a fluorescent probe. The concomitant changes of protein expression were analysed with Western blot. Results: Human dermal fibroblasts were induced to premature senescence by sub-cytotoxic doses of irradiated UVB. Strong senescence-associated β-galactosidase activity and increased intracellular superoxide anion were observed in human dermal fibroblasts irradiated by UVB. Tiron blocks UVB-induced glutathione depletion and increase of superoxide anion and protects against UVB-induced senescence-like characteristics in human dermal fibroblasts. Compared with normal fibroblasts, UVB-irradiated human dermal fibroblasts showed a higher ratio of active (hypophosphorylated) to inactive (phosphorylated) forms of Rb and p38, upregulation of p53 or p16 and c-Myc and insulin-like growth factor 1 (IGF-1) downregulation. After treatment with tiron, p53, p16 c-Myc and IGF-1 as well as phosphorylation Rb and p38 could partially recover. Conclusion: These results indicate that tiron protects against UVB-induced senescence-like characteristics in human dermal fibroblasts via the inhibition of production of superoxide anion and glutathione depletion, and modulation of related senescence proteins.     

Culture and drug biotransformation capacity of adult human keratinocytes from post-mortem skin

Summary 'I'hc aim of this study was to analyse viability, growth, differentiation and drug metabolic capacity of cultured human keratinocytes obtained from post-mortem skin. Epidermal cells were prepared from 1-day post-mortem paired sun-exposed (outer) and sun-protected (inner) sites of the upper arm. of donors aged 47–80 years, The percentage of viable cells obtained from post-mortem skin was only slightly lower than that usually obtained for keratinocytes isolated from fresh skin, and no alterations of epidermal markers were noted. Keratinocytes isolated post-mortem from non-exposed skin had a higher viability (78 versus 73%). and a more active proliferation, while their attachment rate, keratin composition, lipid synthesis capacity and transglutaminase activity levels were similar to those of epidermal cells obtained from the sun-exposed skin. Keratinocytes Isolated from postmortem skin expressed various phase I and II activities at levels similar to those obtained with keratinocytes isolated from fresh skin while drug metabolizing enzyme activities were consistently higher in sun-exposed compared to sun-protected cells. The results support the conclusion that skin collected post-mortem can represent an alternative source of viable and functional epidermal cells, and that the functional changes that occur in adult keratinocytes habitually exposed to the sun, affect much more strongly the drug metabolism capacity than the expression of differentiation markers.     

Effects of ultraviolet A and B irradiation on lipid peroxidation and activity of the antioxidant enzymes in keratinocytes in culture.

Human keratinocytes (NCTC 2544) in culture were exposed to various combinations of ultraviolet A (UVA) and UVB irradiation and at 0.5 h postirradiation the level of lipid peroxidation and activities of antioxidant enzymes were measured. The results suggest that UV irradiation is capable of inducing lipid peroxidation reactions, as parameters of which the amount of thiobarbituric acid-reactive material and the number of conjugated diene double bonds were measured. Both UVA and UVB irradiation were also found to affect the activities of antioxidant enzymes. Following UVB irradiation the activity of superoxide dismutase (Cu/Zn form) was decreased, and combination of increasing doses of UVA irradiation to a given dose of UVB irradiation decreased the activity of both catalase and superoxide dismutase. In summary, this study suggests that both UVA and UVB irradiation are capable of inducing lipid peroxidation reactions and an impairment of the enzymic antioxidant system in human keratinocytes in culture.     

A comparative study of superoxide dismutase, catalase, and glutathione peroxidase activities and nitrate levels in vitiligo patients

BACKGROUND: Several groups have shown the involvement of oxidative stress in the pathophysiology of vitiligo. METHODS: In this study, we examined the erythrocyte and plasma activities of glutathione peroxidase and Cu/Zn superoxide dismutase, plasma nitrite/nitrate levels, and erythrocyte catalase activity in 23 vitiligo patients and 25 controls. RESULTS: The results show that erythrocyte superoxide dismutase activity and plasma nitrite/nitrate levels are high in vitiligo patients. CONCLUSIONS: Our study confirms that oxidative stress is involved in the pathophysiology of vitiligo, as indicated by the high levels of erythrocyte superoxide dismutase activity and plasma nitrite/nitrate.     

