الفهرس 
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Abstract
Acrylamide (ACR) is a chemical that naturally forms in starchy food products during high-temperature cooking, including frying, baking, roasting and also industrial processing, in this study we aimed to evaluate the toxic effect of ACR in nervous and reproductive systems of male rats through molecular, biochemical, pathological and immunohistochemical examinations. Also to evaluate the protective effects of portulaca oleracea seed hydroethanolic extract (PSE) on acrylamide -induced toxicity. PSE was subjected to phytochemical investigation using ultra-high-performance liquid chromatography (UPLC) coupled with quantitative time of flight mass spectrometry (qTOF-MS).
A number of 42 male Wister albino rats were divided into six groups each group has 7 rats including negative control, ACR-intoxicated group (10 mg/kg/day), PSE treated groups (200 and 400 mg/kg/day), and ACR + PSE treated groups (200 and 400 mg/kg/day, respectively). All treatments were given intragastrically for 60 days. The ACR treated group showed reduced relative organ body weight, while co-treatment with PSE showed significant increase of the weight. ACR caused a significant decrease in plasma total antioxidant capacity (TAC) and glutathione (GSH) activity, and an increase malondialdehyde (MDA) levels in testes and brain compared to the control group. In contrast, PSE treatment significantly increased the (TAC) and (GSH) activities, and deceased MDA levels. PSE markedly ameliorated brain damage as evidenced by the decreased lactate dehydrogenase (LDH), increased acetylcholinesterase (AchE) activities, as well as the increased brain‐derived neurotrophic factor (BDNF) that were altered by the toxic dose of ACR. Moreover, PSE markedly attenuated ACR-induced histopathological alterations in the cerebrum, cerebellum, hippocampus and sciatic nerve. PSE restored the oxidative status in the brain as indicated by (GSH), lipid peroxidation and increased (TAC). PSE upregulated the mRNA expression of protein kinase B (AKT), which resulted in an upsurge in its downstream cAMP response element-binding protein (CREB)/ brain derived neurotrophic factor (BDNF) mRNA expression in the brain tissue of ACR-intoxicated rats. Histopathological examination of testes of ACR treated group showed severe testicular degeneration in the form of a reduction in the number of the spermatogonial cells, and apoptosis of Leydig cells were also observed. ACR + Co treatment with PSE extract showed improvement of testicular lesions. Immunohistochemical examination exhibited strong casepase-3 immunoreactivity in testes of ACR- treated group. Treatment with PSE extract reduced the induced apoptosis. Moreover, proliferating cell nuclear antigen (PCNA) expression showed significant reduction in a spermatogenic series of ACR treated group unlike control and PSE-treated groups showed a strong immunopositive reaction in secondary spermatocytes and spermatids. Furthermore, PSE markedly downregulated the ACR-inclined glial fibrillary acidic protein (GFAP) expression in the brain tissue. Conclusion: The supplementation with PSE extract may provide a potential protective effect for ACR-induced testicular dysfunction and neurotoxicity in male rats. .