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2025 | 63 | 2 | 205-213

Article title

Histological study of the prefrontal cortex of adult wistar rat exposed to primidone (mysoline)

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EN

Abstracts

EN
Epilepsy is a chronic neurological disorder that often requires long-term administration of antiepileptic drugs (AEDs). Primidone (Mysoline), a first-generation barbiturate-type AED, remains widely prescribed for seizure control and essential tremor. Despite its clinical efficacy, prolonged use of Primidone has been associated with metabolic and neurochemical alterations that could influence cortical function. This study investigated the histological and biochemical effects of Primidone on the prefrontal cortex of adult female Wistar rats. Fifteen healthy rats weighing between 130 and 200 g were randomly divided into three groups of five each: control, low-dose (75 mg/kg), and high-dose (150 mg/kg). The control group received standard feed and water, while the treated groups were administered oral doses of Primidone daily for twenty-eight days. At the end of the exposure period, the rats were sacrificed under anesthesia, and their prefrontal cortices were excised for histological and biochemical analyses. Hematoxylin and eosin staining revealed no significant histoarchitectural alterations or neuronal degeneration across treatment groups compared with the control. However, biochemical assays demonstrated a dose-dependent reduction (p < 0.05) in the activities of key antioxidant enzymes—superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and acetylcholinesterase (AChE)—alongside a marked elevation in malondialdehyde (MDA), an indicator of lipid peroxidation and oxidative stress. These findings suggest that chronic Primidone exposure may impair endogenous antioxidant defense systems in the prefrontal cortex, thereby predisposing neuronal tissues to oxidative injury even in the absence of overt histological damage. The study highlights the need for cautious long-term use of barbiturate-based anticonvulsants and underscores the potential benefits of adjunct antioxidant therapy in mitigating drug-induced neurotoxicity.

Year

Volume

63

Issue

2

Pages

205-213

Physical description

Contributors

  • Department of Human Anatomy and Cell Biology, Faculty of Basic Medical Sciences, Delta State University, Abraka, Delta State, Nigeria
author
  • Department of Human Anatomy and Cell Biology, Faculty of Basic Medical Sciences, Delta State University, Abraka, Delta State, Nigeria
  • School of Petroleum Engineering, Department of Oil and Gas Engineering, China University of Petroleum (East China), Qingdao City, Shandong Province, China

References

  • [1] Castonguay C.-E., Liao C., Khayachi A., et al. Transcriptomic effects of propranolol and primidone converge on molecular pathways relevant to essential tremor. NPJ Genom. Med. 7 (2022) 46
  • [2] Kośmider K., et al. Second-generation antiepileptic drugs and oxidative stress: mechanisms and implications. Neurotox. Res. 45 (2023) 112–132
  • [3] de Munter J., Pavlov D., Gorlova A., et al. Increased oxidative stress in the prefrontal cortex as a shared feature of depressive- and PTSD-like syndromes: effects of a standardized herbal antioxidant. Front. Nutr. 8 (2021) 661455
  • [4] Kamieniak M., et al. The oxidative stress in epilepsy — focus on melatonin. Int. J. Mol. Sci. 25 (2024) 12943
  • [5] Park H.J., Lee Y., Sadigh S., et al. Comparison of malondialdehyde, acetylcholinesterase, and oxidative markers in rodent models of cognitive dysfunction. J. Neurosci. Methods 395 (2024) 115921
  • [6] Lenka A., et al. Primidone intolerance in essential tremor: clinical review and mechanisms. Tremor Other Hyperkinet. Mov. 11 (2021) 22
  • [7] Parsons A.L.M., et al. The interconnected mechanisms of oxidative stress and epilepsy: implications for treatment. Pharmacol. Res. 176 (2022) 106014
  • [8] Quinlan S., et al. Early-life phenobarbital exposure dysregulates the transcriptome and induces long-term neurodevelopmental changes. Front. Pharmacol. 15 (2024) 1340691
  • [9] Fuchs M., et al. Oxidative stress in rat brain during experimental status epilepticus: prevention by antioxidants. Front. Pharmacol. 14 (2023) 1233184
  • [10] Hossain R., Al-Khafaji K., Khan R.A., et al. Quercetin and/or ascorbic acid modulatory effect on phenobarbital-induced sleeping mice: role of antioxidant defenses. Pharmaceutics 14 (2021) 721
  • [11] Belete T.M., et al. Recent progress in the development of new antiepileptic therapeutics: pharmacology and oxidative-stress considerations. Pharmaceuticals 16 (2023) 111
  • [12] Borowicz-Reutt K.K., et al. Role of oxidative stress in epileptogenesis and potential therapeutic approaches. Pharmacol. Rep. 72 (2020) 123–145
  • [13] Jujuboside A., et al. Jujuboside A exhibits antiepileptogenic and neuroprotective effects in a rat seizure model. Biomed. Res. Int. 2022 (2022) 7792791
  • [14] Pasini A.M.F., et al. Effect of antioxidant therapy on oxidative stress in vivo: implications for CNS disorders. Antioxidants (Basel) 11 (2022) 234
  • [15] Saenz-Farret M., et al. Antiseizure drugs and movement disorders: clinical and pharmacological perspectives. Mov. Disord. Clin. Pract. 9 (2022) 876–889
  • [16] Ogunsuyi O.B., et al. Neural acetylcholinesterase and monoamine oxidase alterations in experimental neurotoxicity models: links to oxidative stress. BMC Neurosci. 25 (2024) 90
  • [17] Villeda-González J.D., et al. New paradigms in the study of the cholinergic system and oxidative stress in brain disorders. J. Cell Physiol. 239 (2024) 10210–10226
  • [18] Zhang L., et al. The associations between oxidative stress and epilepsy: review and recent advances. Ann. Clin. Neuro. 2 (2024) 45–59
  • [19] Łukawski K., et al. Oxidative stress and neurodegeneration in animal models: insights into mechanisms and therapeutic targets. Neurotoxicol. Teratol. 92 (2023) 107–123
  • [20] Jomová K., et al. Several lines of antioxidant defense against oxidative stress. Arch. Toxicol. 98 (2024) 1357–1376

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article

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bwmeta1.element.psjd-2ed25c6b-df48-4caf-a2c8-93ce4b7a85e6
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