Oxidative stress and antioxidant markers in patients with alopecia areata: A comparative cross-sectional study

Background: Alopecia areata is a chronic inflammatory skin disease. Oxidative stress may contribute to the pathogenesis of this condition. Aim: To evaluate the serum oxidative stress markers and antioxidant capacity in patients with alopecia areata. Methods: This cross-sectional study was performed on 40 patients with alopecia areata and 40 healthy controls. The fasting blood sugar, C-reactive protein, lipid profile, and serum oxidative markers, including advanced glycation end products and advanced oxidation protein products, were measured in this study. Also, antioxidant enzymes, including paraoxonase-1, lecithin-cholesterol acyltransferase and serum ferric-reducing antioxidant power, were determined. Results: The serum levels of advanced glycation end products and advanced oxidation protein products were significantly higher in patients with alopecia areata, compared to the controls (P < 0.001), whereas the levels of ferric-reducing antioxidant power, paraoxonase-1 and lecithin-cholesterol acyltransferase were significantly lower in patients with alopecia areata, compared to the controls (P < 0.001). The mean fasting blood sugar level was significantly higher in patients with alopecia areata, compared to the controls. The ferric reducing antioxidant power level was significantly associated with the percentage of hair loss (P = 0.01, r = 0.4) and the serum C-reactive protein level (P = 0.03, r = –0.3) in patients with alopecia areata. Limitations: Since the current study had a cross-sectional design, no cause-effect relationship was established between alopecia areata and oxidative stress. The sample size of our study was also small. Conclusion: Based on the present results, the oxidant-antioxidant enzymatic system is impaired in alopecia areata due to the increased oxidative products and decreased antioxidant activity

Factors associated to serum paraoxonase 1 activity in patients with cardiovascular disease

ABSTRACT Objectives: Paraoxonase 1 (PON1) is an enzyme that has antioxidant potential, which confers a protective effect against the atherosclerotic process. However, studies associating genetics, dietary patterns and PON1 activity in individuals with cardiovascular disease (CVD) are scarce. Thus, the aim of the current study was to evaluate the influence of dietary factors on serum PON1 in CVD patients. Subjects and methods: Cross-sectional, sub-study of the BALANCE Program Trial. All patients aged 45 years or older and had evidence of established atherosclerotic disease in the preceding 10 years. Body weight, height, waist circumference, blood pressure, lipid profile and fasting glucose were collected. Food intake was assessed with 24-h dietary recall. Data was analyzed using SAS University Edition and a P value ≤ 0.05 was considered statistically significant. Sample was divided into three groups, according to the PON1 T(-107)C genotype (CC, CT and TT) and serum PON1 activity (Low, Medium, High). Results: There were no genotype differences for major factors. However, the systolic blood pressure was lower for CT individuals (p<0.05). Intake of cholesterol, saturated fatty acids (SFA) and monounsaturated fatty acids (MUFAS) was higher in patients with lower PON1 activity. Lipid ingestion tended to be higher in patients with lower PON1 activity (p=0.08). In the multivariate logistic regression model, SFA intake (P=0.03), genotype (P=0.09), gender (P=0.04), age (P=0.07) and carbohydrate intake (P=0.16) contributed the most to the serum PON1 activity. Conclusion: Based on these findings, nutritional guidance for these patients becomes essential, since dietary components interact with serum PON1 activity more than genotype.

