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Protective effects of melatonin against polystyrene nanoplastic–induced placental dysfunction and adverse pregnancy outcomes in rats
Summary
In pregnant rats, exposure to nanoplastics (tiny plastic particles found in everyday pollution) damaged the placenta and harmed pregnancy outcomes by increasing cell-damaging stress. Melatonin, a hormone your body makes naturally (and that's sold as a sleep supplement), helped protect against this damage when given to the rats. While this is early animal research and hasn't been tested in humans yet, it raises hopeful questions about whether melatonin could someday help protect pregnancies from the growing problem of plastic pollution in our environment.
Plastic pollution has emerged as a major environmental and health concern. This study investigated the adverse effects of polystyrene nano-plastics (PSNP) on placental structure and pregnancy outcomes, as well as the potential protective role of melatonin during gestation. Pregnant Wistar rats were divided into four groups: control, PSNP-exposed (10 mg/kg, oral gavage), melatonin-treated (10 mg/kg, intraperitoneal), and combined PSNP-melatonin. PSNP was administered from gestational day 0 until delivery, while melatonin was given 7-12 days prior to mating and continued throughout gestation. Macroscopic and microscopic examinations, morphometric analyses, assessment of antioxidant enzymes (SOD, GPX, CAT), malondialdehyde (MDA) levels, and immunohistochemical evaluation of BCL2 and P53 were performed. PSNP exposure resulted in increased thickness of the decidua and junctional zones, elevated MDA levels, decreased antioxidant enzyme activity, upregulation of P53, and downregulation of BCL2, indicating enhanced oxidative stress and alterations in apoptosis-related marker expression. Additionally, PSNP exposure reduced litter size while increasing offspring weight. Melatonin administration significantly attenuated oxidative stress, restored antioxidant enzyme activity, modulated the expression of apoptosis-related markers, and improved placental morphology and pregnancy outcomes. These findings suggest that melatonin mitigates PSNP-induced placental damage, possibly by reducing oxidative stress and modulating apoptosis-related signaling. In conclusion, melatonin may stabilize the uterine-placental microenvironment under PSNP-induced environmental stress, highlighting its potential protective role in maternal-fetal health and its relevance for future translational and clinical investigations.