Sister Chromatid Exchange Analysis Research Articles

In vitro genotoxicity of rocuronium bromide in human peripheral lymphocytes

Rocuronium bromide (RB), an aminosteroid type neuromuscular blocking agent, acts by reducing or inhibiting the depolarising effect of acetylcholine on the terminal disc of the muscle cell. To our knowledge, there is no adequate information on the genotoxic effects of RB, up to now. In the present study, possible genotoxic effects of RB have been determined by means of sister chromatid exchange (SCE), chromosome aberration (CA) and micronucleus (MN) analyses in human peripheral blood lymphocytes. The human peripheral blood lymphocytes were exposed to three different concentrations of RB (60, 80 and 100μg/mL) for 24- and 48-h. In this study, RB increased the frequency of CAs, however, did not increase the frequency of SCEs. RB did not decrease the proliferation index (PI) and mitotic index (MI). Accordingly, RB increased the frequency of micronucleus (MN) but did not decrease the nuclear division index (NDI). Findings from this study suggest that rocuronium bromide is clastogenic but not cytotoxic to cultured human peripheral blood lymphocytes.

Genetic Risk Assessment in Traffic Policemen of Chennai City by Sister Chromatid Exchange Analysis

Urban atmosphere contains a variety of chemicals which are potentially genotoxic and carcinogenic. An increased risk of lung cancer in certain occupational groups is due to exposure to traffic-related pollution. Few reports are available in India on the genetic damage caused by exposure to automobile exhaust pollution on traffic policemen. Therefore, the present work was undertaken to study the genetic risk assessment in traffic policemen of Chennai city by Sister Chromatid Exchange Analysis. The study subjects consisted of 56 traffic policemen who worked in high density traffic areas of Chennai city and 25 office workers unexposed to traffic as controls were used. Sister chromatid exchanges (SCEs) were analyzed in peripheral blood lymphocytes drawn from both subjects. The results expressed as mean SCEs/cell was found significantly ( p<0.001) higher in traffic policemen (10.62±0.57) compared to the unexposed control subjects (6.49±0.31). These subjects were divided further into two sub-groups such as smokers and alcohol consumers which were not influence the incidence of SCEs/cell. However, a statistically significant (p<0.001) difference was observed between smokers and alcohol consumers than that of control subjects. This is the first studyof the risk assessment of Chennai city traffic police exposed to vehicular pollution.

Lack of association between GSTT1 polymorphism and endogenous or benzo[a]pyrene-induced sister chromatid exchanges as analyzed in metaphase or G2-phase lymphocytes

The objectives of the present work are (1) to verify whether genetic polymorphism in the detoxification gene GSTT1 influences the endogenous sensitivity in terms of sister chromatid exchanges (SCEs)/cell in healthy donors and (2) to test whether in vitro exposure to B[a]P in terms of SCEs/cell can be associated with polymorphism of GSTT1 gene. The presence or absence of the homozygous deletion in GSTT1 gene was determined in peripheral blood cells using multiplex-PCR. For SCEs quantitation, the cytogenetic method used thus far is based on the analysis in metaphase chromosomes. Consequently, G2-arrested cells are not included in the analysis. To overcome this shortcoming of the conventional method, we applied here SCE analysis in G2-phase prematurely condensed chromosomes (G2-PCCs) induced by calyculin-A, using a modified fluorescence-plus-Giemsa staining protocol. Compared to metaphase, a statistically significant increase in the yield of SCEs was notified in the G2-phase analysis after 48h exposure of peripheral blood lymphocytes to 0.01-1mM B[a]P, in both GSTT1-positive and -null donors. Therefore, the analysis of SCEs in the G2-phase using calyculin-A induced PCC methodology was shown to be more sensitive compared to the analysis at the metaphase level. Nevertheless, the results obtained do not show an association between the GSTT1 polymorphism with increased endogenous and/or B[a]P-induced SCE-frequencies in peripheral blood lymphocyte chromosomes in vitro. These results highlight not only the effect of B[a]P on cell cycle kinetics but also they demonstrate that conventional cytogenetic analysis at metaphase underestimates the cytogenetic effects of chemicals that delay cell cycle progression in G2-phase.

