Stress In Vitiligo Research Articles

An Evaluation of the Hematological Markers of Systemic Inflammation and Oxidative Stress in Vitiligo: A Case-Control Study.

Introduction Melanocyte dysfunction in vitiligo is considered to be due to genetics, inflammation, and autoimmunity. Research has shown that oxidative stress plays a significant role in triggering these conditions. Currently, there are several markers indicating hematological inflammation and oxidative stress. This study aimed to investigate the status of inflammation and oxidative stress markers in vitiligo. Methods This study included patients with vitiligo and age-gender-matched healthy controls.C-reactive protein (CRP), neutrophil-to-lymphocyte ratio (NLR), monocyte-to-lymphocyte ratio (MLR), platelet-to-lymphocyte ratio (PLR), and monocyte-to-high-density lipoprotein ratio (MHR) and extent of vitiligo were calculated and compared. Results The study included 138 participants (69 vitiligo and 69 controls). The mean was 41.46 years with a female predominance (55.1%). The patient group demonstrated higher levels of platelets, neutrophils, CRP, NLR, MLR, PLR, and HDL and lower levels of lymphocytes and HDL compared to the control group (p>0,05).The only significantly different value between the groups was MHR (p=0.03). The generalized vitiligo group demonstrated higher levels of platelets, neutrophils, monocytes, CRP, NLR, PLR, and MLR, and lower levels of lymphocytes and HDL compared to the localized group. The only significantly different values between the groups were MHR and MLR (p=0.02, p=0.03). Conclusion This study found that MHR and CRP values were higher in vitiligo patients. Additionally, MHR and MLR values were higher in patients with generalized vitiligo. These results suggest that MHR is a reliable indicator marker for systemic inflammation and oxidative stress in vitiligo.

Antioxidant mechanisms of mesenchymal stem cells and their therapeutic potential in vitiligo.

Vitiligo is a skin pigmentation disorder caused by melanocyte damage or abnormal function. Reac-tive oxygen species Reactive oxygen species can cause oxidative stress damage to melanocytes, which in turn induces vitiligo. Traditional treatments such as phototherapy, drugs, and other methods of treatment are long and result in frequent recurrences. Currently, mesenchymal stem cells (MSCs) are widely used in the research of various disease treatments due to their excellent paracrine effects, making them a promising immunoregulatory and tissue repair strategy. Furthermore, an increasing body of evi-dence suggests that utilizing the paracrine functions of MSCs can downregulate oxidative stress in the testes, liver, kidneys, and other affected organs in animal models of certain diseases. Addition-ally, MSCs can help create a microenvironment that promotes tissue repair and regeneration in are-as with oxidative stress damage, improving the disordered state of the injured site. In this article, we review the pathogenesis of oxidative stress in vitiligo and promising strategies for its treatment.

Aquaporin-3 Downregulation in Vitiligo Keratinocytes Increases Oxidative Stress of Melanocytes.

Oxidative stress-induced melanocyte apoptosis is linked to the immune system and plays a critical role in the pathogenesis of vitiligo. Aquaporin-3 (AQP3), which is downregulated in vitiligo keratinocytes, regulates intracellular H2O2 accumulation. However, the role of AQP3 in oxidative stress is uncertain in vitiligo. This study investigated the effect of downregulated AQP3 on oxidative stress in vitiligo using lesional and non-lesional skin specimen sets from vitiligo patients and primary cultured adult normal human epidermal keratinocytes, with or without downregulation and overexpression of AQP3 in the presence or absence of H2O2 treatment. The levels of nuclear factor E2-related factor 2 (NRF2) and/or its main target, NAD(P)H quinone dehydrogenase 1 (NQO-1), were lower in the lesional keratinocytes and cultured keratinocytes with AQP3 knockdown, but were increased in keratinocytes upon AQP3 overexpression. Ratios of NRF2 nuclear translocation and NQO-1 expression levels were further reduced in AQP3-knockdown keratinocytes following H2O2 treatment. The conditioned media from AQP3-knockdown keratinocytes treated with H2O2 contained higher concentrations of reactive oxygen species (ROS). Moreover, the number of viable melanocytes was reduced when the conditioned media were added to the culture media. Overall, AQP3 downregulation in the keratinocytes of patients with vitiligo can induce oxidative stress in neighboring melanocytes, leading to melanocyte death.

The Role of Oxidative Stress in Vitiligo: An Update on Its Pathogenesis and Therapeutic Implications.