Paraoxonase 1 serum activity in women: the effects of menopause, the C(-107)T polymorphism and food intake

ABSTRACT Objective The aims of this study were to investigate changes in serum paraoxonase 1 (PON1) activity in women at the pre and postmenopausal stages and its association with the PON1 C(-107)T polymorphism and food intake profile. Subjects and methods A cross-sectional study with female patients aged between 35 and 59 years old was conducted. Women were divided into two groups: premenopausal (n = 40) and postmenopausal (n = 36). Women enrolled in the study had serum PON1, total cholesterol, HDL, LDL, glucose and HbA1c, as well as the BMI measured. Additionally, women were genotyped for the PON1 T(-107)C polymorphism and the food intake profile was obtained through interview. Results Glucose (p = 0.03), HbA1c (p = 0.002) and total cholesterol (p = 0.002)concentrations were higher in post than premenopausal women, however PON1 activity was not different (p > 0.05). Carriers of the C allele had higher PON1 activity (CC: 88.9 ± 6.5 U/mL and CT: 79.9 ± 4.7 U/mL) than women of the TT genotype (66.6 ± 5.9 U/mL) (p < 0.05). However, the model predicting PON1 activity was slightly better when genotype, total fat and cholesterol content in the diet were all included. Conclusion In sum, we observed that the PON1 C(-107)T genotype was the major regulator of PON1 activity, and menopause had no effect on PON1 activity. The lipid and glycemic profile were altered in postmenopausal women.

Assessment Of Serum Paraoxonase-1 Enzyme Activity, Malondialdehyde And Vitamin-c In Oral Premalignancies

Background:Oral premalignancies are a group of disease or syndromes which if left untreatedcanleadtocancer.ItcarriesagreatsignificanceinIndianperspective. Theactual figure of oral cancers arising from oral premalignancies is not known and to predict accuratelythemalignanttransformationsofthemisstillnotpossible.Oxidativestressisa known player behind cancerogenesis. Recently decreased Paraoxonase-1 activity and increasedoxidativestressmarkerswarefoundtobeassociatedwithOralSquamousCell Carcinoma. So, thereis astrongpossibilityofasimilar findingin Oral Premalignanciestoo. Aim: This studyaims to investigatethecor-relation between serum PON-1 activityand oxidative stress markers (MDA& Vitamin C) in patients with Oral Premalignancies. MaterialandMethods:Atotalof62patientswithclinically diagnosedoralpremalignant lesions anddiseasedcontrolswerechosenforthe study. Venous bloodsampleswerecollectedandPON-1,MDA (inse-rum)&Vitaminc (inplasma) wereanalysed spectro-photometrically. Results:A significant decreased serum PON-1 activity (P<0.05) and concomitant significantlyincreased serum MDA(P<0.05)anddecreased Vitamin Clevels (P<0.05) were observedinpremalignanciescomparedtothecontrols.Thesefinding weremorepronounced inOral Leukoplakia (OL) thaninOral Submucous Fibrosis (OSMF)withasignificantdifference.Meanlevelsoftheanalysedparameters differedaccordinglyin theclinicalgrades of oral premalignancies. Conclusion:Itcanbeenvis-agedthatserumPON-1activity andincreasedoxidativestress mightbe acontributingfactorbehindpathogenesisandprogressionofOralPremalignant Diseases

Paraoxonase (PON1) L55M and Q192R polymorphisms in major depression and bipolar affective disorder

Abstract Background Oxidative and nitrosative stress pathways, along with immune-inflammatory response, might play an important role in the pathogenic mechanisms underlying major depression and bipolar disorder. Objective The aim of the present study is to investigate paraoxonase 1 polymorphisms and its correlations with disease parameters in patients with major depression and bipolar affective disorder. Methods PON1 L55M and Q192R single nucleotide polymorphisms were analyzed in a group consisted of 100 patients with major depression, and 100 patients with bipolar affective disorder and 96 healthy controls. Polymorphisms were analyzed by using polymerase chain reaction. Results Our findings reported no association between Q192R and L55M polymorphisms of PON1 and major depression and bipolar disorder. Additionally, there was no association between the PON1 genotypes and disease variables in both depressed and bipolar patients. Discussion Evaluating the different stages of patients with affective disorders and and investigating the connection between PON1 polymorphisms and treatment outcomes will help us to clarify the relationship between PON1 and mood disorders.