Genetic Risk Assessment in Traffic Policemen of Chennai City by Sister Chromatid Exchange Analysis

Urban atmosphere contains a variety of chemicals which are potentially genotoxic and carcinogenic. An increased risk of lung cancer in certain occupational groups is due to exposure to traffic-related pollution. Few reports are available in India on the genetic damage caused by exposure to automobile exhaust pollution on traffic policemen. Therefore, the present work was undertaken to study the genetic risk assessment in traffic policemen of Chennai city by Sister Chromatid Exchange Analysis. The study subjects consisted of 56 traffic policemen who worked in high density traffic areas of Chennai city and 25 office workers unexposed to traffic as controls were used. Sister chromatid exchanges (SCEs) were analyzed in peripheral blood lymphocytes drawn from both subjects. The results expressed as mean SCEs/cell was found significantly ( p<0.001) higher in traffic policemen (10.62±0.57) compared to the unexposed control subjects (6.49±0.31). These subjects were divided further into two sub-groups such as smokers and alcohol consumers which were not influence the incidence of SCEs/cell. However, a statistically significant (p<0.001) difference was observed between smokers and alcohol consumers than that of control subjects. This is the first studyof the risk assessment of Chennai city traffic police exposed to vehicular pollution.

Sister Chromatid Exchange Frequency in Early Embryos and Offspring Derived from IVF or ICSI in Mice

To demonstrate chromosomal injuries associated with in vitro fertilization (IVF) and intracytoplasmic sperm injection (ICSI), sister chromatid exchange (SCE), an indicator of DNA damage, was investigated and the cytogenetic influence of embryonic manipulation on chromosomes of early embryos and offspring was investigated. SCE analysis was performed in early embryos and offspring obtained by IVF, ICSI, or in vivo fertilization (control). To label chromosomes of early embryos, the embryos were cultured in BrdU-supplemented medium for 2 cell cycles. For offspring, BrdU solution was repeatedly injected intraperitoneally. Chromosome samples prepared from the embryos and the bone marrow cells of offspring were stained by the Fluorescence plus Giemsa (FPG) method. In the IVF and ICSI groups, the rates of early development, implantation and offspring were lower than those in the control group. The SCE frequency of early embryos was significantly higher in the IVF and ICSI groups than in the control group (P < 0.05). In contrast, the SCE frequency of offspring in the IVF and ICSI groups was not significantly different from that in the control group. These findings suggest that embryos having serious DNA damage due to embryonic manipulation may be eliminated in a relatively early developmental step and may not reach term.

Sister chromatid exchange (SCE) and high-frequency cells (HFC) in peripheral blood lymphocytes of healthy Tunisian smokers

Cigarette smoking is a major public health problem in Tunisia as it concerns up to 30–35% of the adult population, raising important national issues on tobacco-related disease. The aim of this study was to establish whether cigarette smoking increases sister chromatid exchange (SCE) in peripheral blood lymphocytes of smokers (n=14) compared with non-smokers (n=15) in Sfax, Tunisia. The smokers were subdivided in two subgroups according to the duration of the smoking habit: heavy smokers (>10 years) and light smokers (≤10 years). After signing a consent form, volunteers provided a blood sample (5ml) to establish cell cultures during 72h. For SCE analysis, 30 second-division metaphases were examined from each subject. We determined the frequency of SCE, the percentage of high-frequency cells (HFC) and that of the high-frequency cell individual (HFI). The results show a significantly higher SCE frequency in smokers (8.65±1.43) than in non-smokers (7.16±1.3; p<0.01). A significant difference in SCE frequency was also shown when comparing the two subgroups of smokers (p<0.05). Interestingly, no significant difference was found when comparing the light smokers with non-smokers (7.82±1 vs 7.16±1.3, respectively, p>0.05). The percentages of HFC and HFI were significantly higher in smokers (11.2±7.8% and 78.6%, respectively) than in non-smokers (4±2.2% and 20%, respectively, p<0.01). Our study indicates that the genotoxic effects in lymphocytes from healthy Tunisian smokers are most likely caused by cigarette-smoke constituents. This effect was mainly observed in smokers who had been smoking during more than 10 years. These results provide scientific evidence to urge the prevention of tobacco consumption.

