stillbirth/глутатион

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Glutathione prevents preterm parturition and fetal death by targeting macrophage-induced reactive oxygen species production in the myometrium.

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Preterm birth is an inflammatory process resulting from the massive infiltration of innate immune cells and the production of proinflammatory cytokines in the myometrium. However, proinflammatory cytokines, which induce labor in vivo, fail to induce labor-associated features in human myometrial

Reduced glutathione in hepatitis E infection and pregnancy outcome.

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OBJECTIVE To study reduced glutathione (GSH) as a marker of oxidative stress in hepatitis E virus (HEV) infection during pregnancy, and to clarify its association with pregnancy outcome. METHODS A total of 30 pregnant and 30 non-pregnant women with HEV infection were enrolled in the present study,

Stillbirth and slow metabolizers of caffeine: comparison by genotypes.

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BACKGROUND Cytochrome P4501A2 (CYP1A2) and N-acetyltransferase 2 (NAT2) are key enzymes in the metabolism of caffeine. The polymorphism of these genes facilitates the detection of fast and slow metabolizers, and if caffeine is causally related to stillbirth, we expect slow metabolizers to have a

Protective effect of N-acetylcysteine against fetal death and preterm labor induced by maternal inflammation.

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OBJECTIVE Intrauterine and maternal systemic infections are proposed causes of preterm labor. The resulting prematurity is associated with 75% of infant mortality and 50% of long-term neurologic handicaps. We hypothesize that free radicals generated in large quantities during an inflammatory

Effect of N-acetylcysteine on lipopolysaccharide-induced intra-uterine fetal death and intra-uterine growth retardation in mice.

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Lipopolysaccharide (LPS) has been associated with adverse developmental outcome, including embryonic resorption, intra-uterine fetal death (IUFD), intra-uterine growth retardation (IUGR), and preterm delivery. Reactive oxygen species (ROS) have been associated with LPS-induced developmental

Potentiation of ethyl methanesulfonate-induced germ cell mutagenesis and depression of glutathione in male reproductive tissues by 1,2-dibromoethane.

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EDB significantly depressed GSH in caput and cauda epididymis, but not in testis, 2 hours following injection. This depression was dose-related. EDB enhanced EMS-induced dominant lethal mutations at mating weeks 2 and 3 (of 6). At mating week 2 the fetal death rate was increased two-fold, while at

Melatonin alleviates lipopolysaccharide-induced placental cellular stress response in mice.

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Melatonin protects mice from lipopolysaccharide (LPS)-induced fetal death and intra-uterine growth retardation. Nevertheless, its molecular mechanism remains obscure. In the present study, we investigated the effects of melatonin on LPS-induced cellular stress in placenta. Pregnant mice were given

Assessment of serum thyroid hormone concentrations in lambs with selenium deficiency myopathy.

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OBJECTIVE To assess changes in serum concentrations of thyroid hormones associated with selenium deficiency myopathy in lambs. METHODS 35 lambs with selenium deficiency myopathy and 30 healthy lambs. METHODS Blood samples were collected via jugular venipuncture from lambs with selenium deficiency

Effects of dietary sodium selenite supplementation on salicylate-induced embryo- and fetotoxicity in the rat.

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The effects of dietary supplementation with sodium selenite (3.0 or 4.5 ppm Se) for 8 weeks prior to and throughout gestation on sodium salicylate induced embryo- and fetotoxicity (resorptions, fetal deaths, malformations, fetal weight reduction) have been studied in the rat. Salicylate was

Oxidant balance markers at birth in relation to glycemic and acid-base parameters.

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In diabetic pregnancies, suboptimal glycemic control is a risk factor for fetal acidemia and stillbirth. We hypothesized that the diabetic intrauterine milieu (hyperglycemia, hyperinsulinemia, changes in acid-base status) might predispose to oxidative stress. We studied 70 newborns whose mothers had

Combined effect of prenatal solvent exposure and GSTT1 or GSTM1 polymorphisms in the risk of birth defects.

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Exposure to solvents during pregnancy has long been suspected to increase the risk of congenital malformations. Glutathione S-transferases (GSTs) are enzymes essential for the detoxification of various chemicals. Our objective here was to assess whether GST polymorphisms might modify the association

Prevention of fetal demise and growth restriction in a mouse model of fetal alcohol syndrome.

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Two peptides [NAPVSIPQ (NAP) and SALLRSIPA (ADNF-9)], that are associated with novel glial proteins regulated by vasoactive intestinal peptide, are shown now to provide protective intervention in a model of fetal alcohol syndrome. Fetal demise and growth restrictions were produced after

Maternal occupational chemical exposures and biotransformation genotypes as risk factors for selected congenital anomalies.

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In a case-control study using an assessment of occupational tasks by an industrial hygienist, the authors investigated whether women's occupational exposures increased risks of delivering infants with cleft palate (CP), cleft lip with or without cleft palate (CLP), conotruncal defects, or limb

Gene cloning and characterization of the protein encoded by the Neospora caninum bradyzoite-specific antigen gene BAG1.

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Neospora caninum is an Apicomplexan parasite that causes repeated abortion and stillbirth in cattle. The aim of this study was to clone the gene encoding the N. caninum orthologue (NcBAG1) of the Toxoplasma gondii bradyzoite-specific protein TgBAG1 and characterize its expression pattern in the

Reactive oxygen species are involved in lipopolysaccharide-induced intrauterine growth restriction and skeletal development retardation in mice.

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OBJECTIVE Maternal infection is a cause of adverse developmental outcomes including embryonic resorption, intrauterine fetal death, and preterm labor. Lipopolysaccharide-induced developmental toxicity at early gestational stages has been well characterized. The purpose of the present study was to

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