Comparison of ultraviolet B-induced imbalance of antioxidant status in foreskin- and abdominal skin-derived human fibroblasts

Ultraviolet B radiation (UVB) is involved in the development of deleterious cutaneous damage. Several changes could be attributed to UVB-induced reactive oxygen species attacks in fibroblasts. However dermal cells from young and adult skin could respond differently to oxidative stress. So antioxidant status and its consequences on cytotoxicity and apoptosis were compared in child foreskin fibroblasts (FF) and adult abdominal skin fibroblasts (AF) in response to UVB. Basal levels of lipid peroxidation tended to be higher in AF than in FF, which could be related to a reshaping of antioxidant defences (higher catalase and lower superoxide dismutase activities). AF and FF appeared to react similarly to high UVB doses as regards cytotoxicity and apoptosis which increased significantly 24h after exposure. The enhancement of cell death could be due to the inherent oxidative stress: glutathione appeared significantly decreased in both cell populations. As a consequence AF, but not FF, presented significantly increased levels of lipid peroxidation, which could be explained by the pre-cited differences of basal antioxidant defences. These results suggest that AF and FF do not respond to UVB by the same pathway.     

Mitochondrial impairment in peripheral blood mononuclear cells during the active phase of vitiligo.

Several hypotheses have been made about the pathogenesis of vitiligo, and some of them have considered a systemic involvement in the course of the disease. Evidence has been presented on the role of oxidative stress as the initial event in melanocyte degeneration. In accordance with this view, we determined the levels of some antioxidants, i.e., superoxide dismutase, catalase, reduced glutathione, and vitamin E, in erythrocytes and/or peripheral blood mononuclear cells from patients with active or stable vitiligo and from a control group of healthy subjects. In erythrocytes the parameters evaluated were not significantly different. On the contrary, in peripheral blood mononuclear cells, superoxide dismutase activity was increased in both groups of patients, whereas catalase activity, reduced glutathione and vitamin E levels were decreased exclusively in subjects with active disease. The imbalance of antioxidants was associated with hyperproduction of reactive oxygen species due to a mitochondrial impairment as cyclosporin A, an inhibitor of the permeability transition pores opening, significantly reduced the reactive oxygen species production. Moreover an alteration of the mitochondrial transmembrane potential and a higher percentage of apoptotic cells were observed in active vitiligo patients. Based on these results, we suggest that, in vitiligo, mitochondria might be the target of different stimuli, such as reactive oxygen species generation, cytokines production, catecholamine release, alteration of Ca2+ metabolism, all of which capable of inducing melanocyte degeneration.     

Over-expression of Mn-superoxide dismutase as a marker of oxidative stress in lesional skin of chronic idiopathic urticaria

We studied the involvement of oxidative stress in chronic idiopathic urticaria (CIU), assessing the activities of superoxide dismutase (SOD) and glutathione and the levels of malondialdeyde (MDA), a marker of lipid peroxidation, in samples taken from lesional skin (n = 16) and nonlesional skin (n = 11) of CIU patients. The activity of SOD and glutathione and the levels of MDA were markedly increased in lesional skin as compared with skin of healthy subjects, whereas no differences were detected between nonlesional skin of CIU patients and control samples. Immuno-dot blot assay revealed an up-regulation of Mn-SOD expression in lesional skin. These findings show that oxidative stress is crucially involved in CIU. The evidence of lipid peroxidation and compensatory increase of Mn-SOD and glutathione activities in lesional skin, in the absence of any alteration in uninvolved skin, suggests that oxidative stress is secondary to the development of inflammation.     

Defects in antioxidant defense and calcium transport in the epidermis of xeroderma pigmentosum patients

Summary A comparative study of the antioxidant enzymes superoxide dismutase, catalase, glutathione reductase and thioredoxin reductase was undertaken in two families with xeroderma pigmentosum (XP) and in healthy controls of corresponding skin phototypes. Epidermal blister roofs obtained from the XP patients revealed significant decreases in catalase, thioredoxin reductase, and superoxide dismutase, but glutathione reductase was unaffected. In addition, keratinocytes established from XP patients contained a significantly higher than normal intracellular calcium concentration compared with control cells from a corresponding skin type. Keratinocytes established from an XP obligate heterozygote revealed intermediate levels of calcium between XP homozygotes and controls. Previously high intracellular calcium has been shown to compromise the redox status of keratinocytes by allosteric inhibition of the thioredoxin reductase/thioredoxin electron transfer system. In XP homozygous keratinocytes from sun-exposed epidermis, the intracellular concentration of reduced thioredoxin was decreased to 50% compared with these cells from unexposed skin. Taken together, the results from this study indicate that the epidermis in XP patients lacks effective defense against free radicals and peroxides. In addition to the well-established defect in the normal rates of unscheduled DNA repair, these findings provide an even better explanation for the multiple cutaneous neoplasms in these patients.     

