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Year : 2014  |  Volume : 27  |  Issue : 2  |  Page : 465-468

Oxidants and antioxidants role in acne vulgaris

1 Department of Dermatology and Andrology, Faculty of Medicine, Menoufia University, Menufia, Egypt
2 Department of Medical Biochemistry, Faculty of Medicine, Menoufia University, Menufia, Egypt

Date of Submission14-Apr-2013
Date of Acceptance07-Sep-2013
Date of Web Publication26-Sep-2014

Correspondence Address:
Amira Adel Mahmoud
MBBCh, Kafer Beheda, Mit Ghamer, Dakahlia
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1110-2098.141728

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The aim of the study was to determine the effects of oxidative stress in acne vulgaris by measuring the levels of an oxidant [malondialdehyde (MDA)] and an antioxidant [superoxide dismutase (SOD) enzyme] in acne patients.
Acne vulgaris is one of the common dermatological diseases, and its pathogenesis is multifactorial.
Materials and methods
Twenty-seven consecutive acne patients and 10 controls were enrolled. The parameters of oxidative stress, such as serum SOD and MDA, were measured spectrophotometrically.
There was significantly higher enzymatic level of SOD (P < 0.001) and MDA (P < 0.001) in blood of patient with acne compared with that of healthy control. There was significant positive correlation between serum SOD and serum MDA level.
Oxidative stress exists in acne patients.

Keywords: Acne vulgaris, malondialdehyde, oxidative stress, reactive oxygen species, superoxide dismutase

How to cite this article:
Gaber MA, Dawood AA, Mahmoud AA. Oxidants and antioxidants role in acne vulgaris. Menoufia Med J 2014;27:465-8

How to cite this URL:
Gaber MA, Dawood AA, Mahmoud AA. Oxidants and antioxidants role in acne vulgaris. Menoufia Med J [serial online] 2014 [cited 2021 Oct 28];27:465-8. Available from: http://www.mmj.eg.net/text.asp?2014/27/2/465/141728

  Introduction Top

Acne vulgaris is a chronic inflammatory skin disease caused by changes in the pilosebaceous units [1]. It affects more than 85% of people at some time during their lives. It is more common in male individuals than in female individuals during adolescence. However, it is more common in women than in men during adulthood. Acne vulgaris affects the areas of skin with the greatest proportion of sebaceous follicles; these areas include the face, the upper part of the chest, and the back [2]. Sebaceous hyperplasia, follicular hyperkeratinization, bacterial hypercolonization, as well as immune reactions and inflammations may lead to acne, which has a quite complex pathogenesis [3].  Propionibacterium acnes Scientific Name Search cular lipases, proteases, and hyaluronidases - several enzymes that may play an important role in the inflammatory process [4]. Besides, many researchers think that acne pathogenesis cannot exactly be understood. In acne, sebum produced by the sebaceous glands, content changes, and reactive oxygen species (ROS) may be released from the impacted damaged follicular walls; at the same time, it is thought that this may be the reason for the progress of the inflammation in the pathogenesis of the disease [5]. Oxygen, which is an important and vital component for human, can produce reactive types (superoxide anion, hydrogen peroxide, and hydroxyl radicals) known as ROS. These radicals are formed with the reduction of oxygen to water. Normally, the production of these radicals is slow and they are removed by the antioxidant enzymes existing in the cell. Superoxide dismutase (SOD), catalase (CAT), and glucose-6-phosphate dehydrogenase are some of the important antioxidant enzymes. Malondialdehyde (MDA) is the end product of lipid peroxidation and one of the indicators of oxidative stress. When SOD and CAT enzymes are insufficient for oxidative stress, ROS denotes its impact by starting the lipid peroxidation on the membranes of organs and cells. Although acne vulgaris is the most frequent disease of the young population, only a few studies on antioxidative system in acne pathophysiology have been performed until now [6],[7]. In this study, serum levels of SOD and MDA were measured in patients with acne and in age-matched and sex-matched healthy controls to investigate the role of oxidative stress in acne pathogenesis.

  Materials and methods Top

This controlled study was conducted on 37 patients divided into two groups. Group I (the patient group) included 27 patients with acne. There were 21 women and six men; their ages ranged between 13 and 25) years. Group II (the control group) included 10 age-matched and sex-matched healthy individuals as controls; there were eight women and two men. Their ages ranged between 13 and 25 years. The patients were attendants of out patients clinic of Dermatology Department, Menoufia University Hospital during the period from December 2011 to April 2012. Written consent was taken from all patients and controls; this work was approved by ethical committee of Menofia university faculty of medicine. Patients with other dermatological disease, smoking, and drug intake were excluded. Both patients and controls had no history of any topical and systemic drug therapy, including vitamins and anti-inflammatory drugs at least 3 months before blood collection.

Five ml of venous blood was taken from each patient after taking written consent; the blood was left to clot for 30 min at room temperature then subjected to centrifugation for 10 min at 5000 rotation per minute (rpm), and the serum obtained was stored at -80°C until the time of spectrophotometeric assay of serum MDA and SOD enzyme.

