Intoxication syndrome in patients with pulmonary tuberculosis in relation to the system glutathione transferase gene polymorphism

Stepanova, Natalia; Галимзянов, Х М; Кантемирова, Б. И.

doi:10.22625/2072-6732-2017-9-2-13-16

Cited by 2 publications

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“…Встречаемость таких делеций в популяциях очень высока, поскольку установлено, что до половины европеоидного населения являются гомозиготами по делеции гена GSTM1 и около 15% по делеции гена GSTT1 [6,13]. В настоящее время, показано, что полиморфизм генов GSTM1 и GSTT1, связанный с делецией этих генов играет важную роль в повышенном риске не только некоторых типов рака [13,19], но и более тяжелого течения инфекционных заболеваний, таких как туберкулез, малярия, ВИЧ-инфекция и геморрагическая лихорадка с почечным синдромом [5,7,12,15].…”

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“…Глутатион-S-трансферазы способствуют защите организма от широкого круга химичес-ких соединений, включая реактивные формы кислорода и другие потенциальные мутагены. Имеются исследования, свидетельствующие о связи между тяжестью инфекционного заболевания и наличием у больного мутантных аллелей генов ферментов глутатион-S-трансфераз [5,7,12,15]. Установлено, что носительство мутантных неактивных вариантов генов GSTM1 и GSTT1 часто сопровождается цитогенетической нестабильностью и повышенной чувствительность хромосомного аппарата человека к различным мутагенным факторам [16,18].…”

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Monitoring of cytogenetic instability by micronuclei assay of both immunocompetent and non-immunocompetent cells in tick-borne encephalitis patients depending on variants of glutathione-S-transferase genes in the genotype

Ильинских

Замятина

et al. 2019

Russian Journal of Infection and Immunity

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Aim of this study was to study the dynamics of the frequency of cytokinesis-blocked T-lymphocytes with micronuclei in peripheral blood and the frequency of buccal micronucleated epithelium cells for a period of half a year in patients with acute tick-borne encephalitis, depending on burden of active and inactive variants of glutathione-S-transferase genes (GSTM1 and GSTT1) in the patient's genotype. We carried out micronucleus assay in immunocompetent and non-immunocompetent cells in 54 patients with acute tick-borne encephalitis and 35 healthy persons (control) residing in the Tomsk and Tyumen regions. To analyze the frequency of cytokinesis-blocked micronucleated T-lymphocytes was used venous peripheral blood as material for phytohemagglutinin-stimulated cultures, and to study the frequency of buccal micronucleated cells, samples of the buccal mucous membrane epithelial cells were obtained. To carried out both techniques of micronucleus assay, cytological preparations were prepared, which were stained using the Giemsa or Felgen methods. The material for the study was obtained repeatedly during admission of patients to treatment, and also after 1 week, 1, 3 and 6 months. Polymerase chain reaction was used to analyze the alleles of the GSTM1 and GSTT1 genes. As a result of this analysis was found a significant increase in the frequency of micronucleated cells in tick-borne encephalitis patients compared with the control group. In addition, the frequency of cytokinesis-blocked micronucleated T-lymphocytes was increased significantly higher than the one of micronucleated buccal cells. The most significant and prolonged increase in the frequency of micronucleated cells was associated with the mutant inactive variants of the genes GSTM1 (0/0) and GSTT1 (0/0). In the patients with burden the inactive forms of these genes, the cytogenetic instability of the cytokinesis-blocked blood T-lymphocytes could persist for up to six months. In case of buccal cells, the frequency of micronucleated cells was close to the one in the control group as early as 1-3 months after a course of treatment. Conclusion. It was found that the most increased and prolonged frequency of cytogenetically instable cells persisted in cytokinesis-blocked T-lymphocytes of peripheral blood of patients with tick-borne encephalitis who were carriers of the genotype with inactive variants of both GSTM1 (0/0) and GSTT1 (0/0 ) glutathione-S-transferase genes.

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Monitoring of cytogenetic instability by micronuclei assay of both immunocompetent and non-immunocompetent cells in tick-borne encephalitis patients depending on variants of glutathione-S-transferase genes in the genotype

Ильинских

Замятина

et al. 2019

Russian Journal of Infection and Immunity

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Isoniazid-Induced Liver Injury: Pharmacogenetic Aspects

Краснова

Николаев

2022

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Inter-individual differences in anti-tuberculosis chemotherapy outcomes have been demonstrated in clinical practice, such as, achievement of intended therapeutic effect in some patients, and insufficiency or absence of response to treatment in others, with development of adverse drug reactions, especially, isoniazid-induced liver injury. Isoniazid-induced liver injuries are the main reason for isoniazid discontinuation, which further leads to considerably reduced effectiveness of anti-tuberculosis chemotherapy, increased relapse risk, and secondary drug-resistance of M. tuberculosis. Hepatotoxic reactions to chemotherapy are predicated by mutations in genes encoding enzymes participating in isoniazid biotransformation: N-acetyltransferase 2 (NAT2), cytochrome P450 2Е1, and glutathione-S-transferase.NAT2 gene polymorphism has been identified as risk factor for isoniazid hepatotoxicity. Nucleotide substitutions in NAT2 gene cause modification of enzyme protein structure, reduction of enzyme synthesis and alteration of its activity. Based on genetically-determined isoniazid acetylation rate, patients are referred to three acetylator types: rapid, intermediate, and slow. Correlations have been established in meta-reviews and systematic reviews between slow acetylator type and frequency of hepatotoxic reactions to isoniazid.Based on study findings, interrelation was shown between cytochrome P450 CYP2E1 gene polymorphism and increased risk of liver injury during chemotherapy with isoniazid. Contribution of GSTM1 and GSTT1 genotypes to isoniazid toxicity requires further exploration, as the obtained results were ambiguous and controversial.

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Intoxication syndrome in patients with pulmonary tuberculosis in relation to the system glutathione transferase gene polymorphism

Cited by 2 publications

References 1 publication

Monitoring of cytogenetic instability by micronuclei assay of both immunocompetent and non-immunocompetent cells in tick-borne encephalitis patients depending on variants of glutathione-S-transferase genes in the genotype

Monitoring of cytogenetic instability by micronuclei assay of both immunocompetent and non-immunocompetent cells in tick-borne encephalitis patients depending on variants of glutathione-S-transferase genes in the genotype

Isoniazid-Induced Liver Injury: Pharmacogenetic Aspects

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