Genotoxic assessment in peripheral blood lymphocytes of post-polio individuals using sister chromatid exchange analysis and micronucleus assay

Environmental pollution is a complex issue because of the diversity of anthropogenic agents, both chemical and physical, that have been detected and catalogued. The consequences to biota from exposure to genotoxic agents present an additional problem because of the potential for these agents to produce adverse change at the cellular and organism levels. Past studies in virus have focused on structural damage to the DNA of environmental species that may occur after exposure to genotoxic agents and the use of this information to document exposure and to monitor remediation. In an effort to predict effects at the population, community and ecosystem levels, in the present study, we attempt to characterize damage occurring through genotoxic agents like 5-bromo-2-deoxyuridine, BrdU, using sister chromatid exchange technique and the formation of micronuclei (MN) in the peripheral lymphocytes of the post-polio syndrome sequelae affected by poliovirus. Analysis of structural chromosomal aberrations (CAs) and involvement of the specific chromosome break were pursued in this study. They revealed a significantly higher incidence of CAs (chromatid and chromosome breaks) in patients compared with controls, where the specific chromosome break has emerged as specific. Also, the maximum numbers of breaks were found to be in chromosome 1 at the position 1p36.1. The results also suggest a correlation between CAs and content of MN.

Cytogenetic analysis of peripheral blood lymphocytes of hospital staff occupationally exposed to low doses of ionizing radiation

Ionizing radiation is known to induce mutations and cell transformations, predominantly by causing single-strand and double-strand DNA breakage, thereby leading to chromosome instability and carcinogenesis. The aim of this study was to evaluate genotoxic effects in hospital staff exposed to low-dose ionizing radiation in comparison with a selected control group, by using the cytokinesis-blocked micronucleus (CBMN) and sister chromatid exchange (SCE) tests in peripheral blood lymphocytes. The study included 40 exposed radiology staff and 30 control subjects. The frequency of micronuclei (MN) was significantly increased in radiation-exposed groups compared with control persons (p < 0.05). The frequency of SCE did not show any significant difference in the exposed individuals in comparison to the controls. Our results showed that low-level chronic occupational exposure to ionizing radiation causes an increase of MN frequency in chromosomes, even though the absorbed doses were below the permissible limits. Our studies indicate that the CBMN assay is considered to be sensitive test in contrast to SCE analysis to evaluate chromosomal damage induced by ionizing radiation.

Evaluation of genotoxic effects of semicarbazide on cultured human lymphocytes and rat bone marrow

Semicarbazide (SEM) belongs to the hydrazine family of chemicals, some members of which are known to possess carcinogenic potential. Information on the potential hazard of SEM itself is incomplete and the possibility that it is genotoxic cannot be ruled out. SEM is widely used as a residue marker for the banned veterinary drug nitrofurazone. Also, it occurs as a break-down product of azodicarbonamide (ADC), a chemical used as a flour treatment. Furthermore, it may form as a reaction product of hypochlorite action on food additives. In the present study, we investigated the possible genotoxic effects of SEM with respect to the following cytogenetic end-points: (1) in vitro micronucleus (MN) formation and sister-chromatid exchange (SCE) induction in human lymphocytes and (2) in vivo micronucleus induction on rat bone marrow polychromatic erythrocytes (PCEs). Comparing MN and SCE frequencies on control and examined concentrations (0.5, 2.5, 5, 10 and 20 μg ml −1) did not reveal statistically significant differences except, marginally, the highest concentration (20 μg ml −1) in SCE analysis. On the other hand, oral administration of 50, 100 and 150 mg kg −1 b.w. of SEM showed a statistically significant effect in MN frequencies on Wistar rats’ bone marrow PCEs, with no dose–response pattern.

The manuscripts for these Proceedings were received by the Publisher: end of June 2009

Pesticides are widely used throughout the world in agriculture to protect crops and in public health to control diseases. Nevertheless, exposure to pesticides represents a potential risk to humans. This paper describes a study of possible genetic damage in the people living in regions contaminated with complex mixture of pesticides in Göksu Delta. In this study, used methods were chromosomal aberration (CA), sister chromatid exchange analysis (SCE) in the peripheral blood lymphocytes, and micronucleus (MN) assay in the buccal epithelial cells. In the present investigation, 32 affected subjects consist of 16 smoking and 16 non-smokings and an equal number of control subjects were assessed for genome damage. Micronucleus (MN), Broken egg (BE), Karyorrhexis (KR), Karyolysis (KL) and Binucleus (BN) frequencies were higher in affected subjects than in controls. Smoking had a statistically significant effect on the Micronucleus, Karyorrhexis and Binucleus frequencies for both the control and the exposed group. Also smoking and exposure affected the frequency of sister chromatid exchange and chromosomal aberrations compared with control groups.

