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

Abstract

Purpose

To determine if Toxoplasma gondii (T. gondii) infection may play a role in the development of schizophrenia in genetically susceptible persons with regard to genes encoding glutathione S-transferase T1 (GSTT1) and M1 (GSTM1).

Methods

A total of 78 cases with psychiatric diagnosis of schizophrenia were compared with 91 healthy controls. For detection of IgG antibodies, enzyme-linked immunosorbent assay was used. Genotyping of GSTM1 and GSTT1 was performed by multiplex PCR. Chi-square and logistic regression were used for statistical analyses.

Results

A higher frequency of the GSTT1 active gene in schizophrenic patients was observed. When risk categories based on the combination of T. gondii status and GSTs polymorphisms were compared, risk of schizophrenia increased in T. gondii positive/GSTT1 absent subjects (OR = 4.75, p = 0.05) compared with T. gondii negative/GSTT1 absent group. When T. gondii positive subjects had the GSTT1 active genotype, the risk increased linearly (OR = 10.20, p < 0.001). Odds ratio in T. gondii positive groups were almost the same in combination with the GSTM1 active genotype (OR = 4.45, p = 0.003) or null genotype (OR = 4.37, p = 0.006).

Conclusions

Our results showed an additive effect for T. gondii and GSTT1 active genotype as risk factors for schizophrenia in Iranian population. This is a small pilot study and replicating the study with larger groups of patients in multinational investigation to clarify these findings is recommended.

Keywords:

• Iran
• glutathione S-transferase
• polymorphism
• schizophrenia
• Toxoplasma gondii

Acknowledgements

The authors thank Dr. Hassan Farrashbandi (Department of Psychiatry, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran) for his kind assistance in sample collection.

Disclosure statement

The authors declared that there is no conflict of interest.

Additional information

Funding

This study was supported by Shiraz University [Grant number: 94GRD1M2003].

Notes on contributors

Maryam Ansari-Lari

Maryam Ansari-Lari, M.D., Community Medicine. Epidemiologic research on public health and zoonoses.

Zahra Zendehboodi

Zahra Zendehboodi, Ph.D., Molecular and cellular biology. Research on gene polymorphism.

Malihe Masoudian

Malihe Masoudian, Ph.D., Biotechnology. Research on bioinformatics and genetic engineering.

Fahimeh Mohammadi

Fahimeh Mohammadi, D.V.M., Private Clinician.