Vitiligo is an autoimmune skin disorder caused by dysfunctional pigment-producing melanocytes which are attacked by immune cells. Oxidative stress is considered to play a crucial role in activating consequent autoimmune responses related to vitiligo. Melanin synthesis by melanocytes is the main intracellular stressor, producing reactive oxygen species (ROS). Under normal physiological conditions, the antioxidative nuclear factor erythroid 2-related factor 2 (Nrf2) pathway functions as a crucial mediator for cells to resist oxidative stress. In pathological situations, such as with antioxidant defects or under inflammation, ROS accumulate and cause cell damage. Herein, we summarize events at the cellular level under excessive ROS in vitiligo and highlight exposure to melanocyte-specific antigens that trigger immune responses. Such responses lead to functional impairment and the death of melanocytes, which sequentially increase melanocyte cytotoxicity through both innate and adaptive immunity. This report provides new perspectives and advances our understanding of interrelationships between oxidative stress and autoimmunity in the pathogenesis of vitiligo. We describe progress with targeted antioxidant therapy, with the aim of providing potential therapeutic approaches.

Post-Traumatic Stress in Vitiligo Patients: A Neglected but Real-Existing Psychological Impairment.

BackgroundVitiligo is the most common depigmentation disorder. This disease causes disfiguration and induces psychological burdens, leading to significantly impaired quality of life. Limited research about disease-related post-traumatic stress (PTS) has been conducted in vitiligo patients.ObjectiveTo evaluate the prevalence, severity, and risk factors of post-traumatic stress in vitiligo patients.MethodsThis case-control study was performed from January 2021 to April 2021. A survey questionnaire including baseline information, post-traumatic stress symptoms evaluation, life quality evaluation was conducted. According to the severity of post-traumatic stress symptoms, patients were grouped and compared. The logistic regression model was conducted to analyze the risk factors for post-traumatic stress disorder (PTSD).ResultsA total of 337 patients were included. A 30.3% of vitiligo patients (102/337) in present cohort had PTS and 12.5% patients (42/337) were confirmed for developing into PTSD. The multivariate logistic regression revealed educational level<university (OR=2.32, 95% CI=1.97–2.93, P=0.003), vitiligo in face and neck (OR=2.65, 95% CI=2.08–3.12, P=0.008), vitiligo in feet and hands (OR=1.86, 95% CI=1.54–2.12, P<0.001) and surgical treatment (OR=3.53, 95% CI=3.12–4.02, P<0.001) were risk factors for PTSD. PTS severity was significantly associated with vitiligo disease activity score (rho=0.54, R2=0.29, P=0.002), vitiligo area scoring index score (r=0.55, R2=0.30, P=0.012), and dermatology life quality index score (r=0.61, R2=0.37, P=0.004).ConclusionVitiligo-related PTS is prevalent in vitiligo patients and causes psychological impairment. Dermatologists should realize and identify this condition carefully and offer proactive intervention to improve patients’ quality of life.

Oxeiptosis: a novel pathway of melanocytes death in response to oxidative stress in vitiligo

Vitiligo is a cutaneous depigmenting autoimmune disease caused by the extensive destruction of epidermal melanocytes. Convincing data has defined a critical role for oxidative stress in the pathogenesis of vitiligo. Oxeiptosis is a caspase-independent cell death modality that was reportedly triggered by oxidative stress and operative in pathogen clearance. However, whether oxeiptosis exists in oxidative stress-induced melanocytes demise in vitiligo remains undetermined. In the present study, we initially found that other cell death modalities might exist in addition to the well-recognized apoptosis and necroptosis in H2O2-treated melanocytes. Furthermore, AIFM1 was found to be dephosphorylated at Ser116 in oxidative stress-induced melanocytes death, which was specific to oxeiptosis. Moreover, KEAP1 and PGAM5, upstream of the AIFM1 in oxeiptosis, were found to operate in melanocytic death. Subsequently, the KEAP1-PGAM5-AIFM1 signaling pathway was proved to be involved in oxidative stress-triggered melanocytes demise through the depletion of KEAP1 and PGAM5. Altogether, our study indicated that oxeiptosis might occur in melanocytes death under oxidative stress and contribute to the pathogenesis of vitiligo.

The Role of Oxidative Stress in the Pathogenesis of Vitiligo: A Culprit for Melanocyte Death.