Sister chromatid exchanges and chromosomal aberrations in Chinese hamster ovary (CHO-K1) cells treated with the insecticide pirimicarb

Pirimicarb and its formulation Aficida ® (50% pirimicarb) effects were studied on CHO-K1 cells employing sister chromatid exchange (SCE), chromosomal aberrations (CA), cell-cycle progression and mitotic index analyses. Continuous treatments were performed within 10–300 μg/ml concentration-range. Pirimicarb, but not Aficida ®, induced a concentration-dependent increase of abnormal cells. Pirimicarb induced a greater frequency of chromatid/isochromatid breaks than Aficida ® did. Regression analyses showed a concentration-dependent increase in the frequency of chromatid-type breaks for both compounds whereas only the frequency of isochromatid-type breaks did in those pirimicarb-treated cultures. SCEs in pirimicarb- or Aficida ®-treated cultures were significantly higher than control values with concentrations of 100–200 μg/ml. Both test compounds induced equivalent frequency of SCEs. A delay in cell-cycle kinetics was observed for pirimicarb and Aficida ® within 100–300 and 200–300 μg/ml concentration-range, respectively. An inhibition of MI was observed for both chemicals regardless of tested concentrations. Finally, the CAs appears to be a higher sensitive bioassay to detect DNA damage at lower concentrations of pirimicarb than SCEs does. The results demonstrated that pirimicarb and Aficida ® exert geno-cytotoxicity, at least in CHO-K1 cells.

Micronuclear and sister chromatid exchange analyses in peripheral lymphocytes of patients with oral lichen planus – a pilot study*

The purpose of this study was to determine the genetic instability of peripheral blood lymphocytes from patients diagnosed with oral lichen planus (OLP) by investigation of frequencies of micronuclei (MN) and sister chromatid exchange (SCE). A total of 22 newly diagnosed and untreated patients with OLP of same severity scores and twenty healthy controls participated in this study. They were all non-smokers with no previous history or family history of cancer. The periodontal status, flow rate and buffering capacity of whole mouth saliva were recorded. SCE and MN analyses were performed on peripheral blood lymphocytes of OLP patients and healthy controls. The frequencies of MN (50.00 +/- 22.36) and SCE (6.89 +/- 1.48) in OLP patients were found to be significantly elevated compared with that in normal individuals (25.20 +/- 9.52 and 5.93 +/- 1.31; z = 3.946, P = 0.0001; z = 2.346, P = 0.019). There were no significant differences in the MN frequency and SCE between the two subgroups with reticular or erosive types of OLP. These pilot data indicate an increased genomic instability in peripheral blood lymphocytes of a cohort of Turkish patients diagnosed with oral lichen planus as compared with that of healthy individuals. As patients with OLP may have an increased or potential risk for oral malignancy, these assays could be used in translational research to monitor beneficial effects of interventions and long-term prognosis.

Evaluation of the genotoxicity of Fusarium mycotoxin moniliformin in human peripheral blood lymphocytes

Mycotoxins are fungal secondary metabolites that can be found in contaminated food and feed. There is some evidence to suggest that certain mycotoxins may be mutagenic. Here, we investigate the genotoxicity of the mycotoxin moniliformin (MON) (3-hydroxycyclobut-3-ene-1,2-dione) in human peripheral blood lymphocytes using chromosomal aberration (CA), sister-chromatid exchange (SCE), and micronucleus (MN) analysis. Lymphocyte cultures were treated for 48 h with six different concentrations of MON between 2.5 and 25 microM. CA, SCE, and MN frequencies were significantly increased in a dose-dependent manner compared with the negative control. The mitotic, replication, and cytokinesis-block proliferation indices were not affected by treatment with MON. The results provide evidence to demonstrate that MON can exert cytogenetic effects in human cells in culture.

