Polymorphisms of glutathione S-transferase M1 (GSTM1) and T1 (GSTT1) and endometriosis risk: a meta-analysis

Ding, Bo; Sun, Wei; Han, Song; Cai, Yefeng; Ren, Mulan

doi:10.1016/j.ejogrb.2014.10.032

Cited by 5 publications

(5 citation statements)

References 33 publications

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“…No difference in the thresholds at 4–32 kHz was noted between the Gstm1 −/− and WT mice or the Gstt1 −/− and WT mice (Figure 3A–E). Numerous studies have identified the Gstm1 / Gstt1 double null genotype in humans and found it to be related to enhanced risk of many complex disorders involving various cancer types 30–34 . Then, we crossed the Gstm1 −/− and Gstt1 −/− mice to obtain mice with ablation of both Gstm1 and Gstt1 .…”

Section: Resultsmentioning

confidence: 99%

“…Numerous studies have identified the Gstm1/Gstt1 double null genotype in humans and found it to be related to enhanced risk of many complex disorders involving various cancer types. [30][31][32][33][34] Then, we crossed the Gstm1 −/− and Gstt1 −/− mice to obtain mice with ablation of both Gstm1 and Gstt1. However, the Gstm1/Gstt1-DKO mice also showed normal ABR thresholds at 4-32 kHz for up to 12 months (Figure 3F-H).…”

Section: Gstt1 and Gstm1 Are Not Essential For Maintaining The Hearin...mentioning

confidence: 99%

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Gstm1/Gstt1 is essential for reducing cisplatin ototoxicity in CBA/CaJ mice

Liu

Wang

et al. 2022

The FASEB Journal

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Cisplatin is a widely used chemotherapeutic agent. However, its clinical utility is limited because of cisplatin‐induced ototoxicity. Glutathione S‐transferase (GST) was found to play a vital role in reducing cisplatin ototoxicity in mice. Deletion polymorphisms of GSTM1 and GSTT1, members of the GST family, are common in humans and are presumed to be associated with cisplatin‐induced hearing impairment. However, the specific roles of GSTM1 and GSTT1 in cisplatin ototoxicity are not completely clear. Here, under cisplatin treatment, simultaneous deletion of Gstm1 and Gstt1 lead to a more profound hearing loss in CBA/CaJ mice (Gstm1/Gstt1‐DKO) than in wild‐type mice. The Gstm1/Gstt1‐DKO mice, in which phase II detoxification genes were upregulated, exhibited more severe oxidative stress and higher outer hair cell apoptosis in the cochleae than the control mice. Thus, our study revealed that Gstm1 and Gstt1 protect auditory hair cells from cisplatin‐induced ototoxicity in the CBA/CaJ mice, and genetic screening for GSTM1 and GSTT1 polymorphisms could help determine a standard cisplatin dose for cancer patients undergoing chemotherapy.

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Section: Resultsmentioning

confidence: 99%

Section: Gstt1 and Gstm1 Are Not Essential For Maintaining The Hearin...mentioning

confidence: 99%

Gstm1/Gstt1 is essential for reducing cisplatin ototoxicity in CBA/CaJ mice

Liu

Wang

et al. 2022

The FASEB Journal

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“…Previously, the relationship between the GSTM1 polymorphism and the risk of endometriosis has been widely studied [13][14][15][16][17][18][19]. Despite inconsistent results, mos-t studies [15,[20][21][22] have confirmed that null mutations in GSTM1, a genotype that may lead to a lack of corresponding enzyme activity, may significantly increase the risk of endometriosis in women. In particular, several meta-analysis results [20][21][22][23][24][25][26] have shown that the GSTM1-null genotype is a potentially valuable genetic marker for the risk of endometriosis.…”

Section: Introductionmentioning

confidence: 99%

“…Despite inconsistent results, mos-t studies [15,[20][21][22] have confirmed that null mutations in GSTM1, a genotype that may lead to a lack of corresponding enzyme activity, may significantly increase the risk of endometriosis in women. In particular, several meta-analysis results [20][21][22][23][24][25][26] have shown that the GSTM1-null genotype is a potentially valuable genetic marker for the risk of endometriosis. However, the role of GSTM1 polymorphisms in endometriosis-related infertility has not been reported thus far.…”

Section: Introductionmentioning

confidence: 99%

Genetic Variation of Glutathione S-Transferase M1 Is Associated with Patients with Ovarian Endometriosis and Endometriosis-Related Primary Infertility

