Evaluation of serum paraoxonase, 1 and its association with serum cholinesterase as a cause of congenital anomalies

Abhra Ghosh, Jagriti Bhardwaj, Robin Singh, Divya Baruhee


Background: Birth defects are conditions of prenatal origin that are present at birth, potentially impacting an infant's health, development, and/or survival. Several environmental toxins affect the growth of the fetus during the intrauterine period by affecting various cellular components. Pesticides and industrial chemicals are known toxins that can hinder the developmental process. In this study, authors are evaluating the relation of cholinesterase and paraoxonase-1 with visible congenital anomalies.

Methods: Sixty babies delivered in the labor room were selected for the study. They were divided into two groups. Thirty newborns with visible congenital anomalies were included in Group I. Only babies with visible congenital anomalies were taken as inclusion criteria for this group. This group was compared with Group II, which were taken as controls and consisted of 30 healthy newborns without any congenital anomalies. Serum cholinesterase and serum paraoxonase-1 were estimated and statistical tests were applied.

Results: Serum cholinesterase and serum paraoxonase-1 were significantly low in the babies with visible congenital anomalies. Serum cholinesterase levels showed a statistically significant positive correlation with serum paraoxonase 1 level in both the groups.

Conclusions: Decrease in acetylcholinesterase by various environmental toxins and the associated decrease in serum paraoxonase level imposes significant oxidant stress and the resultant risk of developing congenital anomalies.


Congenital anomalies, Cholinesterase, Paraoxonase 1

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Impact: Congenital anomalies. Available at: congenital-anomalies#tab=tab_3. Accessed on 8th June 2020.

Congenital anomalies (birth defects). Available at: disease/ gynaecology-and-obstetrics/congenital-anomalies-birth-defects. Accessed at 8th June 2020.

Khoury MJ. Epidemiology of birth defects. Epidemiol Rev. 1989;11:244-8.

Wellesley D, Boyd P, Dolk H, Pattenden S. An aetiological classification of birth defects for epidemiological research. J Med Genet. 2005;42:54-7.

Brennand DM, Jehanli AM, Wood PJ, Smith JL. Raised levels of maternal serum secretory acetylcholinesterase may be indicative of fetal neural tube defects in early pregnancy. Acta Obstet Gynecol Scand. 1998;77:8-13.

Loft AG, Høgdall E, Larsen SO, Nørgaard-Pedersen B. A comparison of amniotic fluid alpha-fetoprotein and acetylcholinesterase in the prenatal diagnosis of open neural tube defects and anterior abdominal wall defects. Prenat Diagn. 1993;13:93-109.

Engel SM, Berkowitz GS, Barr DB, Teitelbaum SL, Siskind J, Meisel SJ et al. Prenatal organophosphate metabolite and organochlorine levels and performance on the Brazelton Neonatal Behavioral Assessment Scale in a multi-ethnic pregnancy cohort. Am J Epidemiol. 2007;165:1397-404.

Gonzalez HL, Martín CFR, Luna RM, Canto HJ, Pinto ED, Perez HN, et al. Paraoxonase 1 polymorphisms and haplotypes and the risk for having offspring affected with spina bifida in Southeast Mexico. Birth Defects Res A Clin Mol Teratol. 2010;88:987-94.

Roy PS, Ghosh A. Cholinesterase as marker of congenital anomalies. Int J Sci Res. 2018;7(9):19-20.

Venkataraman B, Iyer G, Narayanan R. Erythrocyte and plasma cholinesterase activity in normal pregnancy. Indian J Physiol. 1990;34:26-8.

Elejalde BR, Peck G, Elejalde MM de. Determination of cholinesterase and acetylcholinesterase in amniotic fluid. Clin Genet. 2008;293:196-203.

Lozano-Paniagua D, Gómez-Martín A, Gil F, Parrón T, Alarcón R, Requena M, et al. Activity and determinants of cholinesterases and paraoxonase-1 in blood of workers exposed to non-cholinesterase inhibiting pesticides. Chem Biol Interact. 2016;259:160-7.

Farahat T, Shaheen HM, Sanad Z, Farag NA. Organophosphate pesticide exposure during pregnancy and adverse perinatal outcome. J Womens Health Care. 2016;5:336.

Thiermann H, Kehe K, Steinritz D, Mikler J, Hill I, Zilker T, et al. Red blood cell acetylcholinesterase and plasma butyrylcholinesterase status: important indicators for the treatment of patients poisoned by organophosphorus compounds. Arh Hig Rada Toksikol. 2007;58:359-66.

Bryk B, BenMoyal-Segal L, POdoly E, Livanh O, Eisenkraft A, Luria S, et al. Inherited and acquired interactions between AChE and PON1 polymorphisms modulate plasma acetylcholinesterase and paraoxonase activities. J Neurochem. 2005:92:1216-27.

Hofmann JN, Keifer MC, Furlong CE, De Roos AJ, Farin FM, Fenske RA, et al. Serum Cholinesterase inhibition in relation to paraoxonase-1 (PON-1) status among organophosphate-exposed agricultural pesticide handlers. Environ Health Perspect. 2009:117:1402-8.

Turgut G, Özcan A, Çakmak E, Baş L, Tatlıdede S, Öztürk O, et al. Paraoxonase-1 192 enzyme polymorphism in non-syndromic clefting: In patients and parents. J Cell Mol Biol. 2008:67.

Araoud M, Neffeti F, Douki W, Najjar MF, Kenani A. Paraoxonase 1 correlates with butyrylcholinesterase and gamma glutamyl transferase in workers chronically exposed to pesticides. J Occup Health. 2010;52:383-8.

Hernandez AF, Gomez MA, Pena G, Gil F, Rodrigo L, Villanueva E, Pla A. Effect of longterm exposure to pesticides on plasma esterases from plastic greenhouse workers. J Toxicol Environ Health. 2004;67:1095-108.

Richard SA, Frank EA, D'Souza CJ. Correlation between cholinesterase and paraoxonase 1 activities: case series of pesticide poisoning subjects. Bioimpacts. 2013;3:119.

Bhattacharya N, Phillip GS (eds.). Human fetal growth and development: first and second trimesters. Switzerland: Springer; 2016:94.

Kaushik A, Sharma HR, Jain S, Dawra J, Kaushik CP. Pesticide pollution of river Ghaggar in Haryana, India. Environ Monit Assess. 2010;160:61-9.

Singh S, Kumar V, Singh P, Thakur S, Banerjee BD, Rautela RS, et al. Genetic polymorphisms of GSTM1, GSTT1 and GSTP1 and susceptibility to DNA damage in workers occupationally exposed to organophosphate pesticides. Mutat Res Genet Toxicol Environ Mutagen. 2011;725:36-42.