Viewing teratogens through the lens of nicotinamide adenine dinucleotide (NAD+)

Paul R Mark1,2, Sally L Dunwoodie3,4,5

  • 1Department of Pediatrics, Division of Medical Genetics, Helen DeVos Children's Hospital, Spectrum Health, Grand Rapids, Michigan, USA.

Birth Defects Research
|December 1, 2022
PubMed
Abstract

Insights

Nicotinamide adenine dinucleotide (NAD+) depletion is linked to human diseases and birth defects. Teratogens impacting NAD+ metabolism may explain how these defects and miscarriages occur.

Area of Science:

  • Biochemistry
  • Developmental Biology
  • Toxicology

Background:

  • Nicotinamide adenine dinucleotide (NAD+) depletion is associated with human diseases.
  • Genetic blockage of NAD+ synthesis causes birth defects and miscarriage in humans.
  • NAD+ deficiency in mice leads to congenital anomalies and miscarriage.

Purpose of the Study:

  • To evaluate how NAD+/NADH perturbations affect teratogenesis mechanisms.
  • To review the impact of various teratogens on NAD+ and NAD+/NADH ratios.

Main Methods:

  • Literature evaluation of NAD+/NADH perturbations in teratogenesis.
  • Review of teratogen literature, including infectious, physical, maternal health, and drug factors.

Main Results:

  • Teratogens can affect NAD+ by altering its metabolism, decreasing intracellular availability, or reducing production.
  • These alterations in NAD+ present a plausible mechanism for birth defect development.

Conclusions:

  • Viewing teratogens through their impact on NAD+ offers insight into birth defect mechanisms.
  • Understanding NAD+ pathways is crucial for identifying teratogenic risks and preventing congenital anomalies.

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