Vitiligo is a common chronic acquired pigmentation disorder characterized by loss of pigmentation. Among various hypotheses proposed for the pathogenesis of vitiligo, oxidative stress-induced immune response that ultimately leads to melanocyte death remains most widely accepted. Oxidative stress which causes elevated levels of reactive oxygen species (ROS) can lead to dysfunction of molecules and organelles, triggering further immune response, and ultimately melanocyte death. In recent years, a variety of cell death modes have been studied, including apoptosis, autophagy and autophagic cell death, ferroptosis, and other novel modes of death, which will be discussed in this review in detail. Oxidative stress is also strongly linked to these modes of death. Under oxidative stress, ROS could induce autophagy by activating the Nrf2 antioxidant pathway of melanocytes. However, persistent stimulation of ROS might eventually lead to excessive activation of Nrf2 antioxidant pathway, which in turn will inactivate autophagy. Moreover, ferroptosis may be triggered by oxidative-related transcriptional production, including ARE, the positive feedback loop related to p62, and the reduced activity and expression of GPX4. Therefore, it is reasonable to infer that these modes of death are involved in the oxidative stress response, and that oxidative stress also acts as an initiator for various modes of death through some complex mechanisms. In this study, we aim to summarize the role of oxidative stress in vitiligo and discuss the corresponding mechanisms of interaction between various modes of cell death and oxidative stress. These findings may provide new ideas for exploring the pathogenesis and potential therapeutic targets of vitiligo.

Factors associated with perceived stress in patients with vitiligo in the ComPaRe e-cohort

Factors associated with perceived stress in patients with vitiligo in the ComPaRe e-cohort

Oxidative stress and the cholinergic system in non-segmental vitiligo: Effect of narrow band ultraviolet b.

Despite exhaustive research, melanocyte disappearance and the evolution of vitiligo remain enigmatic, and although multi-factorial, oxidative stress appears as a major player. The role of cutaneous cholinergic system in vitiligo pathogenesis has also been reported in some studies. To evaluate and correlate the influence of phototherapy on cutaneous cholinergic system and oxidative stress in vitiligo. Acetyl choline (ACh), its receptors; nicotinic (nAChR) and muscarinic (mAChR); acetylcholine esterase (AChE) and H2 O2 levels were estimated in de-pigmented and re-pigmented lesions of 30 vitiligo patients before and after NB-UVB phototherapy and in 30 controls. ACh and H2 O2 levels were measured by colorimetry. AChE and acetylcholine receptors expression were measured by quantitative real-time PCR. Mean ACh and H2 O2 levels were significantly higher in vitiligo lesions before NB-UVB (P<.001) whereas AChE enzyme level was significantly lower (P<.001) compared to both re-pigmented and control skin. Additionally, mean mAChR was significantly higher and mean nAChR was significantly lower in vitiligo lesions before NB-UVB versus controls and re-pigmented skin (P<.001). Also, H2 O2 and AChE showed negative correlation whereas ACh and mAChR showed significant positive correlation. Although all the studied parameters showed significant changes after treatment and subsequent re-pigmentation, a significant difference continued to exist between all vitiligo skin and controls. Cholinergic system is strongly involved in vitiligo pathogenesis through H2 O2 inhibition of AChE which could be reversed by NB-UVB. Moreover, the strong activation of mAChRs may reflect genetic and/or acquired errors, direct up-regulation by ACh and H2 O2 or both.

Correlation between malondialdehyde levels and disease activity in vitiligo

Background: Vitiligo is an acquired depigmented skin disease that occurs due to the death of melanocytes. There are various presumed theories about the cause of melanocyte death in vitiligo; one of them is oxidative stress theory. Lipid peroxidation is the primary manifestation of oxidative stress, producing malondialdehyde (MDA) as its end product. Malondialdehyde is a stable marker to assess the occurrence of oxidative stress. This study aims to prove the differences in serum MDA levels in the active vitiligo, stable vitiligo, and normal control groups.Method: This research is an analytical cross-sectional study involving 64 vitiligo patients with active and stable lesions and 20 normal controls. The study was conducted at Sanglah General Hospital Denpasar in February - November 2019. Serum MDA levels were measured to assess oxidative stress. The measurement of MDA levels was carried out by a spectrophotometer instrument using Competitive-ELISA method.Results: In this study, there were significant differences in MDA levels between active, stable vitiligo patients, and control group (p=0.000) with active vitiligo type have the highest MDA mean, followed by stable type and control group respectively.Conclusion: Increased serum MDA levels are an indicator of oxidative stress in vitiligo, which leads to melanocyte death and manifests as increased vitiligo disease activity. The results of this study support the role of oxidative stress in vitiligo pathogenesis and the use of oxidative stress indicators like serum MDA levels as biomarker in evaluating vitiligo disease activity.

