Paraoxonase-1 genetic polymorphisms and susceptibility to DNA damage in workers occupationally exposed to organophosphate pesticides

Singh, Satyender; Kumar, Vivek; Thakur, Sachin; Banerjee, Basu Dev; Rautela, Rajender Singh; Grover, Shyam Sunder; Rawat, Devendra Singh; Pasha, Syed Tazeen; Jain, Sudhir; Ichhpujani, Rattan; Rai, Arvind

doi:10.1016/j.taap.2011.01.014

Cited by 58 publications

(41 citation statements)

References 51 publications

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“…23,[76][77][78][79][80][81][82][83][84][85][86][87][88][89][90][91] This list is not exhaustive but highlights both established markers of pesticide exposure (such as cholinesterase activity) and emerging biomarkers (such as the ''challenge assay,'' which assesses the DNA repair capacity of cells). It should be noted that most of these biomarkers are not used in the clinic at present; however, they have usefulness in research studies that aim to determine the etiology of cancers that have been linked to agrochemical exposure.…”

Section: Biomarkers Relevant To Pesticide-induced Cancersmentioning

confidence: 99%

Increased cancer burden among pesticide applicators and others due to pesticide exposure

Alavanja

Ross

Bonner

2013

CA A Cancer J Clinicians

287

209

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A growing number of well-designed epidemiological and molecular studies provide substantial evidence that the pesticides used in agricultural, commercial, and home and garden applications are associated with excess cancer risk. This risk is associated both with those applying the pesticide and, under some conditions, those who are simply bystanders to the application. In this article, the epidemiological, molecular biology, and toxicological evidence emerging from recent literature assessing the link between specific pesticides and several cancers including prostate cancer, non-Hodgkin lymphoma, leukemia, multiple myeloma, and breast cancer are integrated. Although the review is not exhaustive in its scope or depth, the literature does strongly suggest that the public health problem is real. If we are to avoid the introduction of harmful chemicals into the environment in the future, the integrated efforts of molecular biology, pesticide toxicology, and epidemiology are needed to help identify the human carcinogens and thereby improve our understanding of human carcinogenicity and reduce cancer risk. CA Cancer J Clin 2013;63:120-142.

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Section: Biomarkers Relevant To Pesticide-induced Cancersmentioning

confidence: 99%

Increased cancer burden among pesticide applicators and others due to pesticide exposure

Alavanja

Ross

Bonner

2013

CA A Cancer J Clinicians

287

209

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“…18,19 GSTT1 and NAT2 had no effect on DNA damage caused by OP exposure. However, OP exposed individuals with the concomitant GSTM1 and GSTT1 null genotypes experienced higher levels of DNA damage than those with the positive genotypes.…”

mentioning

confidence: 89%

“…Individuals with the null genotypes are suspected to be more susceptible to effects of OPs due to its reduced or absent metabolizing properties. 18,27 Four epidemiological studies have been conducted to determine whether GST (GSTM1 and GSTT1) and NAT2 DNA variants modify OP neurotoxicity and the results differ between these studies. In India, Abhishek et al 26 found that GSTT1 played a key role in OP susceptibility but GSTM1 had no effect on DNA damage.…”

mentioning

confidence: 99%

DNA variants and organophosphate neurotoxicity among emerging farmers in the Western Cape of South Africa

Glass

Dalvie

Holtman

et al. 2017

American J Industrial Med

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BackgroundPrevious epidemiological studies investigating modification of organophosphate (OP) neurotoxicity by xenobiotic metabolizing enzymes (XMEs) polymorphisms have produced inconsistent results.MethodsA cross‐sectional study of 301 emerging farmers was conducted. Neurotoxicity testing included forward and backward recall, digit span, and vibration sensitivity testing. Questionnaire data included demography, potential confounders, and work history of pesticide exposures. Genomic DNA was analyzed from study participants for DNA variants of two glutathione S‐transferases (GSTM1 and GSTT1), N‐acetyltransferase 2 (NAT2), and Paraoxonase 1 (PON1).ResultsThere was evidence of OP pesticide neurotoxicity modification by rs1799931 (NAT2), rs662 (PON1), and the null allele of GSTM1 in multivariate analysis. The strongest evidence of modification was observed for rs1799931 (NAT2) on the relationship between pesticide poisoning and impaired vibration sense.ConclusionsDNA variants of NAT2, PON1, and GSTM1 may modify OP neurotoxicity, and this requires further exploration.