Exogenous hydrogen sulphide supplement accelerates skin wound healing via oxidative stress inhibition and vascular endothelial growth factor enhancement

Hydrogen sulphide (H₂S) is an important gasotransmitter with several physiological functions. However, the roles and the detailed mechanisms of H₂S on skin wound healing are not known well. In the present study, 129S1/SvImJ mice were intraperitoneally injected with NaHS (50 μmol/kg/d) for 2 weeks. Then, a round wound of 6 mm diameter with depth into the dermis was made. The skin wound area, blood perfusion, superoxide production, malondialdehyde (MDA) levels, total antioxidant capacity (T‐AOC), expression of vascular endothelial growth factor (VEGF), dynamin‐related protein 1 (DRP1) and optic atrophy 1 (OPA1) were measured. After NaHS (50 μmol/L) pre‐administration for 4 hours, cell migration rate, DRP1, OPA1 and α–smooth muscle actin (α‐SMA) expression, superoxide production and mitochondrial membrane potential in primary skin fibroblasts were measured. Tube formation in human umbilical vein endothelial cells (HUVECs) and cell migration in human keratinocytes were also measured. The results showed that NaHS pretreatment significantly accelerated wound healing and improved blood flow in the wound after operation. NaHS increased VEGF expression in the wound and promoted tube formation in HUVECs. Meanwhile, NaHS attenuated reactive oxygen species (ROS) production, suppressed MDA level but restored T‐AOC in the wound. NaHS also promoted skin fibroblasts migration and α‐SMA expression after scratch. Moreover, NaHS alleviated ROS, increased mitochondrial membrane potential, decreased DRP1 but enhanced OPA1 expression in skin fibroblasts after scratch. NaHS also accelerated human keratinocytes migration after scratch. Taken together, exogenous H₂S supplementary accelerated the skin wound healing, which might be related to oxidative stress inhibition and VEGF enhancement.     

The role of free oxygen radicals in the aetiopathogenesis of rosacea

A possible link between superoxide dismutase activity and malondialdehyde level with the clinical manifestations of rosacea was investigated. We found differences in superoxide dismutase activities between mild rosacea (stages I and II) and severe involvement (stage III) groups, as well as between disease and control groups that were statistically significant (P < 0.05). In the mild involvement group (stages I and II), the superoxide dismutase activity was higher than in the control group (P < 0.05), while the malondialdehyde levels did not differ from the control. In the severe involvement group (stage III), the superoxide dismutase activity was lower than in the control group (P < 0.05), and this was coupled to a raised level of malondialdehyde (P < 0.05). These findings clearly show that in the mild involvement phase of rosacea patients, superoxide dismutase activity was stimulated to protect the skin against reactive oxygen species so that the malondialdehyde levels were maintained. In contrast, in more severe disease, due to a decrease in the capacity of the antioxidant defence system, the malondialdehyde levels were increased. These findings support the 'antioxidant system defect hypothesis' in rosacea patients.     

Aging- and photoaging-dependent changes of enzymic and nonenzymic antioxidants in the epidermis and dermis of human skin in vivo.

This is a comprehensive study of the changes in major antioxidant enzymes and antioxidant molecules during intrinsic aging and photoaging processes in the epidermis and dermis of human skin in vivo. We show that the activities of superoxide dismutase and glutathione peroxidase are not changed during these processes in human skin in vivo. Interestingly, the activity of catalase was significantly increased in the epidermis of photoaged (163%) and naturally aged (118%) skin (n = 9), but it was significantly lower in the dermis of photoaged (67% of the young skin level) and naturally aged (55%) skin compared with young (n = 7) skin. The activity of glutathione reductase was significantly higher (121%) in naturally aged epidermis. The concentration of alpha-tocopherol was significantly lower in the epidermis of photoaged (56% of young skin level) and aged (61%) skin, but this was not found to be the case in the dermis. Ascorbic acid levels were lower in both epidermis (69% and 61%) and dermis (63% and 70%) of photoaged and naturally aged skin, respectively. Gluta thione concentrations were also lower. Uric acid did not show any significant changes. Our results suggest that the components of the antioxidant defense system in human skin are probably regulated in a complex manner during the intrinsic aging and photoaging processes.     

E6* oncoprotein expression of human papillomavirus type-16 determines different ultraviolet sensitivity related to glutathione and glutathione peroxidase antioxidant defence

Clinical observations of non-melanoma skin cancer in immunocompromised patients, such as organ transplant recipients, suggest co-operative effects of human papillomavirus (HPV) and ultraviolet (UV) radiation. The aim of the present study is to evaluate UV sensitivity and DNA damage formation according to antioxidant status in HPV16-infected keratinocytes. We used SKv cell lines, infected with HPV16 and well characterized for their proliferative and tumorigenic capacities. We showed that SKv cell lines presented various E6* (a truncated form of E6) RNA levels. We demonstrated that the higher oncoprotein RNA expression level was associated with a higher resistance to solar-simulated radiation, more specifically to UVB radiation and to hydrogen peroxide. Moreover, this high resistance was associated with a low oxidative DNA damage formation after UV radiation and was related to high glutathione content and glutathione peroxidase activities. Therefore, the results of our study suggest that E6* levels could modulate the glutathione/glutathione peroxidase pathway providing a mechanism to protect HPV-infected keratinocytes against an environmental oxidative stress, such as UV radiation.     