721 Abnormal autophagosome formation increased melanocyte sensitivity to H2O2-induced oxidative stress in vitiligo

Autophagy is a controlled self-digestion process which can protect cells against oxidative damage. Dysregulated autophagy has been demonstrated to increase melanocyte sensitivity to oxidative stress in vitiligo. However, the exact mechanism is still not clear. This study aimed to determine the implications of autophagy for melanocyte survival in response to oxidative stress. Our results demonstrated that the autophagic flux in PIG1 exposure to H2O2 was significantly enhanced compared with that in PIG3V, which were accompanied by high level of ROS accumulation, membrane potential changes, and increased apoptosis. It indicates that vitiligo melanocytes exhibited hypersensitivity to H2O2-induced oxidative injury due to dysregulated autophagy. To further explore the mechanism, we performed RNA sequencing to compare the RNA expression in PIG1 and PIG3V cells exposed to H2O2, the bioinformatic analysis indicate that autophagosome formation was impaired in vitiligo melanocytes, our in vitro study also showed that inhibition of autolysosome degradation can not lead to autophagosome accumulation in vitiligo melanocytes, confirming that the impairment of autophagosome formation is responsible for the defects of autophagy in vitiligo melanocytes, the further study also showed that overexpression of HSF1, the main transcription factor for Atg5 and Atg12, could reduce H2O2-induced oxidative damage of vitiligo melanocytes. Our data demonstrated that owing to the deficiency of HSF1 expression, the autophagosome formation was blocked, which resulted in autophagy impairment and further increase the sensitivity of vitiligo melanocytes to oxidative stress. Our results indicating that targeting autophagy may be a potential therapy option.

Determination of oxidative stress in vitiligo by measuring superoxide dismutase levels in vitiliginous skin

Objective This study was conducted to determine the association between oxidative stress and vitiligo by measuring antioxidant enzyme superoxide dismutase (SOD) in vitiliginous skin. Background Vitiligo is an acquired depigmenting disease characterized by milky white patches of skin due to local destruction and loss of the epidermal melanocytes. Complex genetic, immunological, neural and self-destructive mechanisms interplay in its pathogenesis. According to autocytotoxic hypothesis, oxidative stress has been suggested to be the initial pathogenic event in melanocyte degeneration. Oxidative stress is defined as a disruption of the delicate balance between the formation of reactive oxygen species and the antioxidant defense system, The dismutation of superoxide (O2-) by SOD to hydrogen peroxide (H2O2) is generally considered to be the primary antioxidant defense of the body, because this enzyme prevents the further generation of free radicals. SOD exists in virtually every oxygen-respiring organism, and its major function is to catalyze dismutative reaction. Patients and methods We determined the activity of SOD in lesional skin only of 20 female patients with vitiligo. The ages of the patients ranged from 18 to 53 years. A total of 17 patients had nonsegmental vitiligo and three had segmental vitiligo, and 10 age-matched and gender-matched apparently healthy volunteers with no past, present or family history of vitiligo, served as a control group. Every case and control was subjected to skin biopsy, and SOD assay of the obtained biopsy was carried out by spectrophotometry. Results A significant difference was found between cases and controls with regard to tissue SOD (P = 0.01, Conclusion There was a significant association between oxidative stress and vitiligo.

Usefulness of ischemia-modified albumin in predicting oxidative stress in patients with vitiligo.

To investigate the emphasis of oxidative stress in the pathogenesis of vitiligo through an evaluation of ischemia-modified albumin (IMA). Results/methodology: IMA was of higher statistical significance in patients than in the control group (IMA: 0.57 ± 0.2 vs 0.52 ± 0.2 ΔABSU; p < 0.0001). IMA (p < 0.0001; OR: 8.9; 95% CI = 3.1-26.1) was found as an independent predictor of oxidative stress. Increases in affected body surface area and age were found to be independent risk factors for IMA. The sensitivity, specificity and positive and negative predictive values and capacity of IMA were higher than other studied biomarkers. IMA can be detected in the condition of oxidative stress in vitiligo; it has great potential as a biomarker of said condition, when compared with other studied biomarkers.