Zhang

et al. 2021

Public Health Genomics

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Background: The aim of the study was to investigate the role of the genetic variation of glutathione S-transferase M1 (GSTM1) in the development of ovarian endometriosis and endometriosis-related primary infertility risk. Methods: This case-control study included 564 women with ovarian endometriosis and 576 normal women in the control group in northern China. The polymorphism of GSTM1 was genotyped by polymerase chain reaction (PCR)/ligase detection reaction method. To assess the biological significance of polymorphisms, the level of GSTM1 mRNA expression in patients’ endometrial tissues with different genotypes was detected by quantitative real-time PCR (qRT-PCR). Results: Compared with the positive genotype, the null genotype of GSTM1 was associated with the risk of developing ovarian endometriosis (OR = 1.29, 95% CI = 1.02–1.62). Further analysis showed that patients with a null genotype also had a significantly higher risk of primary infertility than patients with positive genotypes (OR = 1.59, 95% CI = 1.01–2.49). In addition, we found that GSTM1 mRNA expression was present in the endometrial tissue of all patients, but the expression level of patients with a positive genotype was nearly 10 times higher than that of patients with a negative genotype. Conclusion: Our results suggest that the GSTM1 polymorphism is not only related to the genetic susceptibility to ovarian endometriosis but also a potential molecular marker of primary infertility in patients with ovarian endometriosis.

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“…By contrast, homozygous whole gene deletions of GSTT1 or GSTM1 cause a lack of the respective enzyme function. These GST genes polymorphisms have been linked to inflammation and immune processes in a number of reports ( Bekris et al, 2005 , Aguilera et al, 2004 , Babushok et al, 2013 , Liang et al, 2013 , Živković et al, 2013 , Ding et al, 2014 ).…”

Section: Introductionmentioning

confidence: 99%

Polymorphisms of glutathione S-transferase and methylenetetrahydrofolate reductase genes in Moldavian patients with ulcerative colitis: Genotype-phenotype correlation

et al. 2016

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BackgroundGlutathione S-transferases (GSTM1, GSTT1, and GSTP1) and methylenetetrahydrofolate reductase (MTHFR) are important enzymes for protection against oxidative stress. In addition, MTHFR has an essential role in DNA synthesis, repair, and methylation. Their polymorphisms have been implicated in the pathogenesis of ulcerative colitis (UC). The aim of the present study was to investigate the role of selected polymorphisms in these genes in the development of UC in the Moldavian population.MethodsIn a case-control study including 128 UC patients and 136 healthy individuals, GSTM1 and GSTT1 genotypes (polymorphic deletions) were determined using multiplex polymerase chain reaction (PCR). The GSTP1 rs1695 (Ile105Val), MTHFR rs1801133 (C677T), and MTHFR rs1801131 (A1298C) polymorphisms were studied with restriction fragment length polymorphism (RFLP) analysis. Genotype–phenotype correlations were examined using logistic regression analysis.ResultsNone of the genotypes, either alone or in combination, showed a strong association with UC. The case-only sub-phenotypic association analysis showed an association of the MTHFR rs1801133 polymorphism with the extent of UC under co-dominant (p corrected = 0.040) and recessive (p corrected = 0.020; OR = 0.15; CI = 0.04–0.63) genetic models. Also, an association between the MTHFR rs1801131 polymorphism and the severity of UC was reported for the over-dominant model (p corrected = 0.023; coefficient = 0.32; 95% CI = 0.10–0.54).ConclusionThe GST and MTHFR genotypes do not seem to be a relevant risk factor for UC in our sample. There was, however, evidence that variants in MTHFR may influence the clinical features in UC patients. Additional larger studies investigating the relationship between GST and MTHFR polymorphisms and UC are required.

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Polymorphisms of glutathione S-transferase M1 (GSTM1) and T1 (GSTT1) and endometriosis risk: a meta-analysis

Cited by 5 publications

References 33 publications

Gstm1/Gstt1 is essential for reducing cisplatin ototoxicity in CBA/CaJ mice

Gstm1/Gstt1 is essential for reducing cisplatin ototoxicity in CBA/CaJ mice

Genetic Variation of Glutathione S-Transferase M1 Is Associated with Patients with Ovarian Endometriosis and Endometriosis-Related Primary Infertility

Polymorphisms of glutathione S-transferase and methylenetetrahydrofolate reductase genes in Moldavian patients with ulcerative colitis: Genotype-phenotype correlation

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