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“…neuropsychological disorders, disruption of the endocrine system, developmental anomalies, hypersensitivity, disorders of the immune system and cancer development). 3 Paraoxonase (aryldialkylphosphatase, EC 3.1.8.1) is a calcium-dependent enzyme and possess the activities of organophosphatase, arylesterase and lactonase. It hydrolyzes organophosphorus insecticides (e.g.…”

Section: Introductionmentioning

confidence: 99%

Association Between PON1 L55M Polymorphism and PON1 Enzyme Activity in Patients with Leukemia.

Eras¹,

Tombak²,

Yalın³

et al. 2017

UHOD

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Paraoxonase 1 (PON1) is an important antioxidant enzyme which has a role in preventing the effects of systemic oxidative stress. The purpose of our study was to investigate the possible association between PON1 L55M polymorphism and leukemia development and to determine the relationship between PON1 genotypes and PON1 enzyme activities. Genotypes of 102 cases and 112 healthy controls were determined by PCR-RFLP. PON1 enzyme activity was determined according to Eckerson's method. The ratio of MM genotype belonging to PON1 L55M polymorphism in control group was 6.3% and was 7.8% in patients with leukemia (p= 0.39). PON1 enzyme activity was 118.8 ± 115.1 U/mL in control group, while decreased to 75.6 ± 64.4 U/mL in patients with leukemia (p= 0.004). PON1 enzyme activities of the individuals with MM genotypes belonging to PON1 L55M polymorphism was 57.43 ± 21.61 U/ mL in control group and decreased to 39.18 ± 45.61 U/mL in leukemic patients. Our results suggest that, PON1 L55M polymorphism genotype ratios do not affect leukemia development. However, reduced PON1 enzyme activity and also the combination of PON1 L55M polymorphism with reduced PON1 enzyme activity are associated with the increased risk of leukemia. Furthermore, older age may be a risk factor for developing leukemia. PON1 enzim aktivitesi Eckerson yöntemi ile ölçüldü. PON1 L55M polimorfizmine ait MM genotip oranları kontrol grubunda %6.3 iken lösemili hastalarda % 7.8 idi (p= 0.39). PON1 enzim aktivitesi kontrol grubunda 118.8 ± 115.1 U/mL iken lösemili hastalarda düşük olarak saptandı (75.6 ± 64.4 U/mL, p= 0.004). PON1 L55M polimorfizmine ait MM genotipli bireylerin PON1 enzim aktivitesi kontrol grubunda 57.43 ± 21.61 U/mL iken lösemili hastalarda düşük olarak saptandı (39.18 ± 45.61 U/mL). Bizim bulgularımız PON1 L55M polimorfizmi genotip oranlarının lösemi gelişimini etkilemediğini göstermektedir. Bununla birlikte, düşük PON1 enzim aktivitesi tek başına ve PON1 L55M polimorfizmi ile birlikte lösemi riski artışı ile ilişkilidir. Ayrıca ileri yaş lösemiye yakalanma olasılığını yükseltir.

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Paraoxonase-1 genetic polymorphisms and susceptibility to DNA damage in workers occupationally exposed to organophosphate pesticides

Cited by 58 publications

References 51 publications

Increased cancer burden among pesticide applicators and others due to pesticide exposure

Increased cancer burden among pesticide applicators and others due to pesticide exposure

DNA variants and organophosphate neurotoxicity among emerging farmers in the Western Cape of South Africa

Association Between PON1 L55M Polymorphism and PON1 Enzyme Activity in Patients with Leukemia.

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