MDA determination

Serum MDA level was determined by colometric method [8]. On the basis of the reaction of MDA with thiobarbituric acid in acidic medium at temperature of 95°C for 30 min to form thiobarbituric acid reactive product, the absorbance of the resultant pink product can be measured at 534 nm. The kit used was provided by Bioenergetic company.

Measurement of serum SOD

The method used for this assay relies on the ability of the enzyme to inhibit the phenazine methosulphate-mediated reduction of nitroblue tetrazolium dye by colometric method [9].

Assay procedure

R4 should be diluted 100 times immediately before use (0.1 ml + 9.9 ml distilled water) and discarded after use.

Sample should be diluted to give an inhibition percentage between 30 and 60.

Buffer (R1) 1 ml + NBT (R2) 0.1 ml + NADH (R3) 0.1 ml+sample (control) 0.05 (sample or DW, respectively).

Measure the increase in absorbance at 560 nm for 5 min for control (D?A control ) and sample (D?A sample ) at 25°C [9].

Statistical methods

Data were analyzed by the SPSS version 11.0 statistical package.

The quantitative data were expressed as mean and SD. The qualitative data were expressed as number and percentage and analyzed by the c2 -test and Student's t-test for normally distributed variables and for abnormally distributed variables, respectively. The Mann-Whittney test was used. Correlations between variables were calculated by Spearman's correlation coefficient. All these tests were used as tests of significance at P value less than 0.05.

  Results Top

The present study included 27 patients and 10 age-matched and sex-matched healthy controls. Cases included six male patients and 21 female patients, with a mean ± SD of 18.3 ± 3.1 years. Regarding the disease severity, 12 patients had mild acne, 13 patients had moderate acne, and two patients had severe acne.

Serum sample was taken from each individual of both groups, and SOD level and MDA level were estimated.

High statistically significant increase in SOD enzyme levels (P = 0.001) was found in the patient group compared with the control group, and high statistically significant increase was found in MDA levels in the patient group compared with the control group. ([Table 1] and [Table 2], respectively).

There was no statistically significant correlation between MDA and severity (r = −0.154, P = 0.44). There was no statistically significant correlation between SOD and severity (r = −0.119, P = 0.55). Statistically highly significant positive correlation was found between MDA and SOD levels (r = 846, P = 0.001) [Table 3].
Table 1: Comparison between group I and group II with respect to SOD level

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Table 2: Comparison between group I and group II with respect to MDA level

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Table 3: Correlation between superoxide dismutase enzyme and malondialdehyde levels

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  Discussion Top

Acne vulgaris is a chronic inflammatory skin disease of the pilosebaceous unit [1]. It is characterized by seborrhea, comedones, erythematous papules and pustules, less frequently by nodules, deep pustules or pseudocysts, and in some cases is accompanied by scarring [10]. The traditional etiologic factors include increased sebum production, ductal hyperkeratosis, abnormality of the microbial flora within the pilosebaceous unit, and mediators of inflammation [11].

ROS are toxic molecules and play critical roles in many of the inflammatory skin diseases [5],[12]. Propionibacterium acnes taking part in acne pathogenesis cause the release of some chemotactic factors leading to neutrophils accumulation. This situation causes damages to follicular epithelia after the release of some inflammatory factors such as lysosome enzymes as a result of phagocytosis. ROS is released from the active neutrophils in the inflammatory tissue. These oxidants attack DNA and/or membrane lipids and cause chemical damage to them, including the healthy tissue [5],[13],[14]. Production of ROS is a particularly destructive aspect of oxidative stress. Such species include free radicals and peroxides. Some of the less reactive of these species (such as superoxide) can be converted by oxidoreduction reactions with transition metals or other redox cycling compounds (including quinones) into more aggressive radical species that can cause extensive cellular damage [15]. The first line of defense against superoxide free radicals in the body is the SOD, which is considered the most effective antioxidant. In brief, SOD keeps oxygen under control [16].

MDA is a highly reactive 3-carbon dialdehyde produced as a byproduct of polyunsaturated fatty acid peroxidation and arachidonic acid metabolism [17]. MDA is one of the most frequently used indicators of lipid peroxidation. However, on a group basis, data support that MDA may be a potential biomarker for oxidative stress [18].

In our study, it was found that there was high statistically significant increase in SOD enzyme level in the patient group compared with the control group. Statistically, no significant correlation was found between SOD level and severity of the disease. In addition, there was no statistically significant correlation between SOD levels and age and sex in the patients groups.

Our findings are in agreement with the study by Ozer and colleagues, who investigated 43 acne patients, including 30 women and 13 men, and 46 healthy controls, including 28 women and18 men. They reported that erythrocyte SOD activity was increased in patients with acne than in the control group. They reported negative correlation between SOD level and the disease severity. In addition, they reported no correlation among ages or sexes and serum antioxidant enzymes level [19].

However, Samantha Crofskey, who investigated a total of 23 patients (13 men) with mild (n = 6), moderate (n = 10), or severe (n = 7) acne vulgaris, along with 23 age-matched and sex-matched controls, reported no significant difference in SOD activities between the patients and control groups [20].

