Kunduz-Afghanistan, Kunduz city of Afghanistan | Afghanistan
Primary Affiliation: Kunduz University-Afghanistan - Kunduz-Afghanistan, Kunduz city of Afghanistan , Afghanistan
PubMed Central Citations
39PubMed Central Citations
Molecular Biology Research Communications
ABSTRACT Glutathione S-transferases (GSTs; EC: 22.214.171.124) are a ubiquitous family of eukaryotic and prokaryotic phase II metabolic isozymes. Genes encoding GSTM1 (OMIM: 138350), and GSTT1 (OMIM: 600436) are members of class mu and theta, respectively. The most common polymorphism in the GSTM1 is a deletion of the whole GSTM1 gene with a lack of enzyme activity. A homozygous deletion in the GSTT1 has also been reported (null genotypes of GSTT1). The aim of the present study was to investigate the association between GSTM1 and GSTT1 polymorphisms and risk of dependency to opium sap. The present study was performed in Shiraz (southern Iran). In total, 71 males dependent to opium sap and 590 healthy males (as a control group) were included in this study. The genotypes of GSTM1 and GSTT1 polymorphisms were determined by PCR. Our data indicate that neither GSTM1 (OR=0.78, 95% CI: 0.47-1.27, P=0.325) nor GSTT1 (OR=1.25, 95% CI: 0.70-2.21, P=0.442) null genotypes significantly associated with the risk of opium sap dependence. There is no additive effect of the null genotypes of GSTT1 and GSTM1 in relation to the risk of dependency to opium sap. The present study indicated that the null genotypes of GSTT1 and GSTM1 are not risk factor for opium sap dependence.
Psychiatry Res 2015 Oct 12;229(3):1055-6. Epub 2015 Aug 12.
Department of Biology, College of Sciences, Shiraz University, Shiraz 71454, Iran. Electronic address:
Egyptian Journal of Medical Human Genetics
Background and purpose Monoamine oxidase A (MAOA, Xp11.3; OMIM: 309850) can modulate the level of neurotransmitters in the central nervous system. A 30 bp variable number of tandem repeat (VNTR) genetic polymorphism on the promoter region of the MAOA can modulate the transcriptional activity of the gene. Association between this polymorphism and dependency to methamphetamine was investigated. Subjects and methods A total of 65 methamphetamine abusers (52 males and 13 females) and 635 healthy controls (525 males and 110 females) were included in the present case–control study. Genotypic analysis for the MAOA VNTR polymorphism was determined by conventional PCR. Based on transcriptional activity of the VNTR alleles, the alleles were categorized into two classes: L allele (2R and 3R alleles) and H allele (3.5R, 4R and 5R alleles), which have low and high transcriptional activities, respectively. Results Our data show that the H allele significantly increases the risk of methamphetamine dependence in males (OR = 2.03, 95% CI: 1.04–3.67, P = 0.037). The H allele seems positively associated with the risk of dependency to methamphetamine among females, but the observed OR did not reach the significance level, probability due to small sample size of the patients. Conclusion The present study supports the role of the VNTR polymorphism on the promoter region of the MAOA on methamphetamine dependence. Keywords Methamphetamine dependence; Monoamine oxidase A; MAOA; Polymorphism; VNTR
Access Macedonian Journal of Medical Sciences.
Abstract AIM: Prodynorphin (PDYN; OMIM: 131340) is the precursor of the dynorphin related peptides which plays an important role in drug abuse. Previous studies have been shown that the expression of PDYN is regulated by a genetic polymorphism of VNTR in the promoter region of the gene. MATERIALS AND METHODS: The present case-control study was performed on 52 (41 males, 11 females) methamphetamine dependence patients and 635 (525 males, 110 females) healthy blood donors frequency matched with the patients according to age and gender, as a control group was participated in the study. RESULTS: The genotypes of VNTR PDYN polymorphism were determined using PCR method. The HL (OR = 1.22, 95%CI: 0.67-2.20, P = 0.500) and LL (OR = 0.86, 95%CI: 0.28-2.57, P =0.792) genotypes does not alter the risk of methamphetamine dependence, in comparison with the HH genotypes. CONCLUSION: The present study revealed no association between the VNTR polymorphism in the promoter region of the PDYN gene and methamphetamine dependence risk. Full text: http://www.id-press.eu/mjms/article/view/337/457
Molecular Biology Research Communications (MBRC); Journal of Shiraz Univesity-Iran
Glutathione S-transferases (GSTs; EC: 126.96.36.199) are ubiquitous multifunctional enzymes, which play a key role in cellular detoxification. Functional genetic polymorphisms in genes encoding GSTM1 (a member of GST class mu; OMIM: 138350), and GSTT1 (a member of GST class theta; OMIM: 600436) have been well defined. The functional null alleles of GSTM1 and GSTT1 represent deletions of GSTM1 and GSTT1 genes, respectively. The aim of the present study is to investigate the association between GSTM1 and GSTT1 polymorphisms and methamphetamine dependence. The present population-based case-control study was performed in Shiraz (southern Iran). In total, 52 methamphetamine dependence (11 females, 41 males) and 635 healthy controls (110 females, 525 males) were included in this study. The genotypes of GSTM1 and GSTT1 polymorphisms were determined by PCR. Neither GSTM1 (OR=0.92, 95% CI: 0.52-1.61, P=0.771) nor GSTT1 (OR=0.71, 95% CI: 0.33- 1.54, P=0.381) null genotypes were significantly associated with risk of methamphetamine dependence. It should be noted that although there was no association between the GSTM1 null genotype and risk of methamphetamine dependence, in both genders, there was significant interaction between gender and GSTM1 polymorphism (P=0.029). The combination genotypes of the GSTM1 and GSTT1 polymorphisms revealed that the genotypes of these two polymorphisms had no additive effect in relation to the susceptibility to methamphetamine dependence. The present study revealed that genetic polymorphisms of GSTT1 and GSTM1 are not risk factors for methamphetamine dependence.
Psychiatry Res 2014 Nov 5;219(3):690-2. Epub 2014 Jul 5.
Department of Biology, College of Sciences, Shiraz University, Shiraz 71454, Iran; Institute of Biotechnology, Shiraz University, Shiraz, Iran. Electronic address: