Cytogenetic effects of tick-borne encephalitis in residents of the north of Western Siberia with alimentary-constitutional obesity depending on the polymorphism of the genes of glutathione-S-transferase

Abstract

Backgraund. Tick-borne encephalitis (TBE), one of the large-scale public health problems of the Siberian region, can cause significant cytogenetic damage in humans by stimulating oxidative stress. Active functioning of the detoxification system including enzymes of glutathione-S-transferase is intended to protect the genetic structure of cells in the body, while at the same time, there are studies showing the defective functioning of this system in individuals with obesity. Aims. Aim of this work is to study the longevity of term of TBE-induced cytogenetic damage in patients with different alleles of genes of glutathione-S-transferase, suffering from alimentary-constitutional obesity compared with the control. Materials and methods. We were examined 133 female residents of the northern areas of Tomsk region from 35 to 44 years old who were hospitalized for infection TBE at local medical clinics. All individials were divided into two subgroups. Patients of the 1st subgroup (control) had a body mass index (BMI) within 2126, the 2nd subgroup had BMI showing severe obesity (BMI 3545). Buccal cells for cytogenetic and molecular analysis were taken several times: 12 days after hospitalization, 1 week, 1 month, 3 months, and 6 months after beginning of the disease. Methods of immunoassay and polymerase chain reaction (PCR) was used to confirm the diagnosis of TBE. As an untreated control were examined 126 healthy female residents of the same age groups. All individuals signed informed consent. In the analysis of deletions in the genes GSTM1 and GSTT1 was used multiplex PCR. We studied at least 1000 epithelial buccal cells from each individual. Results. In patients with high BMI rates revealed a significant increase in the frequency of the buccal cells with cytogenetic damage, compared to the control group. TBE disease was significantly increased the frequency of the cytogenetically damaged cells in this group of patients. The cytogenetic aberrations persisted in their body for six months after hospitalization. In patients with normal BMI rates TBE induced significantly less changes. The recovery of normal cytogenetic status was observed in this group 3 months after hospitalization. Analysis of the glutathione-S-transferase gene variants showed that in TBE patients with normal BMI and non-active alleles of these genesthe frequency of micronucleated epithelial cellswere significantly increased compared to the patients with the activeGSTM1 (+) / GSTT1 (+)genes. In the patients with alimentary obesity such patterns were not observed. Conclusions. Thus,infection with TBE in patients with obesity induced significant increase in both the frequency of cytogenetically damaged cells and the longevity of their persistency in the body compared to these in control group. Polymorphisms in genes of glutathione-S-transferase had no significant effect on the indices.