The study conducted by Sarici et al. [20] involved 32 patients with acne vulgaris in the patient group and 34 healthy adults in the control group. The parameters of oxidative stress, such as CAT, SOD, xanthine oxidase, nitric oxide, and MDA, in the venous blood of patients were measured spectrophotometrically. The values were compared with those of the control group. The results showed significantly lower SOD and CAT activity in the patient group than in the control group.

It was thought that SOD level may be increased as a reaction to oxidant stress occurring as a result of oxidant/antioxidant imbalance in the cell.

In our study, we obtained a higher level of MDA in acne patients than in the control group. Our findings are in agreement with the study by Ozer et al. [19] who reported high level of MDA in patients with acne vulgaris compared with controls.

In addition, our findings are in agreement with the study by Sarici et al. [20] who reported that serum levels of MDA and xanthine oxidase activity in patients with acne vulgaris were significantly higher than those of the controls.

High level of MDA in acne vulgaris can be explained on the basis that inflammation appears to be a source of ROS [21].

In our study, there was statistically significant correlation between MDA and SOD levels among the patients group.

According to the present results, we conclude that the statistically significant high levels of MDA in patient with acne vulgaris reflect the presence of oxidative stress state that can lead to cell injury and inflammation in acne vulgaris. In addition, the statistically significant high levels of SOD enzyme in lesions of acne vulgaris and its negative correlation with severity of the disease attribute oxidative stress to the increase in antioxidant, at least SOD enzyme.

These findings clearly indicate that oxidative stress exists in acne and may play an important role in its pathogenesis.

In planning acne therapy, synergistic effects should be considered by selecting antiacne agents that have different mechanisms of action and targets on the pathogenesis of acne. Until new products are developed, it will be useful to prefer at least one antioxidant-featured drug along with the combined acne treatment.

  Acknowledgements Top

Conflicts of interest

There are no conflicts of interest.

  References Top

1.Goodman G. Acne and acne scarring - the case for active and early intervention. Aust Fam Physician 2006; 35 :503-504.  Back to cited text no. 1
2. Harper J, Fulton J. Acne vulgaris. eMedicine Articles. Available at: http://www.emedicine.com/derm/topic2.htm [Accessed on 19 August 2007].  Back to cited text no. 2
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9. Nishikimi M, Appaji N, Yagi K. The occurrence of superoxide anion in the reaction of reduced phenazine methosulfate and molecular oxygen. Biochem Biophys Res Commun 1972; 46 :849-854.  Back to cited text no. 9
10.Simpson NB, Cunliffe WJ. In: Burns T, Breathnach S, Cox N, Griffiths C, eds. Disorders of the sebaceous glands. Rook′s textbook of dermatology. 7th ed. Malden, MA: Blackwell Science; 2004. 43.1-43.75.  Back to cited text no. 10
11.Bergfeld WF. The pathophysiology of acne vulgaris in children and adolescents, Part 1. Cutis 2004; 74 :92-97.  Back to cited text no. 11
12.Oztas MO, Balk M, Ogus E, Bozkurt M, Ogus IH, Ozer N. The role of free oxygen radicals in the aetiopathogenesis of rosacea. Clin Exp Dermatol 2003; 28 :188-192.  Back to cited text no. 12
13.Akamatsu H, Horio T, Hattori K. Increased hydrogen peroxide generation by neutrophils from patients with acne inflammation. Int J Dermatol 2003; 42 :366-369.  Back to cited text no. 13
14.Brown SK, Shalita AR. Acne vulgaris. Lancet 1998; 351 :1871-1876.  Back to cited text no. 14
15.Valko M, Morris H, Cronin MT. Metals, toxicity and oxidative stress. Curr Med Chem2005; 12 :1161-1208.  Back to cited text no. 15
16.Sindhu RK, Ehdaie A, Farmand F, Dhaliwal KK, Nguyen T, Zhan CD, et al. Effect of vitamins C and E on oxidative stress markers and endothelial function. BMJ.2005; 32 :275  Back to cited text no. 16
17.McGillivray SE, Suite PBM, Vancouver WA. Short term altered macro nutrient status on acne. Northwest Life Science Specialties. LLC 2007; 148 :41.  Back to cited text no. 17
18.Atmaca M. Antioxidant enzyme and malondialdehyde levels in patients with social phobia. Clin Chem 2008; 47 :887.  Back to cited text no. 18
19.Ozer A, Ergul B, Sezai S. Oxidative stress in patients with acne vulgaris. Mediators Inflamm 2005; 2005 :380-384.  Back to cited text no. 19
20.Sarici G, Cinar S, Armutcu F. Oxidative stress in acne vulgaris. J Eur Acad Dermatol Venereol 2009; 24 :763-767.  Back to cited text no. 20
21.Raha S, Robinson BH. Mitochondria, oxygen free radicals and apoptosis. Am J Med Genet 2001; 106 :62-70.  Back to cited text no. 21


  [Table 1], [Table 2], [Table 3]

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