Drug and chemical toxicology · 2026
Potential protective effects of nano-hydroxyapatite and vitamin-B12 against acrylamide-induced neurotoxicity in rat cerebella.
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Abdel-Moaty Zamzam Nasrallah, Amin Yahia A, Ali Rana A, Galal Ahmed Talaat, El-Nahas Safaa, Tito Abd Elhameed Basma, Ouies Salwa M, Abd-El Baki Ahmed Maha
Аннотация
BACKGROUND: Acrylamide (ACR) is a common industrial substance that is used in the manufacture of many laboratory materials, formed during food processing, and is known to cause neurotoxicity and brain damage. Protective substances such as Nano-hydroxyapatite and vitamin B12 (Vit.B12) may play a modulatory role in mitigating this neural damage. The current study aimed to investigate the neurotoxicity and brain damage induced by ACR exposure and the ameliorative effects of nano-hydroxyapatite and Vit.B12 against these neural toxic effects.
METHODS: Forty male rats were divided into four groups (10 for each): Control group received distilled water, ACR group received a daily dose of 10 mg/kg bw ACR, ACR+Nano-HA received ACR (10 mg/kg) plus nano-HA (150 mg/kg), and ACR+Vit.B12 group that received ACR (10 mg/kg) plus Vit.B12 (1 mg/kg) for 5 weeks. Oxidant/antioxidant biomarkers, including catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), and malondialdehyde (MDA), were measured in blood. Histological investigations, Semithin sections, and an electron micrograph of the cerebellum were performed. Immunohistochemical staining with an anti-GFAP antibody was performed to determine the severity of astrocytosis.
RESULTS: ARC exposure caused cerebellar degeneration, significant reduced Purkinje cell numbers, significant decreased layers thickness, and significantly decreased antioxidant biomarkers, but markedly elevated oxidative stress biomarker levels. Moreover, marked histological alterations and astrocytosis were observed, as evidenced by the increased number of G-FAP immunopositive cells in cerebellar tissues compared with the other groups.
CONCLUSION: Acrylamide exposure severely damages cerebellar tissue, primarily through oxidative stress. The combination of nano-hydroxyapatite and vitamin B12 provided neuroprotection, with vitamin B12 producing the most noticeable recovery.
METHODS: Forty male rats were divided into four groups (10 for each): Control group received distilled water, ACR group received a daily dose of 10 mg/kg bw ACR, ACR+Nano-HA received ACR (10 mg/kg) plus nano-HA (150 mg/kg), and ACR+Vit.B12 group that received ACR (10 mg/kg) plus Vit.B12 (1 mg/kg) for 5 weeks. Oxidant/antioxidant biomarkers, including catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), and malondialdehyde (MDA), were measured in blood. Histological investigations, Semithin sections, and an electron micrograph of the cerebellum were performed. Immunohistochemical staining with an anti-GFAP antibody was performed to determine the severity of astrocytosis.
RESULTS: ARC exposure caused cerebellar degeneration, significant reduced Purkinje cell numbers, significant decreased layers thickness, and significantly decreased antioxidant biomarkers, but markedly elevated oxidative stress biomarker levels. Moreover, marked histological alterations and astrocytosis were observed, as evidenced by the increased number of G-FAP immunopositive cells in cerebellar tissues compared with the other groups.
CONCLUSION: Acrylamide exposure severely damages cerebellar tissue, primarily through oxidative stress. The combination of nano-hydroxyapatite and vitamin B12 provided neuroprotection, with vitamin B12 producing the most noticeable recovery.