Sudden infant death syndrome: deletions of glutathione-S-transferase genes M1 and T1 and tobacco smoke exposure

Anthea Mawick,Marielle Vennemann,Heidi Pfeiffer

doi:10.1007/s00414-021-02556-5

Anthea Mawick, Marielle Vennemann + Show 1 more

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https://doi.org/10.1007/s00414-021-02556-5

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Abstract

In developed countries, sudden infant death syndrome (SIDS) is the leading cause of death in infants in their first year of life. The risk of SIDS is increased if parents smoked during pregnancy and in presence of the child. Glutathione S-transferases (GSTs) catalyse the conjugation of glutathione with electrophilic compounds and toxins, making them less reactive and easier to excrete. As a gene dose effect was observed for GSTM1 and GSTT1, the aim of this study was to investigate whether there is a connection between homozygous or heterozygous gene deletions of GSTM1 or GSTT1 and the occurrence of SIDS. We found that heterozygous deletion of GSTM1 occurred significantly more frequently in the SIDS case group compared to the control group. A homozygous deletion of GSMT1 was slightly more frequently in the control group. A homozygous gene deletion of GSTT1 showed no significant difference between the SIDS group and the control group. We also found that in the SIDS group, the number of victims that were exposed to cigarette smoke was significantly higher than the number of victims without cigarette smoke exposure and that the mean lifetime of children whose mothers smoked was shorter in comparison with non-smoking mothers. In SIDS cases with homozygous gene deletions of GSTM1, the median life span of children with tobacco smoke exposure was 60 days shorter than without smoke exposure. In conclusion, the absence of these two genes is not the only trigger for SIDS but could be a critical aspect of SIDS aetiology, particularly in SIDS cases with smoking parents.

Highlights

Sudden infant death syndrome (SIDS) is defined as “the sudden death of an infant under one year of age which remains unexplained after a thorough investigation, including a complete autopsy, examination of the death scene, and review of the clinical history.” (San-Diego-definition) [1]
The aim of our study is to investigate a possible connection between the occurrence of SIDS and the deletion of the GSTM1 or GSTT1 gene, taking into account the smoking behaviour of the mother and her partner during pregnancy and after birth
The corresponding curves, in which the ΔCt values were plotted against log DNA concentration to compare these efficiencies, show a slope of − 0.03 for GSTM1 and RNaseP and a slope of − 0.005 for GSTT1 and RNaseP (Fig. 1), which meets the requirements for the use of the ΔΔCt method in both cases

Summary

Introduction

Sudden infant death syndrome (SIDS) is defined as “the sudden death of an infant under one year of age which remains unexplained after a thorough investigation, including a complete autopsy, examination of the death scene, and review of the clinical history.” (San-Diego-definition) [1]. The distinct decrease of children dying of SIDS can be attributed, inter alia, to the “Back-to-Sleep” Campaign that originated in 1994 and is nowadays known as the “Safe-to-Sleep” Campaign [3, 4]. This campaign was launched by a consortium of US health agencies to educate parents and caregivers about how to practice safe infant sleep and thereby reduce the risk of SIDS. For a long time, smoking during pregnancy has been known as a risk factor for low birth weight, growth retardation, premature birth [7], stillbirth [8], and the occurrence of SIDS among others [7, 9, 10].

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