RESEARCH PAPER
Lack of association between two genetic polymorphisms of SOD2 (rs2758339 and rs5746136) and the risk of opium dependency
 
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Department of Biology, College of Sciences, Shiraz University, Shiraz 71467-13565, Iran
 
 
Submission date: 2017-01-21
 
 
Acceptance date: 2017-03-23
 
 
Online publication date: 2017-07-06
 
 
Publication date: 2019-12-20
 
 
Corresponding author
Mostafa Saadat   

Department of Biology, College of Sciences, Shiraz University, Shiraz, 71454 Iran. Tel.: +9871 36137432; fax: +9871 32280926.
 
 
Pol. Ann. Med. 2017;24(2):194-198
 
KEYWORDS
ABSTRACT
Introduction:
Superoxide dismutase-2 (EC 1.15.1.1; SOD2, OMIM: 147460) is a tetrameric enzyme which contains manganese in its active site. It is an important enzyme involved in the cellular detoxification by converting highly toxic superoxide radicals into less reactive molecules, hydrogen peroxide and oxygen. Several single nucleotide polymorphisms have been well defined in the gene encoding SOD2, including the potentially functional polymorphisms of rs2758339 and rs5746136.

Aim:
The aim of the present study is to investigate the associations between the rs2758339 (A/C substitution) and rs5746136 (A/G substitution) polymorphisms and the risk of dependency to opium.

Material and methods:
The present case–control study was performed in Shiraz (southern Iran) on 143 opium dependent and 569 healthy controls. The genotypes of the rs2758339 and rs5746136 polymorphisms were determined by polymerase chain reaction.

Results and discussion:
Statistical analysis showed that there was no significant association between the study polymorphisms and the risk of opium dependency. A significant linkage disequilibrium was observed between the study SOD2 polymorphisms. Statistical analysis showed that there was no significant association between the haplotypes of the polymorphisms and the risk of opium dependency.

Conclusions:
The present data revealed that the rs2758339 and rs5746136 polymorphisms of SOD2 are not risk factors for dependency to opium.

ACKNOWLEDGEMENTS
The authors are indebted to the participants for their close cooperation. The authors are indebted to Dr. Maryam Ansari- Lari for her critical reading the manuscript and for her contribution in discussion. This study was supported by Shiraz University, Iran.
CONFLICT OF INTEREST
None declared.
REFERENCES (36)
1.
Beckman G, Lundgren E, Tarnvik A. Superoxide dismutase isozymes in different human tissues, their genetic control and intracellular localization. Hum Hered. 1973;23:338–345.
 
2.
Beck Y, Oren R, Amit B, et al. Human Mn superoxide dismutase cDNA sequence. Nucleic Acids Res. 1987;15:9076.
 
3.
Niwa J, Yamada S, Ishigaki S, et al. Disulfide bond mediates aggregation, toxicity, and ubiquitylation of familial amyotrophic lateral sclerosis-linked mutant SOD1. J Biol Chem. 2007;282:28087–28095.
 
4.
Wan XS, Devalaraja MN, St Clair DK. Molecular structure and organization of the human manganese superoxide dismutase gene. DNA Cell Biol. 1994;13:1127–1136.
 
5.
Hernandez-Saavedra D, McCord JM. Association of a new intronic polymorphism of the SOD2 gene (G1677T) with cancer. Cell Biochem Funct. 2009;27:223–227.
 
6.
Ebrahimpour S, Saadat I. Association of CAT C-262T and SOD1 A251G single nucleotide polymorphisms susceptible to gastric cancer. Mol Biol Res Commun. 2014;3:223–229.
 
7.
Zhou Y, Shuai P, Li X, et al. Association of SOD2 polymorphisms with primary open angle glaucoma in a Chinese population. Ophthalmic Genet. 2015;36:43–49.
 
8.
Poggi C, Giusti B, Vestri A, et al. Genetic polymorphisms of antioxidant enzymes in preterm infants. J Matern Fetal Neonatal Med. 2012;25(suppl 4):131–134.
 
9.
Ding G, Liu F, Shen B, et al. The association between polymorphisms in prooxidant or antioxidant enzymes (myeloperoxidase, SOD2, and CAT) and genes and prostate cancer risk in the Chinese population of Han nationality. Clin Genitourin Cancer. 2012;10:251–255.
 
10.
Giusti B, Vestrini A, Poggi C, et al. Genetic polymorphisms of antioxidant enzymes as risk factors for oxidative stressassociated complications in preterm infants. Free Radic Res. 2012;46:1130–1139.
 
11.
Park HY, Kim JH, Lim YH, et al. Influence of genetic polymorphisms on the association between phthalate exposure and pulmonary function in the elderly. Environ Res. 2013;122:18–24.
 
12.
Wiener HW, Perry RT, Chen Z, et al. A polymorphism in SOD2 is associated with development of Alzheimer's disease. Genes Brain Behav. 2007;6:770–775.
 
13.
Cunha-Oliveira T, Rego AC, Oliveira CR. Cellular and molecular mechanisms involved in the neurotoxicity of opioid and psychostimulant drugs. Brain Res Rev. 2008;58:192–208.
 
