Impact of 5-Methoxy-N-Acetyltryptamine on the Developmental Toxicity Induced by Deltamethrin in Mice

Baidaa Abdulaziz Mohamed Salah
Department of Biology, College of Education for Pure Science, University of Mosul, Mosul, Iraq

Mohammed Khalid Shindala
Department of Physiology, Biochemistry and Pharmacology, College of Veterinary Medicine, University of Mosul, Mosul, Iraq

Mahaa A. Al-Obaidi
University of Al-Hamdaniya, Al-Hamdaniya District, Iraq

Abstract

Background: decamethrin (synthetic pyrethroid deltamethrin) and other similar compounds in the gestational period have become more worrisome because they cause neurodevelopmental problems in fetuses through three main mechanisms, which include oxidative imbalance, apoptotic signaling, and neuroinflammatory activation. The body produces the 5-methoxy-N-acetyltryptamine (melatonin) as an antioxidant, which has shown potential to protect against pesticide-caused developmental harm to the fetus. They also affect maternal brain architecture. Aim: The research investigated how deltamethrin exposure during pregnancy affects mouse brain development. The ability of melatonin to protect against oxidative stress and Bax-induced cell death in fetus brain and CD45-related   maternal brain inflammation.

 Methods: The study used thirty-two pregnant albino mice. Animals were split into four groups containing eight pregnant mice each.  Group I   received distilled water, group II dosed orally with 1 mg/kg of deltamethrin, group III injected with    12.5 mg/kg   of melatonin intraperitoneally (IP), and the groupIV administrated of both melatonin (12.5 mg/kg) and deltamethrin (1 mg/kg. Both chemicals were given to animals during the period 7-17 days of gestation. The research investigated fetal growth markers together with maternal oxidative stress indicators (MDA and GSH), routine tissue analysis results, and Bax and CD45 protein expression through immunohistochemical testing. Furthermore, some other parameters. Results: The exposure to deltamethrin caused significant fetal growth problems and decreased brain weight of embryos, depleted glutathione levels, severe brain tissue damage, increased Bax protein levels, and elevated CD45 immune responses in the maternal brain, which activated cell death mechanisms and neuroinflammatory responses. The combination of melatonin with other toxicants like deltamethrin resulted in a substantial reduction of pathological changes through enhanced antioxidant defense and decreased apoptosis and inflammation but did not restore all affected parameters to normal levels.

Conclusion: Deltamethrin causes developmental neurotoxic effects during pregnancy through multiple pathways, which include oxidative stress, apoptotic cell death, and neuroimmune system disruption. Melatonin shows restricted neuroprotective effects, which make it a potential therapeutic agent for pesticide-induced brain damage that affects fetal brain development.

Keywords: Deltamethrin ,Melatonin ,Developmental Neurotoxicity ,Oxidative Stress ,Neuroinflammation, Pregnancy