Study on the Correlation of Gene Polymorphism with Antiplatelet Efficacy of Clopidogrel in PAD Patients / 中国药房

OBJECTIVE:To investigate the correlation of gene polymorphism in peripheral artery disease(PAD)patients with antiplatelet efficacy of clopidogrel. METHODS:Reviewing related domestic and foreign literatures in recent years,the correlation of gene polymorphism in PAD patients with antiplatelet efficacy of clopidogrel was summarized and analyzed. RESULTS&CON-CLUSIONS:At present,a variety of genes associated with clopidogrel antiplatelet efficacy and major adverse cardiovascular events (MACE)have been identified,including cytochrome P450(CYP)2C19,adenosine three phosphate binding cassette B subfamily 1 (ABCB1),paraoxonase 1 (PON1) and adenosine diphosphate P2Y12 receptor (P2Y12),etc. CYP2C19*2,*3 allele may reduce the antiplatelet effect of clopidogrel. Their correlation has been confirmed by a number of studies,and study results are broadly con-sistent. Mutations in the ABCB1 C3435T and PON1 Q192R sites may lead to a lower response to clopidogrel and increase the risk of MACE;but there is a lack of large-scale prospective clinical studies,and the present results are inconsistent. P2Y12 gene poly-morphism in PAD patients has not been found to be significantly associated with clopidogrel efficacy.

Association of altered serum levels of Chemerin, Paraoxonase-1 (PON1), Asymmetric Dimethyl arginine (ADMA) and obesitin the development of Polycystic Ovarian Syndrome (PCOS) in Egyptian women

Chemerinwas recently added to the adipokine family and was identified in human ovarian follicles and follicular fluid that suggests a direct correlation between chemerin and PCOS. Asymmetric dimethyl arginine (ADMA) is involved in endothelial dysfunctionthe atherogenic potential of ADMA has been investigated in young patients with PCOS. Oxidative stress is considered to be implicated in the pathophysiology of PCOS.Paraoxonase 1 (PON1) is an antioxidant enzyme and its concentration has been shown to be inversely associated with oxidative stress. Objectives: Evaluation of serum chemerin, ADMA, PON1in obese and non-obese polycystic ovarian patients to postulate their role in pathogenesis of PCOS. Methods: Ninetynuligravida women aged 20-35 (60 with PCOS and 30 controls) were recruited. Fasting blood was obtained on day 2 or 3 of the menstrual cycle. Clinical evaluation, hormonal profile, Chemerin, ADMA and PON1 were assessed. Results: There was a significant increase in serum chemerinlevels in PCOS obese group when compared with PCOS non obese patients and healthy controls non obese and obese respectively. Serum ADMA level was increased significantly in PCOS obese group as compared to the PCOS non obese group , control non obese and control obese. Paraoxonase was decreased stepwise significantly from the control non obese group and control obese group to PCOS non obese patients then PCOS obese patients to. Conclusions: it could be suggested that increased chemerin has a role in PCOS development andaltered ADMA and PON1 associated withobesity and oxidative stress may exacerbate the condition.

Correlation Between Serum Paraoxonase Activity and High Density Lipoprotein Levels in Type2 Diabetes Predisposing to Aterosclerosis.

Human serum paraoxonase is physically associated with HDL and has been implicated in the detoxification of organophosphates and possibly in the prevention of LDL lipid peroxidation and therefore retards atherosclerosis. HDL levels are inversely related to the risk of developing atherosclerosis. We investigated the serum activity and concentration of paraoxonase and HDL levels in 104 subjects (42 diabetic patients without complications, 42 controls, 20 diabetic patients with complications.). Paraoxonase activity was found to be lower in diabetic patients than in controls. Similarly there was reduction in HDL levels in cases suggesting a positive correlation between HDL and paraoxonase levels.

