Effects of exposure to low-level artificial light at night and melatonin supplementation on maternal‑fetal outcomes in pregnant mice: Insights from placental and decidual pathways

Abstract

Exposure to low-level artificial-light at night (L-ALAN) during pregnancy is increasingly common and disrupt melatonin (MT) synthesis. MT maintains circadian rhythm homeostasis and placental/decidual functions. This study aimed to investigate the effects of prenatal L-ALAN exposure and MT intervention on maternal–fetal outcomes and underlying mechanisms. Pregnant C57BL/6 J mice were exposed to L-ALAN (2 lx during night) with or without MT supplementation (10 mg/kg/day, intragastrically) and assessed at embryonic day 16.5 or after natural delivery. Maternal serum and placental MT levels, and related maternal–fetal outcomes were evaluated. Morphological, circadian-omics, and RT-qPCR analyses were conducted to evaluate structural and functional changes in the maternal-placenta-decidual-fetal tissues. Circadian rhythmicity of core-circadian-clock-genes was evaluated using Jonckheere-Terpstra-Kendall (JTK)-CYCLE analysis. L-ALAN reduced nocturnal maternal serum and placental MT peaks, gestational-weight-gains, P4/E2 ratio, maternal liver and spleen indices, placental and fetal weights, and offspring survival. Placental and decidual structural and functional markers were also impaired. L-ALAN disrupted core-circadian-clock-gene expression and increased inflammatory cytokines in the maternal-placenta-decidual-fetal tissues. MT supplementation partially attenuated several of these alterations, whereas maternal organ indices, fetal weights, and fetal liver inflammatory responses were not significantly restored. Gestational L-ALAN exposure suppressed circulating and placental MT secretion, induced gestational hormonal and metabolic dysfunctions and decreased placental/fetal weights. Impaired maternal–fetal interface architecture and function, secondary to circadian rhythm disturbances and inflammatory activation, underlies these detrimental effects, while MT supplementation partially attenuated selected L-ALAN-associated alterations. As the C57BL/6 J strain exhibits deficient pineal MT synthesis, these findings primarily reflect alterations in peripheral (circulating and placental) MT availability.

The authors' abstract, as published at the source. Cell Biology and Toxicology, 2026 · DOI ↗