Absence of cytogenetic effects in children and adults with attention-deficit/hyperactivity disorder treated with methylphenidate

Attention-deficit/hyperactivity disorder (ADHD) is the most common psychiatric condition with onset in childhood, and in more than 50% of cases it persists into adulthood as a chronic disorder. Over five million methylphenidate (MPH) prescriptions were issued in the USA in 2003, mostly for children. A previous report [R.A. El-Zein, S.Z. Abdel-Rahman, M.J. Hay, M.S. Lopez, M.L. Bondy, D.L. Morris and M.S. Legator Cytogenetic effects in children treated with methylphenidate, Cancer Lett. 230 (2005) 284–291.] described the induction of chromosome abnormalities by MPH in children treated for three months, contrary to most of the in vitro and in vivo studies reported since then. We present new relevant information concerning the cytogenetic effects of MPH in children and adults. We include a prospective sample of 12 children and 7 adults with a new diagnosis of ADHD and naive to MPH. We analyzed the cytogenetic effects on peripheral lymphocytes before and three months after starting MPH therapy. The cytogenetic analyses included a cytokinesis-block micronucleus (CBMN) assay, a sister chromatid exchange (SCE) analysis and the determination of chromosome aberrations (CA). Following the same strategy and analyzing the same cytogenetic endpoints that were investigated in the original report [R.A. El-Zein, S.Z. Abdel-Rahman, M.J. Hay, M.S. Lopez, M.L. Bondy, D.L. Morris and M.S. Legator Cytogenetic effects in children treated with methylphenidate, Cancer Lett. 230 (2005) 284–291.], we found no evidence of increased frequency of micronuclei, sister chromatid exchanges or chromosome aberrations induced by MPH in children and adult populations. MPH treatment of children and adults with ADHD resulted in no significant genomic damage (as suggested by the three endpoints studied), results that do not support a potential increased risk of cancer after exposure to MPH.

Increased frequency of sister chromatid exchanges in cigarette smokers

The analysis of sister chromatid exchange (SCE) might be a useful technique for the study of genetic damage in humans exposed to environmental mutagens and carcinogens. To obtain reference values for such studies we have analysed SCE-frequencies in peripheral lymphocytes of 43 healthy, occupationally non-exposed human subjects. Among these subjects cigarette smokers were found to have significantly higher SCE-frequencies (16.2±SD 3.6) than non-smokers (13.1±2.9). When smokers were subdivided into moderate (<10 cig. per day) and heavy (≥10cig. per day) smokers, a clear dose-effect of smoking on the SCE frequency was noted. This observation was supported by a retrospective inquiry into the smoking habits of 18 previously analysed psoriasis patients, among whom SCE-frequencies of 16.8±2.4 and 13.7±3.1 were recorded for smokers and non-smokers, respectively. In a group of 19 laboratory workers there was no significant difference between smokers (18.6±3.3) and non-smokers (19.5±5.0). The significantly increased SCE-frequencies recorded in this group support earlier observations and strongly suggest occupational exposure as a causative factor. The present results indicate that the SCE-frequency in healthy human subjects is influenced by individual smoking habits as well.

Smoking and sister chromatid exchange.

The present survey comprises analysis of sister chromatid exchange (SCE) frequencies in the peripheral blood lymphocytes of 100 subjects: 83 healthy men and women, both cigarette smokers and nonsmokers and 17 children. Both for men (30 smoking, 22 nonsmoking) and for women (13 smoking, 18 nonsmoking) the frequency of SCEs is significantly higher among smokers (group mean 9.6±S.E. 0.2) than among nonsmokers (group mean 8.1±S.E. 0.2). No difference is detected in the frequencies of metaphase chromosome aberrations analysed in the cultured lymphocytes of the same subjects. Young children (17 subjects, mean age 1.5 years) show a significantly lower frequency of SCEs (mean 5.1±0.6) than adults. While the induction of SCEs is known to provide a sensitive indicator of mutagen/carcinogen exposure in experimental assays, it may also give important information of in vivo exposure to genotoxic agents. However, on the basis of the present data, which confirm previous results, the effects of individual smoking habits should carefully be taken into account in evaluations of the effects of exogenous agents on SCE frequencies.

Prometaphase accumulation in murine bone marrow cells following in vivo treatment with alloxan

The aim of this study was to determine the effect of alloxan, an inhibitor of N-acetylglucosaminyl transferase that acts during the G2/M transition, on the course of mitosis in murine bone marrow cells. Mitotic cells from animals treated with different doses of alloxan were analyzed for the frequency of prometaphasic and metaphasic chromosomes based on their morphology and length. The results indicate that alloxan treatment substantially increases the frequency of prometaphase chromosomes. This suggests that N-acetylglucosaminyl transferase is also involved in the G2/M transition in bone marrow cells. Alloxan treatment also provides a method for obtaining large chromosomes for the analysis of chromosome bands, FISH and sister-chromatid exchanges.