Correlation between paraoxonase 1 Q192R polymorphism and ischemic stroke in Chinese Han population / 国际脑血管病杂志

Objective To investigate the correlation between large artery atherosclerotic stroke and paraoxonase 1 (PON1) Q192R polymorphism.Methods Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used to detect the PON1 Q192R polymorphism of 120 patients with large artery atherosclerotic stroke (case group) and 117 healthy subjects (control group).Results There was significant difference in the genotype distribution of PON1 Q192R (x2 =18.727,P＜0.001) and the allele frequency distribution (x2 =16.427,P ＜0.001) between the case group and the control group.Multivariate logistic regression analysis showed that RR genotype was an independent risk factor for large artery atherosclerotic stroke (odds ratio 1.377,95％ confidence interval 1.032-2.185; P =0.026).Conclusions The allelic gene mutation rate of PON1 Q192R in patients with large artery atherosclerotic stroke was significantly higher than that in the healthy population.RR genotype is an independent risk factor for large artery atherosclerotic stroke.

Polimorfismo dos genes NQO1 e PON1 na etiologia das leucemias agudas infantis

As leucemias pediátricas são doenças hetereogêneas, consequentes da combinação de susceptibilidade genética individual e exposições a fatores ambientais. Polimorfismos em genes que codificam enzimas do metabolismo modificam correlações de riscos entre exposições e as leucemias. Baseados nas hipóteses que as leucemias na infância têm origem durante a vida intra-uterina, estudos demonstraram associações de exposições maternas durante a gestação à pesticidas e algumas substâncias medicamentosas. Especulamos se os polimorfismos NQO1C609T, PON1Q192R e PON1L55M poderiam influenciar na etiologia das leucemias infantis. O objetivo principal deste estudo foi determinar a freqüência dos polimorfismos nos genes NQO1 e PON1 em crianças com leucemias agudas e suas mães para avaliar as possíveis associações de riscos entre susceptibilidade genética e exposição ambiental. Foram testadas amostras brasileiras de crianças com diagnóstico de leucemia aguda (578); 393 amostras de crianças saudáveis não-sindrômicas (controles), bem como, amostras das respectivas mães. As genotipagens dos genes NQO1 e PON1 foram realizadas através da técnica de discriminação alélica por PCR em tempo real utilizando sondas TaqMan. O genótipo mutante do polimorfismo NQO1C609T confere um risco para o desenvolvimento de leucemias agudas [OR=2,5; IC95%, 1,05-5,88] às crianças com idade ≥24 meses. Na análise estratificada por subtipo leucêmico, nas leucemias mielóides o genótipo mutante confere um risco elevado [OR=5,44; IC95%, 1,08-27,63] nas crianças entre 13-24 meses de idade. A somatória dos genótipos heterozigoto e homozigoto-mutante do NQO1 apresentou uma tendência de risco 2,0 vezes maior da ocorrência nas leucemias com rearranjos do gene MLL [IC95%, 0,94-4,57]. A presença do alelo polimórfico do NQO1C609T nas mães apresenta risco para leucemias agudas pediátricas [OR=1,76; IC95%, 1,03-3,02]. O polimorfismo PON1L55M apresentou associação de risco para LLA, tanto com o genótipo mutante [OR=3,21; IC95%, 1,21-8,51], quanto com a somatória dos genótipos heterozigoto e homozigoto-mutante [OR= 1,94; IC95%, 1,02-3,68]. Este risco aumenta nas crianças com idade entre 13-24 meses [OR=3,22; IC95%, 1,15-8,99]. Foram realizadas análises de exposição materna a pesticidas, antibióticos e infusões de ervas. O polimorfismo do gene NQO1 não mostrou associação de risco, enquanto os polimorfismos do gene PON1 mostraram associações com as exposições e apresentaram magnitudes de risco independentes do tipo de exposição