Induction of manganese superoxide dismutase in human dermal fibroblasts: a UV-B-mediated paracrine mechanism with the release of epidermal interleukin 1 alpha,interleukin 1 beta,and tumor necrosis factor alpha

BACKGROUND: Reactive oxygen species generated in the skin by UV irradiation promote photoaging and photocarcinogenesis. The manganese (Mn) superoxide dismutase (SOD) is a primary antioxidant enzyme that crucially contributes to the homeostasis of oxygen radicals within the mitochondria, and thus critically participates in the control of senescence and tumor generation. OBJECTIVE: To determine whether repetitive UV-B exposure, as practiced for light hardening during phototherapy for various photodermatoses, can enhance the adaptive antioxidant response by up-regulating MnSOD activity in either the epidermal or the dermal skin compartment. DESIGN: In vitro experiments to determine MnSOD activity levels in cultured human dermal fibroblasts and epidermal cells (HaCaT cells and primary keratinocytes) at different times after direct UV-B exposure or after incubation of human dermal fibroblasts with supernatants from UV-B-irradiated epidermal cells. SETTING: Photobiological research laboratory in a university dermatology department. INTERVENTION: Irradiation of cultured human dermal fibroblasts and epidermal cells with UV-B. MAIN OUTCOME MEASURES: Manganese SOD messenger RNA and activity levels in cultured irradiated or mock-treated skin cells. RESULTS: No increase in MnSOD activity could be detected in fibroblasts or epidermal cells until 24 hours after UV-B irradiation. However, fibroblasts incubated with supernatants from UV-B-irradiated epidermal cells showed a marked increase in specific MnSOD messenger RNA and activity. Removal of interleukin 1alpha, interleukin 1beta, and tumor necrosis factor alpha from the supernatants led to a significant reduction of MnSOD mRNA in fibroblasts. CONCLUSION: Irradiation of the epidermal cells with UV-B induced a release of soluble factors that amplified MnSOD activity in fibroblasts via a paracrine mechanism.     

A comparative study of oxidant–antioxidant status in stable and active vitiligo patients

The pathogenetic mechanisms in vitiligo have not been completely clarified. One of the major hypotheses in the pathogenesis of vitiligo is the oxidative stress hypothesis. The active or stable phase of vitiligo is defined on the basis of the progression or appearance of new lesions in the last 3 months and the absence of new lesions or their progression in the last 6 months, respectively. Eighteen patients with active vitiligo, 18 patients with stable vitiligo, and 40 controls were included in this study. We examined serum levels of malondialdehyde, selenium, vitamin E and A, and the erythrocyte activities of glutathione peroxidase, superoxide dismutase, and catalase. Our results revealed a significantly higher level of serum malondialdehyde, selenium in patients with active disease compared with the controls. Significant higher increase in erythrocytes superoxide dismutase activities was observed in active vitiligo group, erythrocyte glutathione peroxidase activity was decreased significantly in active disease, whereas erythrocyte catalase activity and plasma vitamin E and A levels were not different in vitiligo patients as compared with controls. Our study shows that oxidative stress is involved in the pathophysiology of both active and stable vitiligo but increased imbalance of antioxidants was observed in the blood of active vitiligo patients.I dedicate this article to our dear director (Mme Hentati Basma) who dead in 06/06/06. We will never forget you and you are always in our heart.     

白癜风患者血清及皮损中某些酶及微量元素改变研究

本研究检测白癜风患者血清中超氧化物岐化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、黄嘌呤氧化酶(XOD)活性,丙二醛(MDA)水平及血清、皮肤中锌(Zn)、铜(Cu)、硒(Se)、铁(Fe)含量。结果表明:患者血清中GSH-Px、SOD活性及Cu含量低于对照组(P<0.01),MDA、Fe含量高于对照组(P<0.01).皮损处Zn、Cu、Se或Fe含量分别低于或高于周围外观正常皮肤,治疗后血清SOD、GSH-Px活性增高、Cu、Fe含量显著降低(P<0.01)。提示:白癜风患者自由基防御系统中部分酶活性降低,Zn、Cu、Se缺乏。