Acidic and Basic Forms of Glutathione S-Transferases from
Human Placenta and Comparison with Human Kidney
Glutathione S-Transferase

Steisslinger, Hans Werner; Pfleiderer, Gerhard

doi:10.1159/000469133

Cited by 4 publications

(1 citation statement)

References 11 publications

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“…While no association was observed in our study between RDS occurrence and GST-M1 and T1 polymorphisms, an association between the GST-P1 codon 105 genotype was observed, and a decreased risk of developing RDS was evident in children with the heterozygous or mutated genotypes. GST-P1 is the main isoform in normal placenta and represents 36% of GST activity in this tissue [55]. This nonsynonymous SNP has been associated with reduced enzyme activity [56], hence the reduction in placental steroid biotransformation could permit higher GC concentrations to reach the fetus.…”

Section: Discussionmentioning

confidence: 99%

Glutathione-S-transferase-P1 I105V polymorphism and response to antenatal betamethasone in the prevention of respiratory distress syndrome

Oretti

Marino

Mosca³

et al. 2009

Eur J Clin Pharmacol

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PHARMACOGENETICSGlutathione-S-transferase-P1 I105V polymorphism and response to antenatal betamethasone in the prevention of respiratory distress syndrome Abstract Purpose The aim of this pilot study was to assess the association between polymorphisms in genes that encode for proteins involved in the pharmacokinetics/pharmacodynamics of glucocorticoids and the occurrence of respiratory distress syndrome (RDS) in preterm infants born to mothers treated with a complete course of betamethasone. Methods Sixty-two preterm infants were enrolled. The C1236T, G2677T, and C3435T polymorphisms in the ABCB1 gene, BclI, N363S and ER22/23EK in the NR3C1 gene, I105V in the GST-P1 gene and GST-M1 and GST-T1 deletions were analyzed, and their association with the occurrence of RDS was assessed. Results In univariate analysis, the heterozygous and homozygous presence of the I105V variant in the GST-P1 gene seemed to confer protection against the occurrence of RDS (P=0.032), while no association for all other polymorphisms was observed. In multivariate analysis, selection from the reference model of independent variables based on AIC (Akaike information criteria) maintained three variables in the model: gestation, C3435T, and GST-P1 genotype.

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Section: Discussionmentioning

confidence: 99%

Glutathione-S-transferase-P1 I105V polymorphism and response to antenatal betamethasone in the prevention of respiratory distress syndrome

Oretti

Marino

Mosca³

et al. 2009

Eur J Clin Pharmacol

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Changes in hepatic cytosolic glutathione S-transferase activity and expression of its class-P during prenatal and postnatal period in rats treated with aflatoxin B1

et al. 2006

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The effect of aflatoxin B1 (AFB1) on the expression of glutathione S-transferase-P (GST-P) which is the major isoform of GST in developmental stages has been investigated in rat liver during prenatal and postnatal stages. Following administration of AFB1 (0, 0.5, 1.0, 2.0, 3.0 or 4.0 mg/kg bw) injected I.P on day 8.5 of gestation the number of dead or reabsorbed fetuses and malformed embryos were recorded. Then the fetal livers were processed for measurement of total GST and GST-P activities, using 1-chloro-2,4-dinitrobenzene (CDNB) and ethacrynic acid (ETA) as substrates respectively. RT-PCR using rat GST-P specific primers was performed on mRNA extracted from livers. Besides, the effects of AFB1 on hepatic GST and GST-P were assessed in groups of suckling rats directly injected with the toxin. The results show that a single dose of AFB1 (1.0 or 2.0 mg/kg bw) caused approximately 50-60% depletion in fetal liver GST towards CDNB. Postnatal experiments revealed that liver GST (using CDNB as substrate) was significantly induced (approximately 40%) in suckling rats injected with a single dose of AFB1 (3.0 mg AFB1/kg) 24 h before killing. Liver GST-P expression was unaffected due to AFB1 exposures of rats before and after the birth. This finding was substantiated by western blotting and RT-PCR techniques. These data suggest that AFB1-related induction in rat liver total GST after birth may be implicated in protective mechanisms against AFB1. In contrast, inhibition of this enzyme in fetal liver following placental transfer of the carcinogen may explain high susceptibility of fetal cells to trans-plancental aflatoxins. Furthermore, lack of influence of AFB1 on GST-P expression in developmental stages can role out the involvement of this class of GST in AFB1 biotransformation.

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Glutathione S-Transferases and Esterases in Placenta after Normal and Pre-eclamptic Pregnancies

et al. 2004

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Acidic and Basic Forms of Glutathione S-Transferases from Human Placenta and Comparison with Human Kidney Glutathione S-Transferase

Cited by 4 publications

References 11 publications

Glutathione-S-transferase-P1 I105V polymorphism and response to antenatal betamethasone in the prevention of respiratory distress syndrome

Glutathione-S-transferase-P1 I105V polymorphism and response to antenatal betamethasone in the prevention of respiratory distress syndrome

Changes in hepatic cytosolic glutathione S-transferase activity and expression of its class-P during prenatal and postnatal period in rats treated with aflatoxin B1

Glutathione S-Transferases and Esterases in Placenta after Normal and Pre-eclamptic Pregnancies

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