Pediatric leukemias are heterogeneous diseases which result from the combination of individual genetic susceptibility factors and environmental exposures. Polymorphisms in genes that codify metabolic enzymes alter the risk associations between exposures and leukemias. Based on the prenatal origin of leukemias, studies have demonstrated association between maternal exposures during pregnancy to pesticides or some medicines and childhood leukemia. We speculated whether the polymorphisms NQO1C609T, PON1Q192R and PON1L55M could influence the etiology of the infant leukemias. The main objective of this study was to determine the frequency of these polymorphisms in children with acute leukemia and their mothers to evaluate the possible risk associations between genetic susceptibility and environmental exposures. Samples from children diagnosed with acute leukemia were tested (cases); samples from health children (controls) as well as samples from the respective mothers of both cases and controls were also tested. The genotyping of NQO1 and PON1 was performed using the allelic discrimination real time PCR assay using TaqMan probes. The NQO1C609T mutant genotype was associated with a higher risk of acute leukemia development [OR=2.5; CI95%, 1.05-5.88] in children ≥24 months-old. In the stratified analysis considering the leukemia subtypes, the group of myeloid leukemias presented an increased risk [OR=5.44; CI95%, 1.08-27.63] in children between 13-24 months-old. The sum of NQO1 heterozygous and mutant homozygous alleles showed a trend of 2-fold higher risk of leukemia occurrence in association with MLL gene rearrangements [CI95%, 0.94-4.57]. The polymorphism NQO1C609T within the mothers’ group was associated with childhood leukemias [OR=1.76; CI95%, 1.03-3.02]. The polymorphism PON1L55M presented a risk association with ALL, both considering the homozygous mutant genotype [OR=3.21; CI95%, 1.21-8.51], as well as considering the sum of the heterozygous and the mutant homozygous genotypes [OR= 1.94; CI95%, 1.02-3.68]. This risk increases in children aged between 13-24 months [OR=3.22; CI95%, 1.15-8.99]. The maternal exposures during pregnancy to pesticides, antibiotics and herbal infusions were analyzed in comparison to the genotypes. While no interaction risk associations were observed with the NQO1 polymorphism, the PON1 polymorphisms showed associations with the exposures and presented magnitudes independent of the type of exposure

Effects of Intronic and Exonic Polymorphisms of Paraoxonase 1 (PON1) Gene on Serum PON1 Activity in a Korean Population

Paraoxonase 1 (PON1) hydrolyzes a number of toxic organophosphorous compounds and reduces lipid peroxide accumulation, and PON1 genetic polymorphisms in the coding region modulate serum PON1 activity. In this study, we investigated the association between 3 polymorphisms of PON1 located in intron 5 (17899insdelTT and 17974CT) and exon 6 (192QR) and serum PON1 activity. The genetic polymorphisms and serum activity of PON1 were analyzed in 153 healthy Koreans by using a direct sequencing assay and spectrophotometric method, respectively. A significant linkage disequilibrium (LD) was observed between all tested single nucleotide polymorphisms, with the strongest LD observed between 17899insdelTT and 192QR (D' = 0.984). The 17899insdelTT, 17974CT and 192QR genetic polymorphisms were associated with significant differences in serum paraoxonase activity. In multiple regression analyses, smoking, triglyceride level, high-density lipoprotein (HDL) level, and the 17899insdelTT and 192QR genetic polymorphisms were significant determinants of serum paraoxonase activity, while age, smoking, triglyceride level, HDL level, and the 192QR genetic polymorphism were significant determinants of serum arylesterase activity. These results suggest that although the 192QR genetic polymorphism in the coding region of PON1 is primarily associated with serum PON1 activity, the intronic polymorphisms are also involved in serum PON1 activity, and this association may be mediated by LD.

Proatherogenic or antiatherogenic high density lipoprotein type in acute coronary syndrome and healthy male person.