Fifty years of cytogenetics: A parallel view of the evolution of cytogenetics and genotoxicology

A parallelism exists between human cytogenetics and cytogenetic toxicology. The breakthroughs, mostly coming from and used in clinical genetics, are widely used in genetic toxicology. The birth of human cytogenetics occurred in 1956 when it was published that the diploid number of chromosomes in humans is 46. The first stage in chromosome-induced mutagenesis began in 1938 when Sax published the effects of X-rays on the chromosomes of Drosophila. In 1959, the cytogenetic anomalies for Down, Klinefelter, and Turner syndromes were described, and parallelly in 1960, the first publication on chromosomal aberrations in man caused by ionizing radiation appeared. The cytogenetic analysis of chromosomal aberrations in cell cultures is considered one of the primary methods to evaluate induced mutagenesis. At the end of the 1960s, banding techniques allowed chromosomes to be individually identified, in parallel, the sister chromatid exchange analysis technology was described. Another milestone in the history of induced mutagenesis was the discovery that mutagenic agents were able to alter chromosomal division and segregation in gonads inducing meiotic nondisjunction. Here we review new approaches and applications such as biological dosimetry, translocation scoring using FISH, and micronucleus test. Chromosomal aberrations and micronucleus test are now effective cytogenetic biomarkers of early effect used as cancer predictors. Human cytogenetics has proven to be effective over its 50-year lifespan and, although each new technique that has appeared seemed to announce its end, the fact is that the current state of cytogenetics is in reality a collection of techniques that, while common, are cheap, fast, and wide-ranging. Therefore, in genotoxicology, they continue to be useful to identify mutagenic agents as well as to evaluate and analyze exposed populations.

Genotoxicity of thimerosal in cultured human lymphocytes with and without metabolic activation sister chromatid exchange analysis proliferation index and mitotic index

Thimerosal is an antiseptic containing 49.5% of ethyl mercury that has been used for years as a preservative in many infant vaccines and in flu vaccines. Thimerosal is an organic mercurial compound used as a preservative in biomedical preparations. In this study, we evaluated the genotoxic effect of thimerosal in cultured human peripheral blood lymphocytes using sister chromatid exchange analysis in culture conditions with and without S9 metabolic activation. This study is the first report investigating the genotoxic effects of thimerosal in cultured human peripheral blood lymphocyte cells using sister chromatid exchange analysis. An analysis of variance test (ANOVA) was performed to evaluate the results. Significant induction of sister chromatid exchanges was seen at concentrations between 0.2 and 0.6 microg/ml of thimerosal compared with negative control. A significant decrease (p<0.001) in mitotic index (MI) and proliferation index (PRI) as well as an increase in SCE frequency (p<0.001) was observed compared with control cultures. Our results indicate the genotoxic and cytotoxic effect of TH in cultured human peripheral blood lymphocytes at tested doses in cultures with/without S9 fraction.

Sister chromatid exchange analysis in patients with psoriasis

Psoriasis is a common, chronic inflammatory skin disease with unknown aetiology. An increased reactive oxygen species (ROS) and insufficient antioxidant activity have been determined in psoriatic lesions. The analysis of sister chromatid exchange (SCE) is a cytogenetic technique used to show DNA damage caused by an exchange of DNA fragments between sister chromatids. The study aimed to determine the rates of SCE in psoriatic patients (17 female and 19 male) and healthy controls (15 female and 15 male) as well as superoxide dismutase (SOD), glutathione peroxidase (GP) and catalase (CAT) activity in both groups. We found significantly higher SCE rates in the patients (P < 0.00001). In addition, statistically significant decreased levels of erythrocyte SOD and CAT activities were noted in the patients(P < 0.001 and P < 0.05 respectively). Furthermore, a statistically significant increased erythrocyte GP activity was found in the psoriasis group (P < 0.05). Our results indicate that chromosomal instability may play an important part in the aetiology of psoriasis. In addition, the results support the hypothesis of an imbalance in the oxidant-antioxidant system in psoriasis.