Additive effect of glutathione S-transferase T1 active genotype and infection with<i>Toxoplasma gondii</i>for increasing the risk of schizophrenia

Ansari-Lari, Maryam; Zendehboodi, Zahra; Masoudian, M.; Mohammadi, Fahimeh

doi:10.1080/08039488.2020.1843711

Cited by 3 publications

(5 citation statements)

References 41 publications

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“…For example, it has been associated with carcinogenic processes, such as prostate or serous ovarian cancer, associated with resistance to taxol/carboplatin (Masoodi et al., 2012; Yang et al., 2014; Zhang et al., 2021). Also, not only polymorphism but alterations in gene methylation, such as differential methylation over‐expressed in the regulatory region, are associated with sudden unexplained death and unexpected death in epilepsy [35] or the additive effect of Toxoplasma gondii and genotype GSTT1 in the risk of schizophrenia (Ansari‐Lari et al., 2020) or the increased susceptibility of the GSTT1 polymorphism to develop cardiovascular disease in type 2 diabetes mellitus (Sobha & Ebenezar, 2021) or also with hypertension or asbestosis in populations of Asian origin (Nassereddine et al., 2021).…”

Section: Discussionmentioning

confidence: 99%

“…This gene is located on human chromosome 22q11.2, comprises five exons and is 8 kb long (Kerb et al., 2002; Nakanishi et al., 2022). Several diseases have been associated with gene expression and/or polymorphism of the GSTT1 enzyme, and they include pathologies such as sensitivity to mutagens, Type 2 diabetes mellitus, senile cataract, different carcinomas or de novo autoimmune hepatitis, among others (Al‐Riyami et al., 2022; Ansari‐Lari et al., 2020; Liu et al., 2022; Nassereddine et al., 2021; Nelson et al., 1995; Sobha & Ebenezar, 2021; Stepanova et al., 2021). Moreover, GSTT1 is also involved in activating the p38/MAPKAP kinase 2 (MK2) signal pathway.…”

Section: Introductionmentioning

confidence: 99%

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Analysis of null deletion polymorphism of glutathione S‐transferase theta (GSTT‐1), associated with anti‐GSTT‐1 antibodies development in transplantation

Muro‐Perez,

González‐Martínez,

Martínez‐García

et al. 2023

Int J Immunogenetics

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Glutathione S‐transferase theta 1 (GSTT1) is an enzyme involved in phase II biotransformation processes and a member of a multigene family of detoxifying and clearing reactive oxygen species. GSTT1 is polymorphic like other biotransforming enzymes, allowing variability in hepatic conjugation processes. Immunological recognition of the GSTT1 alloantigen, as evidenced by donor‐specific antibodies formation, has previously been observed in recipients lacking GSTT1 protein (called GSTT1−, GSTT*0, null phenotype or homozygous for the GSTT1 deletion) who receive liver or kidney transplants from GSTT1+ donors and is a risk factor for the development of de novo hepatitis following liver transplants from a GSTT1 expressing donor. Antibodies against GSTT1 are demonstrated in patients who are GSTT1 null and received a transplant from a GSTT1+ donor. Understanding the local population frequency of the GSTT1 deletion is of value in understanding the potential clinical risk of developing post‐transplant complications, which can be attributed to the nonexpression of GSTT1. A population of 173 healthy donors of the Murcia Region in Southeast Spain was evaluated for a null allele of GSTT1 (n = 173). DNA was extracted, and GSTT‐1 null allele detection was performed by real‐time polymerase chain reaction. The frequency of the null GSTT1 genotype (nonexpression or deletion of the homozygous polymorphism of the GSTT1 protein) was 17.9% (n = 31 null allele GSTT1/173 total individuals). Our data suggest that the frequency of null GSTT1 mutations in our population in Southeast Spain is 17.9%, lower than in other Caucasoid populations. This would convert our recipient population into more susceptible to nonlocal potential organ donors and less susceptible to local donors. All recipients bearing this GSTT1 deletion homozygous would be without the protein and triggering an alloantigen in the case of transplantation with a donor without deletion.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Analysis of null deletion polymorphism of glutathione S‐transferase theta (GSTT‐1), associated with anti‐GSTT‐1 antibodies development in transplantation

Muro‐Perez,

González‐Martínez,

Martínez‐García

et al. 2023

Int J Immunogenetics

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“…They showed that the MMP-91562 C allele was only observed in patients diagnosed with schizophrenia and seropositive for Toxo IgG and IgM or IgG alone [ 52 ]. In another study, Ansari-Lari et al tested 78 cases and 91 controls for a polymorphism in Glutathione S-Transferase Theta 1 ( GSTT1) and its association with schizophrenia and Toxo infection [ 53 ]. GSTT1 is located on 22q11.2, a locus previously associated with schizophrenia [ 8 ].…”