Aim: To make proatherogenic/antiatherogenic HDL type criteria using Apolipoprotein A-I (ApoA-I), Paraoxonase-1 (PON-1), Neopterin and HDL-cholesterol levels, which may be useful in clinical practice. Methods: This was a case control study recruiting 52 subjects with Acute Coronary Syndrome (ACS) and 30 control healthy subjects. HDL type was classifi ed into antiatherogenic and proatherogenic based on the levels of ApoA-I, PON-1, Neopterin and HDL-cholesterol. Concentrations of ApoA-I was measured by immunoturbidimetry method, PON-1 was measured by colorimetric method, Neopterin was measured by ELISA, and HDL-C was determined by homogenous method. Univariate logistic regression analysis was done using ACS as a dependent variable and levels of ApoA-I, PON-1, Neopterin and HDL-cholesterol as independent variables. Proatherogenic/antiatherogenic HDL type was determined by using ApoA-I, PON-1, Neopterin and HDL-cholesterol cut off and odd ratios. Results: Patient’s age was 50.89 + 12.63 year, HDL-C was 39.82 + 9.84 mg/dL, Apo A-1 was 119.77 + 32.05 mg/ dL, PON-1 was 41.26 + 18.19 kU/L, Neopterin was 16.22 + 38.10 nmol/L. Cut offs of ApoA-I, PON-1 and Neopterin successively were 124.5 mg/dL, 40.8 kU/L, and 7.016 nmol/L. On univariate logistic regression analysis showed that OR of ApoA-I, PON-1 and Neopterin respectively were 29.759 (95% CI : 4.074 – 217.382), 1.647 (95% CI : 0.412 – 6.586), 4.317 (95% CI : 1.098 – 16.977). Using scoring system, we concluded that total score > 18 was proatherogenic HDL type, and total score < 18 was antiatherogenic HDL type. With this scoring we found 78.85% had proatherogenic HDL type in ACS population. Conclusions: Dysfunctional HDL or proatherogenic/antiatherogenic HDL type can be predicted by using ApoA-I – PON-1 – Neopterin – HDL-cholesterol scoring system. Those with score of 18 are supposed to have antiatherogenic HDL type, and those with score of > 18 were having proatherogenic HDL type.

Paraoxonase 1 gene polymorphisms contribute to coronary artery disease risk among north Indians.

Background: Polymorphisms in paraoxonase 1 (PON1) coding for PON1 enzyme have been studied as genetic markers of coronary artery disease (CAD). PON1 Q192R and PON1 L55M polymorphisms have been analyzed extensively, but data on association and role of these polymorphisms in the etiology of CAD are conflicting. In this study, we tested the genetic association between PON1 Q192R and PON1 L55M polymorphisms and CAD among north Indians. Materials and Methods: Two hundred eighty-five angiographically proven patients with coronary artery disease and 200 sex-matched and ethnically matched controls were genotyped for 2 PON1 polymorphisms by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. Genotype/ allele frequencies were compared in patients and controls using the chi-square test. Results: At PON1-192 locus, there were significant differences between patients and controls (P< 0.05), leading to significant odds ratios for RR genotype (OR= 1.92, CI: 1.19-3.10) and *R allele (OR= 1.30, CI: 1.00-1.70). These odds ratios were higher in the sub-sample of smokers (2.84 and 1.45, respectively). Binary logistic regression analysis also confirmed that *R allele carriers (QR and RR) have a higher risk of CAD (OR= 3.54, CI: 1.67-5.53). PON1-55 locus did not show significant differences between patients and controls, but LL genotype and *L allele were significant risk factors in the nonsmoker group. RL haplotype was also significantly associated with CAD risk (OR= 1.44, CI: 1.08-1.93). Conclusions: PON1-192R allele and RR genotype are significantly associated with CAD patients from the north Indian population (Uttar Pradesh). This association was stronger in smokers, supporting the conclusion that an interaction between PON1 activity and smoking augments CAD risk. Further studies with larger sample size are warranted to confirm these associations in different Indian populations.

