RGD Reference Report - Maternal and paternal environmental risk factors, metabolizing GSTM1 and GSTT1 polymorphisms, and congenital heart disease. - Rat Genome Database

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Maternal and paternal environmental risk factors, metabolizing GSTM1 and GSTT1 polymorphisms, and congenital heart disease.

Authors: Cresci, Monica  Foffa, Ilenia  Ait-Ali, Lamia  Pulignani, Silvia  Gianicolo, Emilio Antonio Luca  Botto, Nicoletta  Picano, Eugenio  Andreassi, Maria Grazia 
Citation: Cresci M, etal., Am J Cardiol. 2011 Dec 1;108(11):1625-31. doi: 10.1016/j.amjcard.2011.07.022. Epub 2011 Sep 3.
RGD ID: 12792220
Pubmed: PMID:21890078   (View Abstract at PubMed)
DOI: DOI:10.1016/j.amjcard.2011.07.022   (Journal Full-text)

Congenital heart defects (CHDs) are the most prevalent of all birth malformations arising from the complex interplay of environmental exposures and genes. Modifiable environmental risk factors are still largely unknown, especially for paternal exposure. The aim of the present study was to examine the association between the environmental exposures of both parents and CHD risk and to explore the modification effect of metabolizing gene polymorphisms in children who lack the genetic capacity to produce the glutathione S-transferase (GST) GSTM1 and GSTT1 enzymes. A total of 330 parents of a child with CHD and 330 parents of a child without any congenital malformations were compared in terms of lifestyle habits and toxicant exposure. GST gene polymorphisms were investigated in 180 patients with CHD (104 males, age 4.9 ± 5.8 years). Paternal smoking (>=15 cigarettes/day) was significantly associated with CHD risk (odds ratio [OR] 2.1, 95% confidence interval [CI] 1.3 to 3.5, p = 0.002). Both maternal (OR 2.6, 95% CI 1.6 to 4.2, p <0.0001) and paternal (OR 2.5, 95% CI 1.6 to 3.8, p <0.0001) occupational/environmental exposures increased the risk of CHD. Also, a significant additive risk (OR 4.5, 95% CI 2.5 to 8.3, p <0.0001) was found when both parents were exposed to toxicants. Both maternal (OR 3.6, 95% CI 1.1 to 11.2, p = 0.03) and paternal (OR 3.3, 95% CI 1.0 to 10.8, p = 0.03) exposure to toxicants increased the CHD risk in children who carried the combined null GST genotypes. The effect for the combined null GST genotypes was also stronger (OR 6.5, 95% CI 1.5 to 28.0) when both parents were exposed. In conclusion, paternal smoking and exposure to toxicants for both parents affect the risk of children with CHD. Polymorphisms in GST genes can modify a person's risk of toxicant exposure-induced disease.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
GSTM1Humancongenital heart disease susceptibilityIAGP DNA:deletion and haplotype:: (human)RGD 
GSTT1Humancongenital heart disease susceptibilityIAGP DNA:deletion and haplotype:: (human)RGD 
Gstm1Ratcongenital heart disease susceptibilityISOGSTM1 (Homo sapiens)DNA:deletion and haplotype:: (human)RGD 
Gstm1Mousecongenital heart disease susceptibilityISOGSTM1 (Homo sapiens)DNA:deletion and haplotype:: (human)RGD 
Gstt1Ratcongenital heart disease susceptibilityISOGSTT1 (Homo sapiens)DNA:deletion and haplotype:: (human)RGD 
Gstt1Mousecongenital heart disease susceptibilityISOGSTT1 (Homo sapiens)DNA:deletion and haplotype:: (human)RGD 

Objects Annotated

Genes (Rattus norvegicus)
Gstm1  (glutathione S-transferase mu 1)
Gstt1  (glutathione S-transferase theta 1)

Genes (Mus musculus)
Gstm1  (glutathione S-transferase, mu 1)
Gstt1  (glutathione S-transferase, theta 1)

Genes (Homo sapiens)
GSTM1  (glutathione S-transferase mu 1)
GSTT1  (glutathione S-transferase theta 1)


Additional Information