Oxidative DNA Damage, Apoptosis, and Astrogliosis Induced by Acrylamide in The Cerebellar Cortex of The Growing Albino Rats and Their Mothers. | ||
| Egyptian Journal of Histology | ||
| Articles in Press, Accepted Manuscript, Available Online from 11 November 2025 | ||
| Document Type: Original Article | ||
| DOI: 10.21608/ejh.2025.379174.2263 | ||
| Authors | ||
| Asmaa Mohamed Tolba* 1; Moatz Mustafa Eltawel2; Amal Soliman Sewelam3; Emtethal Mamdouh El-Bestawy4 | ||
| 11Department of Human Anatomy and Embryology, Faculty of Medicine, Zagazig University, Sharqia Governorate, Zagazig, Egypt | ||
| 2Medical School Student, Kasr El-Ayni, Faculty of Medicine, Cairo University, Giza Governorate 12613, Egypt | ||
| 3Human Anatomy and Embryology,Faculty of Medicine,Zagazig University, Zagazig, Egypt | ||
| 4Human Anatomy and Embryology, Faculty of Medicine, Zagazig University, Egypt | ||
| Abstract | ||
| Introduction: The developmental neurotoxicity of acrylamide (ACR) has increased in concern, but the potential mechanisms of ACR neurotoxicity are still unclear. Aim: This study was designed to evaluate the most significant mechanistic pathway involved in the neurotoxic effects of perinatal acrylamide exposure on the cerebellar cortex of growing albino rats and their mothers and to determine its neurotoxic effects. Materials and Methods: Twenty pregnant albino rats and twenty-six male offspring were used in this study. The pregnant rats were divided into 2 equal groups: the control group which received distilled water and the balanced diet. The ACR-treated group received ACR at a dosage of 10 mg/kg/day orally from the 7th gestational day until weaning. Both the male offspring of the two groups and their mothers were sacrificed on postnatal day 28. Cerebellar tissue sections were stained with hematoxylin and eosin, Glees and Marsland silver stains were used for light microscopic examination. Immunohistochemical detection of glial fibrillary acidic protein (GFAP), Caspase-3, 8hydroxy2’-deoxyguanosine (8-OHdG), and terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL) was performed. Results: ACR induced histopathological changes in the 3 cerebellar cortex layers of mothers and their growing offspring. Maternal administration of ACR during pregnancy and lactation disturbed cerebellar growth via oxidative deoxyribonucleic acid (DNA) damage and apoptosis, in addition to astrogliosis. Statistical analysis of the mean optical density values of GFAP, Caspase3, and 8-OHdG immunoreactivity, and TUNEL staining revealed a highly significant increase in the ACR-treated groups compared with the corresponding control groups. Conclusion: ACR-induced cerebellar injury is mediated via the 8-OHdG /caspase-3 oxidative stress signaling pathway. The intake of ACR should be avoided during pregnancy and lactation. | ||
| Keywords | ||
| Acrylamide; Cerebellar cortex; 8-OHdG; Caspase-3; TUNEL assay | ||
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