Dysregulated autophagy increased melanocyte sensitivity to H2O2-induced oxidative stress in vitiligo

In vitiligo, melanocytes are particularly vulnerable to oxidative stress owing to the pro-oxidant state generated during melanin synthesis and to the genetic antioxidant defects. Autophagy is a controlled self-digestion process which can protect cells against oxidative damage. However, the exact role of autophagy in vitiligo melanocytes in response to oxidative stress and the mechanism involved are still not clear. To determine the implications of autophagy for melanocyte survival in response to oxidative stress, we first detected the autophagic flux in normal melanocytes exposure to H2O2, and found that autophagy was significantly enhanced in normal melanocytes, for protecting cells against H2O2-induced oxidative damage. Nevertheless, vitiligo melanocytes exhibited dysregulated autophagy and hypersensitivity to H2O2-induced oxidative injury. In addition, we confirmed that the impairment of Nrf2-p62 pathway is responsible for the defects of autophagy in vitiligo melanocytes. Noteworthily, upregulation of the Nrf2-p62 pathway or p62 reduced H2O2-induced oxidative damage of vitiligo melanocytes. Therefore, our data demonstrated that dysregulated autophagy owing to the impairment of Nrf2-p62 pathway increase the sensitivity of vitiligo melanocytes to oxidative stress, thus promote the development of vitiligo. Upregulation of p62-dependent autophagy may be applied to vitiligo treatment in the future.

612 Dysregulated autophagy increased melanocyte apoptosis to hydrogen peroxide-induced oxidative stress in vitiligo

612 Dysregulated autophagy increased melanocyte apoptosis to hydrogen peroxide-induced oxidative stress in vitiligo

Vitiligo-Inducing Phenols Activate the Unfolded Protein Response in Melanocytes Resulting in Upregulation of IL6 and IL8

Vitiligo is characterized by depigmented skin patches due to loss of epidermal melanocytes. Oxidative stress may play a role in vitiligo onset, while autoimmunity contributes to disease progression. In this study we sought to identify mechanisms that link disease triggers and spreading of lesions. A hallmark of melanocytes at the periphery of vitiligo lesions is dilation of the endoplasmic reticulum (ER). We hypothesized that oxidative stress results in redox disruptions that extend to the ER, causing accumulation of misfolded peptides, which activates the unfolded protein response (UPR). We used 4-tertiary butyl phenol (4-TBP) and monobenzyl ether of hydroquinone (MBEH), known triggers of vitiligo. We show that expression of key UPR components, including the transcription factor X-box binding protein 1 (XBP1), are increased following exposure of melanocytes to phenols. XBP1 activation increases production of immune mediators interleukin-6 (IL6) and IL8. Co-treatment with XBP1 inhibitors reduced IL6 and IL8 production induced by phenols, while over-expression of XBP1 alone increased their expression. Thus, melanocytes themselves produce cytokines associated with activation of an immune response following exposure to chemical triggers of vitiligo. These results expand our understanding of the mechanisms underlying melanocyte loss in vitiligo and pathways linking environmental stressors and autoimmunity.

Blunted epidermal L‐tryptophan metabolism in vitiligo affects immune response and ROS scavenging by Fenton chemistry, part 2: epidermal H2O2/ONOO–‐mediated stress in vitiligo hampers indoleamine 2,3‐dioxygenase and aryl hydrocarbon receptor‐mediated immune response signaling

Vitiligo is characterized by a mostly progressive loss of the inherited skin color. The cause of the disease is still unknown, despite accumulating in vivo and in vitro evidence of massive oxidative stress via hydrogen peroxide (H(2)O(2)) and peroxynitrite (ONOO(-)) in the skin of affected individuals. The most favored hypothesis is based on autoimmune mechanisms. Since depletion of the essential amino acid L-tryptophan (Trp) severely affects various immune responses, we here looked at Trp metabolism and signaling in these patients. Our in vivo and in vitro data revealed total absence of epidermal Trp hydroxylase activities and the presence of H(2)O(2)/ONOO(-) deactivated indoleamine 2,3-dioxygenase. Aryl hydrocarbon receptor signaling is severely impaired despite the ligand (Trp dimer) being formed, as shown by mass spectrometry. Loss of this signal is supported by the absence of downstream signals (COX-2 and CYP1A1) as well as regulatory T-lymphocytes and by computer modeling. In vivo Fourier transform Raman spectroscopy confirmed the presence of Trp metabolites together with H(2)O(2) supporting deprivation of the epidermal Trp pool by Fenton chemistry. Taken together, our data support a long-expressed role for in loco redox balance and a distinct immune response. These insights could open novel treatment strategies for this disease.

