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Related Concept Videos

Teratogenicity01:07

Teratogenicity

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The ability of a drug to produce structural deformations and functional abnormalities in the developing embryo or the fetus is called teratogenicity, and the drug producing this effect is known as a teratogen. Teratogenic effects include stillbirth, miscarriage, intrauterine growth restriction, and neurocognitive delay. A teratogen may affect the embryo at different stages of development, which is important in determining the type and extent of the damage. During blastocyst formation, the early...
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Pharmacokinetics in Pediatric Patients: Drug Metabolism01:24

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In pediatric care, understanding the nuances of hepatic drug metabolism is crucial, as it significantly differs from that of adults. This divergence is primarily due to the developmental stage of drug-metabolizing enzymes, which affects how medications are processed in the body. In neonates, for instance, the activity of Phase I enzymes—critical for the initial breakdown of drugs—is markedly reduced, functioning at just 20–40% of the levels seen in adults. This reduction poses...
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Nonlinear Pharmacokinetics: Dependence of Elimination Half-Life and Dose Clearance01:23

Nonlinear Pharmacokinetics: Dependence of Elimination Half-Life and Dose Clearance

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The elimination half-life and drug clearance of drugs following nonlinear kinetics can vary with dosage. The Michaelis-Menten parameters and drug concentration influence these factors. As the dose increases, the elimination half-life tends to lengthen, resulting in a reduction in clearance and a disproportionately larger area under the curve. The total clearance can be derived from the Michaelis-Menten equation for drugs following a one-compartment model.
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DNA Methylation of <i>FAM50B</i>/<i>PTCHD3</i> Mediates the Relationships between Low Blood Lead Exposure and Neurobehavioral Development of 0-3 Aged Infants: A Prospective Birth Cohort Study in Southern China.

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Development and Human Extrapolation of Physiologically Based Toxicokinetic Models for Chlorinated Polyfluoroalkyl Ether Sulfonates from Rats.

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Related Experiment Video

Updated: Feb 27, 2026

Author Spotlight: Studying the Impact of Maternal Dietary Deficiencies on Long-Term Offspring Health Outcomes
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Author Spotlight: Studying the Impact of Maternal Dietary Deficiencies on Long-Term Offspring Health Outcomes

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Histidine Metabolic Pathway Modifies the Relationships Between 6:2 Cl-PFESA Exposure and Preterm Birth.

Jianping Cong1,2, Chu Chu3, Zhitao Zhang1

  • 1Shenyang Clinical Medical Research Center for Obstetrics and Gynecology, Liaoning Province Key Laboratory of Assisted Reproduction, Department of Obstetrics and Gynecology, Shenyang Women's and Children's Hospital, Shenyang 110011, China.

Toxics
|February 26, 2026
PubMed
Summary
This summary is machine-generated.

Exposure to chlorinated polyfluoroalkyl ether sulfonic acids (Cl-PFESAs) is linked to preterm birth (PTB). Maternal metabolome profiles, specifically histidine metabolism, may modify this association, offering new insights into reproductive toxicity.

Keywords:
6:2 Cl-PFESAPFAShistidinemetabolomics analysispreterm birth

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Area of Science:

  • Environmental Health
  • Reproductive Toxicology
  • Metabolomics

Background:

  • Limited evidence connects chlorinated polyfluoroalkyl ether sulfonic acids (Cl-PFESAs) to preterm birth (PTB).
  • The impact of Cl-PFESAs on the maternal metabolome concerning PTB is largely unexplored.

Purpose of the Study:

  • To investigate the role of the maternal metabolome in the association between Cl-PFESAs exposure and PTB.
  • To explore potential modifying effects of metabolic pathways on Cl-PFESA-induced PTB risk.

Main Methods:

  • A nested case-control study within the Shenyang birth cohort.
  • Conditional logistic regression analyzed cord blood Cl-PFESA levels and PTB.
  • Maternal blood metabolomics and interaction analysis were performed on a subset of cases and controls.

Main Results:

  • Elevated 6:2 Cl-PFESA levels in cord blood were significantly associated with increased odds of PTB.
  • Metabolomics pathway analysis indicated that histidine metabolism may modify the Cl-PFESA-PTB association.
  • Stratified analysis by histidine levels revealed altered risk associated with cord blood 6:2 Cl-PFESA.

Conclusions:

  • Intrauterine exposure to 6:2 Cl-PFESA is associated with a higher risk of preterm birth.
  • Maternal plasma metabolite profiles, particularly histidine metabolism, may modulate the relationship between Cl-PFESA exposure and PTB.
  • Further research is warranted to elucidate the mechanisms of Cl-PFESA reproductive toxicity.