Section: Gene-environment (Gxe) Interactionsmentioning

confidence: 99%

“…GSTT1 is located on 22q11.2, a locus previously associated with schizophrenia [ 8 ]. They concluded that risk of schizophrenia increased in patients who were infected with Toxo and had a deletion in GSTT1 , although they also mention that other studies have not shown an association between variants in GSTT1 and schizophrenia [ 53 ]. Severance et al investigated the association of complement C4 gene copy number and haplotype groups with schizophrenia and Toxo IgG along with other biomarkers of pathogen exposure.…”

Section: Gene-environment (Gxe) Interactionsmentioning

confidence: 99%

Gene-Environment Interactions in Schizophrenia: A Literature Review

Wahbeh

Avramopoulos

2021

Genes

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Schizophrenia is a devastating mental illness with a strong genetic component that is the subject of extensive research. Despite the high heritability, it is well recognized that non-genetic factors such as certain infections, cannabis use, psychosocial stress, childhood adversity, urban environment, and immigrant status also play a role. Whenever genetic and non-genetic factors co-exist, interaction between the two is likely. This means that certain exposures would only be of consequence given a specific genetic makeup. Here, we provide a brief review of studies reporting evidence of such interactions, exploring genes and variants that moderate the effect of the environment to increase risk of developing psychosis. Discovering these interactions is crucial to our understanding of the pathogenesis of complex disorders. It can help in identifying individuals at high risk, in developing individualized treatments and prevention plans, and can influence clinical management.

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“…Currently, a number of studies had found GSTM1 and GSTT1 polymorphisms to be associated with SZ risk, but some other studies were failed to find this association. [12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27] Antioxidants impairment and oxidative damage could account for the positive results, while other enzymes completely reducing the effects of GST deletion might be responsible for the negative results. However, some studies showed that GSTM1 null genotype was reduced in SZ patients, and a protective effect of GSTT1 null genotype had also been observed.…”

Section: Introductionmentioning

confidence: 99%

Glutathione S-Transferase M1/T1 Polymorphisms and Schizophrenia Risk: A New Method for Quality Assessment and a Systematic Review

Liu¹,

Xu²,

Peng³

2023

NDT

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Background GST genes were reported to be involved in susceptibility to mental disorder. The results between deletions of GST genes and schizophrenia were inconclusive and confusing. Therefore, we performed this updated meta-analysis to outline the association using a new method for quality assessment. Methods Sixteen reported studies were selected, and the overall OR and 95% CI were calculated and analyzed by Review Manager 5.4 and STATE 12. The Newcastle-Ottawa Quality Assessment Scale (NOS) for case–control studies was rewritten to evaluate the quality of published studies, as there was no “Exposure” in these studies and other factors should be suggested to assess the quality. Results There was no significant association between deletions of GST genes and SZ risk ( p > 0.05 in Random model). We also failed to find a significant relation between null genotypes and SZ risk in East Asian population. Based on further analysis of PCR methods, GSTM1 null was weakly associated with SZ risk in 8 studies using multiplex PCR (OR = 1.17, 95% CI = 1.00–1.37, p = 0.05), but GSTT1 null was a protective factor for SZ risk (OR = 0.73, 95% CI = 0.56–0.94, p = 0.02). When stratified by rewritten NOS stars and deductions, GSTM1 null was significantly associated with SZ risk in 9 studies with high quality (OR = 1.24, 95% CI = 1.08–1.43, p = 0.002), and in 10 studies with no deductions (OR = 1.20, 95% CI = 1.05–1.38, p = 0.007). Conclusion GSTM1 null genotype may be a genetic risk factor for SZ in studies using multiplex PCR and high-quality studies. However, GSTT1 null might be a protective factor. Besides, we provided a new method for quality assessment and it was useful and should be promoted in further analysis.

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Additive effect of glutathione S-transferase T1 active genotype and infection withToxoplasma gondiifor increasing the risk of schizophrenia

Cited by 3 publications

References 41 publications

Analysis of null deletion polymorphism of glutathione S‐transferase theta (GSTT‐1), associated with anti‐GSTT‐1 antibodies development in transplantation

Analysis of null deletion polymorphism of glutathione S‐transferase theta (GSTT‐1), associated with anti‐GSTT‐1 antibodies development in transplantation

Gene-Environment Interactions in Schizophrenia: A Literature Review

Glutathione S-Transferase M1/T1 Polymorphisms and Schizophrenia Risk: A New Method for Quality Assessment and a Systematic Review

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