Study of Oxidative Stress in Vitiligo

Vitiligo is an idiopathic, acquired, circumscribed, hypomelanotic skin disorder, characterized by milky white patches of different sizes and shapes. It is due to the destruction of melanocytes resulting in the absence of pigment production of the skin and mucosal surfaces. Oxidative stress has been implicated in pathophysiology of vitiligo. To study the activity of blood Superoxide dismutase (SOD) and Glutathione peroxidase (GPx) in vitiligo patients. A case-control study was conducted in which 100 patients were enrolled after written consent. 50 cases were of active vitiligo and 50 served as control (25 healthy control and 25 with stable vitiligo). SOD-In our study, among the active vitiligo cases 90% had high level of SOD and 10% had normal level of SOD. Among the stable vitiligo controls, 92% had normal level of SOD and 8% had low levels of SOD.The difference between active vitiligo cases and stable vitiligo control as well as with healthy control was statistically significant (P value<0.05). GPx-Among the active vitiligo cases 74% had normal GPx levels, 22% had low and only 4% had high levels of GPx. Among the stable vitiligo controls, 64% had normal GPx levels, 16% had low, and 20% had high levels of GPx. The difference between active vitiligo cases and stable vitiligo control as well as with healthy control was statistically not significant (P value>0.05). Our study shows that oxidative stress is involved in the pathophysiology of vitiligo, as indicated by the high levels of serum superoxide dismutase activity.

Decreased methionine sulphoxide reductase A expression renders melanocytes more sensitive to oxidative stress: a possible cause for melanocyte loss in vitiligo

Methionine is one of the major targets of reactive oxygen species (ROS). It is readily oxidized to methionine-S-sulphoxide and methionine-R-sulphoxide, which can be reduced by methionine sulphoxide reductase (MSR) A and B, respectively. MSR represents a unique repair mechanism in the skin antioxidant network. It functions both as a protein repairer and as a ROS scavenger. However, the expression and activity of MSR are significantly reduced in vitiligo. To investigate whether the decreased expression of MSRA is one of the reasons why melanocytes are especially vulnerable to oxidative stress in vitiligo. Methods We downregulated MSRA expression in immortalized human epidermal melanocyte cell line PIG1 by using the short interfering RNA (siRNA)-targeted gene silencing method. We checked the changes in MSRA transcript and protein level by using reverse transcriptase-polymerase chain reaction and Western blot, respectively. Then we monitored the viability of MSRA-silenced melanocytes under oxidative stress. All statistical analysis was performed by unpaired two-tailed Student's t-test. The siRNA specific for MSRA successfully suppressed MSRA expression in melanocytes. The lower MSRA expression in melanocytes led to an increased sensitivity to oxidative stress, resulting in more cell death. Furthermore, a remarkable loss of viable cells was found in MSRA-silenced melanocytes even in the absence of exogenously added oxidative stress. MSRA is crucial for melanocytes to fight against oxidative stress in vitiligo. In addition, it is also important for normal cell survival. Any means to enhance MSRA appears to have therapeutic potential for the treatment of vitiligo.

Determination of oxidative stress in vitiligo by measuring superoxide dismutase and catalase levels in vitiliginous and non-vitiliginous skin

Vitiligo is an acquired disorder characterized by circumscribed depigmented macules devoid of identifiable melanocytes. Complex genetic, immunological, neural and self destructive mechanisms interplay in its pathogenesis. According to autocytotoxic hypothesis, oxidative stress has been suggested to be the initial pathogenic event in melanocyte degeneration. The aim of our investigation was to evaluate the role of oxidative stress by measuring levels of the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) in lesional and normal skin of patients with vitiligo and in the skin of normal controls. We determined the activity of SOD in lesional and non-lesional skin and CAT in lesional skin only of 25 vitiligo patients and 25 controls by using the spectrophotometric assay and Aebi's method, respectively. There was statistically significant increase in the levels of SOD in vitiliginous and non vitiliginous skin of patient group compared to the control group (P < 0.001). No significant difference was found between the levels of SOD in lesional skin and non-lesional skin of vitiligo patients. The levels of CAT in the skin of patients were found to be significantly lower than those of controls (P < 0.001). There is increased oxidative stress in vitiligo as is indicated by high levels of SOD and low levels of CAT in the skin of vitiligo patients.