ArticleEnvironmental toxicology2026
Acrylamide-Induced Neurotoxicity Is Mitigated by Curcumin and Its Nano Lipid Carrier Formulation in Albino Rats.
Article in Environmental toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- The Mechanism and Application of Traditional Chinese Medicine Nano-Formulations in the Treatment of Renal Fibrosis.International journal of nanomedicine · 2026Review
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5 authors.
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Abstract
Acrylamide (AA) exerts neurotoxicity and genotoxicity in wildlife and humans. This study measured the ability of curcumin, an antioxidant, and curcumin Nano lipid carriers (Cur-NLCs) to alleviate biochemical biomarkers of AA-induced neurotoxicity in the cortex and hippocampus of exposed rats. Thirty adult female albino rats were assigned into one of five experimental groups: (1) negative control, (2) vehicle control, (3) acrylamide (50 mg/kg b.wt), (4) acrylamide (50 mg/kg b.wt) with curcumin (100 mg/kg b.wt), and (5) acrylamide (50 mg/kg b.wt) with Cur-NLCs (10 mg/kg b.wt). Treatments were orally administered to rats for 5 days/week for 2 weeks. Acrylamide administration caused body weight loss, abnormal gait, and histopathological damage to both the cortex and hippocampus. Curcumin and Cur-NLCs treatment reduced the occurrence of abnormal behavior and mitigated histopathological changes observed in rats treated with AA. The level of norepinephrine (NE), dopamine (DA), gamma-aminobutyric acid (GABA), serotonin (5-HT), reduced glutathione (GSH), and adenosine triphosphate (ATP) were all decreased with AA treatment. Following treatment with curcumin, AA-induced reductions in glutathione (GSH), dopamine (DA), 5-hydroxy indole acetic acid (5-HIAA), norepinephrine (NE), adenosine monophosphate (AMP), aspartate (ASP), and gamma-aminobutyric acid were restored to the control level in the cortex. In the hippocampus, GSH, 8-hydroxydeoxyguanosine (8-OHdG), DA, 5-hydroxy tryptamine (5-HT), 5-HIAA, NE, ATP, ASP, GABA and glutamate (Glu) improved to that observed in control rats. Co-treatment with Cur-NLCs also had protective effects on malondialdehyde (MDA) and NE in the cortex, and 5-HIAA and ASP in the hippocampus. Upon comparison, Cur-NLCs at 10 mg/kg/day showed less benefit than curcumin alone (100 mg/kg/day) based on several endpoints of oxidative stress, DNA damage, and histopathology. We conclude there are tissue specific responses to these formulations in the CNS and suggest that a more effective means of treating AA-induced neurotoxicity with these antioxidants may be a mixture of both unmodified curcumin and its Nano-formulation.
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