14.
Ghazavi A, Mosayebi G, Solhi H, et al. Serum markers of inflammation and oxidative stress in chronic opium (Taryak) smokers. Immunol Lett. 2013;153:22–26.
 
15.
Soykut B, Eken A, Erdem O, et al. Oxidative stress enzyme status and frequency of micronuclei in heroin addicts in Turkey. Toxicol Mech Methods. 2013;23:684–688.
 
16.
Payabvash S, Beheshtian A, Salmasi AH, et al. Chronic morphine treatment induces oxidant and apoptotic damage in the mice liver. Life Sci. 2006;79:972–980.
 
17.
Mao J, Sung B, Ji R, et al. Neuronal apoptosis associated with morphine tolerance: evidence for an opioid-induced neurotoxic mechanism. J Neurosci. 2002;22:7650–7661.
 
18.
Zhou J, Li Y, Yan G, et al. Protective role of taurine against morphine-induced neurotoxicity in C6 cells via inhibition of oxidative stress. Neurotox Res. 2011;4:334–342.
 
19.
Saify K, Saadat I, Saadat M. Down-regulation of antioxidant genes in human SH-SY5Y cells after treatment with morphine. Life Sci. 2016;144:26–29.
 
20.
Saify K, Saadat M. Expression patterns of antioxidant genes in human SH-SY5Y cells after treatment with methadone. Psychiatry Res. 2015;230:116–119.
 
21.
Nakatome M, Miyaji A, Mochizuki K, et al. Association between the GST genetic polymorphisms and methamphetamine abusers in the Japanese population. Leg Med (Tokyo). 2009;11(suppl 1):S468–S470.
 
22.
Koizumi H, Hashimoto K, Kumakiri C, et al. Association between the glutathione S-transferase M1 gene deletion and female methamphetamine abusers. Am J Med Genet B: Neuropsychiatr Genet. 2004;126B:43–45.
 
23.
Khalighinasab MR, Saify K, Saadat M. Association between GSTM1 and GSTT1 polymorphisms and susceptibility to methamphetamine dependence. Mol Biol Res Commun. 2015;4:25–32.
 
24.
Khalighinasab MR, Saify K, Saadat M. Association between null alleles of GSTM1 and GSTT1 and dependence to heroin and opium. Psychiatry Res. 2015;228:977–978.
 
25.
Hashimoto T, Hashimoto K, Miyatake R, et al. Association study between polymorphisms in glutathione-related genes and methamphetamine use disorder in a Japanese population. Am J Med Genet B: Neuropsychiatr Genet. 2008;147B:1040–1046.
 
26.
Saify K, Khalighinasab MR, Saadat M. No association between GSTM1 and GSTT1 genetic polymorphisms and susceptibility to opium sap dependence. Mol Biol Res Commun. 2016;5:59–64.
 
27.
Rafiee L, Saadat I, Saadat M. Glutathione S-transferase genetic polymorphisms (GSTM1, GSTT1 and GSTO2) in three Iranian populations. Mol Biol Rep. 2010;37:155–158.
 
28.
Saadat M. Distribution of ACE insertion/deletion (I/D) polymorphism in Iranian populations. Mol Biol Res Commun. 2015;4:63–66.
 
29.
Fallahzadeh-Abarghooei L, Zahedi T, Mirabedi F, et al. Allelic prevalence of intron 3 insertion/deletion genetic polymorphism of DNA double-strand break repair gene XRCC4 in four Iranian populations. Egypt J Med Hum Genet. 2015;16:215–218.
 
30.
Hool LC. Evidence for the regulation of L-type Ca2+ channels in the heart by reactive oxygen species: mechanism for mediating pathology. Clin Exp Pharmacol Physiol. 2008;35:229–234.
 
31.
Saify K, Saadat I, Saadat M. Influence of A-21T and C-262T genetic polymorphisms at the promoter region of the catalase (CAT) on gene expression. Environ Health Prev Med. 2016;21:382–386.
 
32.
Saify K, Khalighinasab MR, Saadat M. Influence of a 50 bp Ins/Del polymorphism at promoter of the superoxide dismutase-1 on gene expression and risk of heroin dependency. Environ Health Prev Med. 2017;22:4.
 
33.
Rajaei M, Saadat I, Saadat M. The novel allele (3R) of the VNTR polymorphism in the XRCC5 promoter region dramatically decreases the gene expression. Biochem Biophys Res Commun. 2013;430:640–641.
 
34.
Kiyohara C, Takayama K, Nakanishi Y. Association of genetic polymorphisms in the base excision repair pathway with lung cancer risk: a meta-analysis. Lung Cancer. 2006;54:267–283.
 
35.
Saadat M, Ansari-Lari M. Polymorphism of XRCC1 (at codon 399) and susceptibility to breast cancer, a meta-analysis of the literatures. Breast Cancer Res Treat. 2009;115:137–144.
 
36.
Saadat M. Apolipoprotein E (APOE) polymorphisms and susceptibility to breast cancer: a meta-analysis. Cancer Res Treat. 2012;44:121–126.
 
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