zearalenone and Premature-Birth

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Topics: Aflatoxins; Aspergillus; Female; Food Contamination; Fusarium; Humans; Infant, Newborn; Male; Mycotoxins; Pregnancy; Premature Birth; Zearalenone

Topics: Adolescent; Adult; Amides; Amnion; Bacterial Infections; Cells, Cultured; Chorioamnionitis; Cyclooxygenase 2; Cytokines; Female; Humans; I-kappa B Kinase; Inflammation Mediators; MAP Kinase Kinase Kinases; Pregnancy; Premature Birth; Thiophenes; Young Adult; Zearalenone

Intrauterine inflammation (IUI) associated with infection is the major cause of preterm birth (PTB) at <32 weeks' gestation and accounts for ∼40% of all spontaneous PTBs. Pharmacological strategies to prevent PTB and improve fetal outcomes will likely require both antimicrobial and anti-inflammatory therapies. Here we investigated the effects of two cytokine-suppressive anti-inflammatory drugs (CSAIDs), compounds that specifically target inflammatory signalling pathways, in an ovine model of lipopolysaccharide (LPS)-induced chorioamnionitis. Chronically catheterized ewes at 116 days gestation (n = 7/group) received an intra-amniotic (IA) bolus of LPS (10 mg) plus vehicle or CSAIDS: TPCA-1 (1.2 mg/kg fetal weight) or 5z-7-oxozeaenol (OxZnl; 0.4 mg/kg fetal weight); controls received vehicle (dimethylsulphoxide). Amniotic fluid (AF), fetal and maternal blood samples were taken 0, 2, 6, 12, 24 and 48 h later; tissues were taken at autopsy (48 h). Administration of TPCA-1 or OxZnl abrogated the stimulatory effects of LPS (P < 0.01 versus vehicle control) on production of PGE2 in AF, with lesser (non-significant) effects on IL-6 production. Fetal membrane polymorphonuclear cell infiltration score was significantly higher in LPS versus vehicle control animals (P < 0.01), and this difference was absent with TPCA-1 and OxZnl treatment. LPS-induced systemic fetal inflammation was highly variable, with no significant effects of CSAIDs observed. Lung inflammation was evident with LPS exposure, but unaffected by CSAID treatment. We have shown in a large animal model that IA administration of a single dose of CSAIDs can suppress LPS-induced IA inflammatory responses, while fetal effects were minimal. Further development and investigation of these compounds in infectious models is warranted.

Topics: Amniotic Fluid; Animals; Anti-Inflammatory Agents; Biomarkers; Catheters, Indwelling; Chorioamnionitis; Disease Models, Animal; Female; Fetal Blood; I-kappa B Kinase; Lipopolysaccharides; Lung; MAP Kinase Kinase Kinases; Phenylurea Compounds; Pregnancy; Premature Birth; Protein Kinase Inhibitors; Sheep, Domestic; Signal Transduction; Thiophenes; Western Australia; Zearalenone

The incidence of idiopathic precocious puberty (IPP) might have an increasing trend. But the causes and risk factors of IPP are unknown. The objective of our study is to evaluate the effects of growth environments and two environmental endocrine disruptors (EDCs), zearalenone (ZEA), and 1,1-dichloro-2,2,bisethylene (p,p'-DDE), on patients with IPP.. Case-control study.. The study consisted of 78 IPP patients at diagnosis and 100 control children matched for age and sex. A questionnaire was designed to collect data on growth environments, and serum ZEA and p,p'-DDE were tested in all subjects. We analyzed data on growth environments, two EDCs, and biological interaction between growth environments and EDCs.. In growth environments, small for gestational age, maternal physical disease during pregnancy, early maternal menarche, early puberty of same-degree relatives, and father's absence in 4- to 6-year olds were risk factors for children with IPP (P<0.05). Serum ZEA concentration, ZEA, and p,p'-DDE-positive rates in the IPP group were significantly higher than those in the control group (P<0.05). There was a biological interaction between growth environments and ZEA (relative excess risk due to interaction =34.562, attributable proportion due to interaction =0.745, synergy index =4.193).. Results suggest possible effects of growth environments and two EDCs on the development of IPP. In addition, growth environments and ZEA have biological interaction that might increase the risk of developing IPP.

Topics: Case-Control Studies; Child; Child, Preschool; Dichlorodiphenyl Dichloroethylene; Endocrine Disruptors; Environmental Pollutants; Female; Humans; Male; Maternal Welfare; Menarche; Premature Birth; Puberty, Precocious; Risk Factors; Socioeconomic Factors; Surveys and Questionnaires; Zearalenone