Assessing the Influence of Intermittent Alcohol Access on Acrylamide-Induced Neuronal Toxicity in an Experimental Rat Model.

acrylamide apoptosis ethanol memory dysfunctions neuroinflammation neurotoxicity oxidative stress

Journal

Brain sciences
ISSN: 2076-3425
Titre abrégé: Brain Sci
Pays: Switzerland
ID NLM: 101598646

Informations de publication

Date de publication:
04 Jun 2024
Historique:
received: 07 05 2024
revised: 27 05 2024
accepted: 03 06 2024
medline: 27 6 2024
pubmed: 27 6 2024
entrez: 27 6 2024
Statut: epublish

Résumé

Tobacco and alcohol have been identified as health risk behaviors associated with significant unfavorable health consequences, ranking within the list of the top ten causes of mortality and disability-adjusted life years (DALY). The combustion of tobacco leads to the formation of acrylamide (ACR), which is well known for its neurotoxic effects. Similarly, alcohol consumption has also been widely recognized for its neurotoxic effects. Both substances can affect neurons and neuroglia cells through various pathways. This study sought to examine the impacts of co-administration of ACR and intermittent-access ethanol (IAE) consumption over a period of one month. The experimental group received 20 mg/kg of ACR, administered orally, along with IAE of 20% ethanol sessions lasting 24 h, three times per week. The cognitive outcomes were assessed utilizing the elevated plus maze (EPM), which was employed as a means of assessing the capability to learn and remember, the novel object recognition (NOR) test, which was employed to assess recognition memory, and the Y-maze, which was used to explore a new environment and navigate. Additionally, ELISA assays were performed to examine underlying mechanisms, including markers associated with inflammation (NF-κB, PGE2, and TNF-α), apoptosis (Bcl2, Bax, and Caspase-3), and oxidative stress (MDA, catalase, and GSH). These markers were assessed in the brain homogenate as part of the investigation. Furthermore, a histopathological study was conducted. The findings indicated that NF-κB levels increased significantly in the combination of ACR and IAE groups (ACR + IAE) compared to either the ACR-alone or IAE-alone groups. However, parallel changes were observed in TNF-α, PGE2, Bax, Bcl-2, Caspase-3, GSH, and CAT levels when comparing the ACR + IAE group to the ACR-alone group. Comparable alterations were noted between the ACR + IAE treatment and IAE-alone groups in TNF-α, Bcl-2, MDA, GSH, and CAT levels. Moreover, the histopathological analysis revealed significant changes between the ACR + IAE and the ACR- or IAE-alone groups. Regarding memory parameters assessed using tests including EPM, NOR, and Y-maze, considerable changes were observed across all treatment groups as opposed to the control. Surprisingly, there were no notable differences in the NOR and Y-maze tasks between the alone and combination treatment. Further study is necessary to explore the long-term alteration of co-administering ACR and IAE on behavior, memory, and neurotoxicity-related mechanisms, in order to elucidate their combined effects more clearly.

Identifiants

pubmed: 38928574
pii: brainsci14060574
doi: 10.3390/brainsci14060574
pii:
doi:

Types de publication

Journal Article

Langues

eng

Subventions

Organisme : Deanship of Graduate Studies and Scientific Research at Qassim University
ID : QU-APC-2024-9/1

Auteurs

Abdulaziz Arif A Alshammari (AAA)

Department of Pharmacology and Toxicology, College of Pharmacy, Qassim University, Buraydah 51452, Saudi Arabia.

Awyed Batah Almutairi (AB)

Pharmacy Care Department, Al Midhnab General Hospital, Qassim Health Cluster, Ministry of Health, Al Mithnab 56526, Saudi Arabia.

Minhajul Arfeen (M)

Department of Medicinal Chemistry and Pharmacognosy, College of Pharmacy, Qassim University, Buraydah 51452, Saudi Arabia.

Abdullah Saleh Alkhamiss (AS)

Department of Pathology, College of Medicine, Qassim University, Buraydah 51452, Saudi Arabia.

Maha A Aldubayan (MA)

Department of Pharmacology and Toxicology, College of Pharmacy, Qassim University, Buraydah 51452, Saudi Arabia.

Ahmad H Alhowail (AH)

Department of Pharmacology and Toxicology, College of Pharmacy, Qassim University, Buraydah 51452, Saudi Arabia.

Vasudevan Mani (V)

Department of Pharmacology and Toxicology, College of Pharmacy, Qassim University, Buraydah 51452, Saudi Arabia.

Classifications MeSH