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Humadi, athraa, Kadhim, Falah. (1405). Developmental Toxicity, Genotoxicity, and Neurobehavioral Alterations Induced by Maternal Exposure to L-Aspartyl-L-Phenylalanine Methyl Ester During Mid-Pregnancy in Rats. , (), -. doi: 10.22059/ijvm.2026.408637.1006011
athraa Nori Humadi; Falah Muosa Kadhim. "Developmental Toxicity, Genotoxicity, and Neurobehavioral Alterations Induced by Maternal Exposure to L-Aspartyl-L-Phenylalanine Methyl Ester During Mid-Pregnancy in Rats". , , , 1405, -. doi: 10.22059/ijvm.2026.408637.1006011
Humadi, athraa, Kadhim, Falah. (1405). 'Developmental Toxicity, Genotoxicity, and Neurobehavioral Alterations Induced by Maternal Exposure to L-Aspartyl-L-Phenylalanine Methyl Ester During Mid-Pregnancy in Rats', , (), pp. -. doi: 10.22059/ijvm.2026.408637.1006011
Humadi, athraa, Kadhim, Falah. Developmental Toxicity, Genotoxicity, and Neurobehavioral Alterations Induced by Maternal Exposure to L-Aspartyl-L-Phenylalanine Methyl Ester During Mid-Pregnancy in Rats. , 1405; (): -. doi: 10.22059/ijvm.2026.408637.1006011

Developmental Toxicity, Genotoxicity, and Neurobehavioral Alterations Induced by Maternal Exposure to L-Aspartyl-L-Phenylalanine Methyl Ester During Mid-Pregnancy in Rats

Iranian Journal of Veterinary Medicine
مقالات آماده انتشار، پذیرفته شده، انتشار آنلاین از تاریخ 29 اردیبهشت 1405
نوع مقاله: Original Articles
شناسه دیجیتال (DOI): 10.22059/ijvm.2026.408637.1006011
نویسندگان
athraa Nori Humadi* ؛ Falah Muosa Kadhim
pharmacology and toxicology/collage of veterinary medicine/ University of Baghdad/ Iraq
چکیده
BACKGROUND: Mid-gestation is a critical developmental window for organogenesis and neurodevelopment. Maternal exposure to L-aspartyl-L-phenylalanine methyl ester during this period may disrupt embryonic programming through oxidative and inflammatory pathways.
OBJECTIVE: This study aimed to investigate the embryo-toxic, genotoxic, and neurobehavioral impacts of L-aspartyl-L-phenylalanine methyl ester administered at doses of 240 and 300 mg/kg during the mid-gestational stage in pregnant rats.
METHODS: Pregnant Wistar albino rats were divided into three groups: control, 240 mg/kg, and 300 mg/kg of L-aspartyl-L-phenylalanine methyl ester. Assessment included fetal growth parameters, DNA fragmentation (COMET assay), pro-inflammatory cytokines (IL-1β, IL-6), and oxidative stress markers. Additionally, offspring neurobehavioral performance was evaluated using Negative Geotaxis, Swimming Rank, and Cleft Avoidance tests, followed by histopathological examination of fetal brain, liver, and heart tissues.
RESULTS: Mid-gestational exposure triggered a significant dose-dependent oxidative-inflammatory surge. Treated embryos exhibited substantial DNA fragmentation and marked elevations in IL-1β and IL-6 levels. Significant fetal growth restriction was observed alongside distinct sensorimotor and functional impairments in neurobehavioral tests. Histopathological analysis revealed degenerative alterations in the brain, liver, and myocardium, which were more severe at the higher dose (300 mg/kg).
CONCLUSION: The mid-gestational window is exceptionally vulnerable to L-aspartyl-L-phenylalanine methyl ester-induced toxicity. The findings highlight persistent structural and functional disturbances, suggesting the need for stage-specific caution regarding artificial sweetener consumption during pregnancy.
Keywords: Artificial sweeteners; DNA integrity; Dose-dependent; Inflammation; Neurobehavioral performance; Oxidative stress.
کلیدواژه‌ها
Artificial sweeteners؛ DNA integrity؛ Inflammation؛ Neurobehavioral performance؛ Oxidative stress
آمار
تعداد مشاهده مقاله: 27





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