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Journals / Türk Biyokimya Dergisi / 2019 / Cilt: 44 - Sayı: 2

Alteration in cholinesterases, γ-aminobutyric acid and serotonin level with respect to thiamine deficiency in Swiss mice

Tiamin Eksikliğine olan farelerde Kolinesteraz, γ-aminobutirik asit ve Serotonin Seviyesinde Değişim

Anupama SHARMA
Renu BIST
Pages
218–223
Publication Date
2022-11-05
DOI
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AI Summary & Key Takeaways

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⚡ TL;DR(Too Long; Didn't Read)

Hence,vitamin B1 deficiency disturbs the cholinergic system andneurotransmitters levels in brain which may lead to neurodegenerative diseases.

📌 3 Key Takeaways

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Objective & Hypothesis:Abstract: Thiamine (vitamin B1), cofactor for variousmulti-enzyme complexes in energy metabolism, and playsa major role in the synthesis of cholinesterases such as acetylcholinesterase (AChE); butyrylcholinesterase (BChE).Present study deals with the changes in the cholinesterases, γ-aminobutyric acid (GABA) and serotonin in micebrain following thiamine deficiency.
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Key Findings & Data:Experimental mice(6–8 week old) were made thiamine deficient by intraperitoneal injection of pyrithiamine hydrobromide and fedwith thiamine-deficient diet.
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Conclusion & Impact:Hence,vitamin B1 deficiency disturbs the cholinergic system andneurotransmitters levels in brain which may lead to neurodegenerative diseases.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Abstract: Thiamine (vitamin B1), cofactor for variousmulti-enzyme complexes in energy metabolism, and playsa major role in the synthesis of cholinesterases such as acetylcholinesterase (AChE); butyrylcholinesterase (BChE).Present study deals with the changes in the cholinesterases, γ-aminobutyric acid (GABA) and serotonin in micebrain following thiamine deficiency. Experimental mice(6–8 week old) were made thiamine deficient by intraperitoneal injection of pyrithiamine hydrobromide and fedwith thiamine-deficient diet. Animals were divided intothree groups, Group I (Control), Group II (thiamine deficient mice for 8 days), and Group III (thiamine deficientmice for 10 days). The higher serotonin level whereas significant decreases in the AChE, BChE and GABA level wererecorded in treated groups as compared to control. Hence,vitamin B1 deficiency disturbs the cholinergic system andneurotransmitters levels in brain which may lead to neurodegenerative diseases.

Özet

Tiamin (vitamin B1), enerji metabolizmasında çeşitli multi-enzim kompleksleri için kofaktör ve Asetilkolinesteraz (AChE), Butirilkolinesteraz (BChE) gibi kolinesterazların sentezinde önemli bir rol oynar; Bu çalışma tiamin eksikliğini takiben farelerde beyindeki kolinesteraz, γ-aminobütirik asit (GABA) ve serotonin değişikliklerini ele almaktadır. Deney fareleri (6–8 haftalık) intraperitoneal pitmiamin hidrobromür enjeksiyonu ile tiyamin eksikliği yapıldı ve tiamin eksikliği olan diyetle beslendi. Hayvanlar 3 gruba ayrıldı, Grup I (Kontrol), Grup II (8 gün boyunca tiamin eksikliği olan fareler) ve Grup III (10 gün boyunca tiamin eksikli fareler). Kontrol grubuna kıyasla tedavi edilen gruplarda daha yüksek serotonin seviyesi, AChE, BChE ve GABA seviyesinde önemli düşüşler kaydedildi. Bu nedenle, B1 vitamini eksikliği, nörodejeneratif hastalıklara yol açabilen beyin içindeki kolinerjik sistemi ve nörotransmiter seviyelerini bozabilir.

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Cite This Article

SHARMA, A., BIST, R. (2022). Alteration in cholinesterases, γ-aminobutyric acid and serotonin level with respect to thiamine deficiency in Swiss mice. Türk Biyokimya Dergisi, Cilt: 44 - Sayı: 2, 218–223. https://ajindex.com/articles/620863

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References (14)

  1. Sharma A, Bist R, Bubber P. Thiamine deficiency induces oxidative stress in brain mitochondria of Mus musculus. J Physiol Biochem 2013;69:539–46
  2. Zastre JA, Sweet RL, Hanberry BS, Ye S. Linking vitamin B1 with cancer cell metabolism. Cancer Metabol 2013;1:16
  3. Shah D, Blockx I, Guns PJ, De Deyn PP, Van Dam D, Jonckers E, et al. Acute modulation of the cholinergic system in the mouse brain detected by pharmacological resting-state functional MRI. Neuroimage 2015;109:151–9
  4. Narvaez C, Ríos JM, Píriz G, Sanchez-Hernandez JC, Sabat, P. Subchronic exposure to chlorpyrifos affects energy expenditure and detoxification capacity in juvenile Japanese quails. Chemosphere 2016;144:775–84
  5. Bist R, Bhatt DK. Augmentation of cholinesterases and ATPase activities in the cerebellum and pons-medulla oblongata, by a combination of antioxidants (resveratrol, ascorbic acid, alphalipoic acid and vitamin E), in acutely lindane intoxicated mice. J Neurol Sci 2010;296:83–7
  6. Sharma A, Bist R. Thiamine deprivation disturbs cholinergic system and oxidative stress in liver of Mus musculus. Int J Pharma Pharma Sci 2014;6:139–43
  7. Auon M, Mahmood F, Khan A, Hussain R. Testicular and genotoxic effects induced by subchronic oral administration of chlorpyrifos in Japanese quail (Coturnix japonica). Pak J Agric Sci 2014;51:1005
  8. Bist R, Bhatt DK. The evaluation of effect of alpha-lipoic acid and vitamin E on the lipid peroxidation, gamma-amino butyric acid and serotonin level in the brain of mice (Mus musculus) acutely intoxicated with lindane. J Neurol Sci 2009;276:99–102
  9. Ellman GL, Courtney KD, Andres V, Jr., Featherstone RM. A new and rapid colorimetric determination of acetylcholinesterase activity. Biochem Pharmacol 1961;7:88–95
  10. Lowry OH, Rosebrough NJ, Farr AL, Randall RJ. The original method for protein estimation. Biol Chem 1951:1951;193–265
  11. Graham LT, Aprison MH. Fluorometric determination of aspartate, glutamate, and gamma-aminobutyrate in nerve tissue using enzymic methods. Anal Biochem 1966;15:487–97
  12. Udenfriend S, Weissbach H, Clark CT. The estimation of 5-hydroxytryptamine (serotonin) in biological tissues. J Biol Chem 1955;215:337–44
  13. Karuppagounder SS, Gibson GE. Thiamine deficiency: a model of metabolic encephalopathy and of selective neuronal vulnerability. In: McCandless DW, editor. Metabolic encephalopathy. New York: Springer, 2008;235–60
  14. Dror V, Eliash V, Rehavi M, Assaf Y, Biton IE, Fattal-Valeyski A. Neurodegeneration