Correlación directa entre FEF25-75 y la actividad de la paraoxonasa plasmática en pacientes asmáticos adultos / Direct correlation between FEF25-75 and plasmatic paraoxonase activity in adult patients with asthma

Introducción: El incremento en la actividad de mieloperoxidasa (AAPO) (EC 1.11.1.7) plasmática ha sido relacionada con la evolución de diferentes patologías destacando las enfermedades crónico-degenerativas que tienen en común el cursar con un estado de estrés oxidativo (EO) concomitante a un proceso inflamatorio persistente. Este es el caso del asma. La enzima paraoxonasa (PON-1) (EC 3.1.1.2), es una arilesterasa que forma parte de la APO A-I de laa HDL. Su función catalítica le permite hidrolizar hidroperóxidos formados durante la lipoperoxídación de lipoproteínas y membranas como consecuencia de un EO. A la PON-1 se ha considerado como protectora de las lipoproteínas al interrumpir la oxidación de las LDL y disminuir el daño a estructuras celulares. Es una actividad enzimática que representa a la defensa antiestrés oxidativo. Objetivos: Demostrar que el estrés oxidativo del paciente asmático puede ser evaluado por el incremento de MPO como marcador de daño oxidante y que la función respiratoria adecuada puede ser relacionada con la capacidad de defensa antioxidante representada por la actividad de la PON-1. Métodos: La actividad de ambas enzimas fue determinada en el plasma de un grupo de pacientes con asma leve a moderada comparado con un grupo control formado por individuos clínicamente sanos. Resultados: En el grupo de pacientes con asma, la actividad de MPO se incrementó en un 42% (57.31 ± 7.2 U vs 33.34 ± 4.7 U p<0.05), mientras que se observó un decremento del 52% (0.09 ±0.1 nmol p-nitrofenol/mg prot vs 0.05 ± 0.01 nmol p-nitrofenol/mg prot p<0.01) en la actividad de la PON-1. La actividad de la MPO mostró una correlación inversamente proporcional con el FEV1 con una r de Spearman de -0.57 y la PON-1 mostró una correlación directamente proporcional con el FEF25-75 con una r de Spearman de 0.64. Conclusiones: Se demuestra por primera vez que los pacientes con asma, en los que se presenta un estado de estrés oxidativo que afecta ...

Introduction: Plasma myeloperoxidase activity (MPO) (EC 1.11.1.7) has been related to several chronic-degenerative diseases such as asthma, which have in common a chronic inflammatory process. Paraoxonase (PON-1) (EC 3.1.1.2), is an arylesterase enzyme that has a hydroperoxide catalytic function. This enzyme is a component of APO A-l located in HDL. PON1 is has been considered to protect lipoproteins, because it interrupts the oxidation process of LDL, conducive to the atherosclerotic process. Objectives: To demonstrate that, a) oxidative stress in asthmatic patients correlates with the MPO activity, and b) demonstrate the role of PON 1 activity as a biomarker of their pulmonary function. Methods: The activity of both enzymes was measured in plasma of patients with asthma and compared to a control group of healthy subjects. Results: In the group of patients with asthma, MPO activity increased 42% (57.31 ± 7.2 U vs 33.34 ± 4.7 U p<0.05), while PON-1 activity decreased 52% (0.09 ±0.1 nmol p-nitrophenol/mg prot vs 0.05 ± 0.01 nmol p-nitrophenol/mg prot p<0.01). MPO activity showed an inverse correlation with FEV, with a Spearman r of -0.57, while PON-1 activiy showed a direct correlation with FEF25-75, Spearman r of0.64. Conclusions: In this study we show, for the first time, that asthma patients, in whom there is a state of oxidative stress that affects the pulmonary function, PON-1 determination can be useful as a predictor of a better pulmonary function, whereas an increment in MPO activity could be associated to an acute inflammatory process, implicating cellular damage. * U = U/mg of protein'.