Effects of adult-onset choline deprivation on the activities of acetylcholinesterase, (Na+,K+)- and Mg2+-ATPase in crucial rat brain regions

Liapi, Charis; Kyriakaki, Argyro; Ζάρρος, Απόστολος; Al-Humadi, Hussam; Stolakis, Vasileios; Gkrouzman, Elena; Anifantaki, Foteini; Skandali, Nikolina; Margaritis, Marios; Tsakiris, Stylianos

doi:10.1016/j.fct.2008.10.012

Cited by 9 publications

(8 citation statements)

References 35 publications

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“…Thus, activation of different PKC isoforms may either activate or inhibit Na + K + activation (Xia et al, 1995). In the same trend, Liapi et al (2009) observed that the differentially affected activities of AchE and Na + K + ATPase could result in modulation of cholinergic neurotransmission, neural excitability, metabolic energy production, Mg +2 homeostasis and protein synthesis in crucial rat brain regions.…”

Section: Discussionmentioning

confidence: 84%

Possible action of grape seed oil on brain toxicity induced by methomyl or imidacloprid of male rats.

Moeen

Amer

Ismail

et al. 2018

Journal of Scientific Research in Science

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The present study was planned to investigate the effect of methomyl or imidacloprid on the brain of male rats. The effect grape seeds oil as an antioxidant was also evaluated. Animals were administered orally with 1/10 and 1/20 of LD 50 methomyl and imidacloprid with 17 and 450 mg /kg bw for four and eight weeks. Grape seeds oil with 4 ml/kg b.wt. was used for protection from methomyl and imidacloprid toxicity. Brain cortex and hippocampus oxidative stress (glutathione S transferase GST, glutathione peroxidase GPX, superoxide dismutase SOD, malondialdhyde MDA and nitric oxide NO), Na + ,K + , ATPase and acetylcholinesterase AChE were determined. The result showed that GST, GPX, MDA, and NO 2 were increased significantly. But SOD, Na + K + ATPase and AChE were significantly reduced in comparison with the control. Grape seed oil induced a significant improvement for the pesticides brain toxicity but not to the level of control. The study suggested that the oil antioxidants not improve the brain toxicity induced by methomyl or imidacloprid.

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Section: Discussionmentioning

confidence: 84%

Possible action of grape seed oil on brain toxicity induced by methomyl or imidacloprid of male rats.

Moeen

Amer

Ismail

et al. 2018

Journal of Scientific Research in Science

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show abstract

“…On the other hand, choline-deficient diets induced deficits of this precursor both in cell membranes and in the ACh synthesizing compartment [186]. Lack of membrane integrity could cause the impairment of energy production in brain mitochondria, leading to increased vulnerability of cholinergic neurons to neurodegenerative signals along with appearance of behavioral deficits [186, 187].…”

Section: Cholinementioning

confidence: 99%

“…Lack of membrane integrity could cause the impairment of energy production in brain mitochondria, leading to increased vulnerability of cholinergic neurons to neurodegenerative signals along with appearance of behavioral deficits [186, 187]. Such reciprocal interactions between aberrant acetyl-CoA/energy and choline metabolisms may trigger vicious cycle of early deterioration of cholinergic neurons under various neurodegenerative conditions.…”

Section: Cholinementioning

confidence: 99%

Acetyl-CoA the Key Factor for Survival or Death of Cholinergic Neurons in Course of Neurodegenerative Diseases

et al. 2013

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Glucose-derived pyruvate is a principal source of acetyl-CoA in all brain cells, through pyruvate dehydogenase complex (PDHC) reaction. Cholinergic neurons like neurons of other transmitter systems and glial cells, utilize acetyl-CoA for energy production in mitochondria and diverse synthetic pathways in their extramitochondrial compartments. However, cholinergic neurons require additional amounts of acetyl-CoA for acetylcholine synthesis in their cytoplasmic compartment to maintain their transmitter functions. Characteristic feature of several neurodegenerating diseases including Alzheimer’s disease and thiamine diphosphate deficiency encephalopathy is the decrease of PDHC activity correlating with cholinergic deficits and losses of cognitive functions. Such conditions generate acetyl-CoA deficits that are deeper in cholinergic neurons than in noncholinergic neuronal and glial cells, due to its additional consumption in the transmitter synthesis. Therefore, any neuropathologic conditions are likely to be more harmful for the cholinergic neurons than for noncholinergic ones. For this reason attempts preserving proper supply of acetyl-CoA in the diseased brain, should attenuate high susceptibility of cholinergic neurons to diverse neurodegenerative conditions. This review describes how common neurodegenerative signals could induce deficts in cholinergic neurotransmission through suppression of acetyl-CoA metabolism in the cholinergic neurons.

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“…For example, tetramers of the "tailed" variant (AChE-T), constitute the main form of AChE in the mammalian brain, while in the mouse brain, stress and anticholinesterase inhibitors induce the expression of unspliced "readthrough" variant (AChE-R) mRNA which produces a monomeric form (Perrier et al 2005). Choline deficiency caused the increase of AChE expression in crucial rat brain regions (hippocampus, hypothalamus, frontal cortex and pons) to a diverse extent (Liapi et al 2009). Taking these facts into consideration, results of our study may be the consequence of competition between AChE variants and their homologs for interactions with the corresponding protein partner in investigated tissues.…”

Section: Discussionmentioning

confidence: 99%

Methionine-choline deprivation alters liver and brain acetylcholinesterase activity in C57BL6 mice

Vučević

Cerović²,

Mladenović³

et al. 2016

gpb

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Choline and methionine are precursors of acetylcholine, whose hydrolysis is catalyzed by acetylcholinesterase (AChE). Considering the possibility of their common deficiency, we investigated the influence of methionine-choline deprivation on AChE activity in liver and various brain regions (hypothalamus, hippocampus, cerebral cortex and striatum) in mice fed with methionine-choline deficient (MCD) diet. Male C57BL/6 mice (n = 28) were randomly and equally divided into following groups: control group fed with standard diet for 6 weeks (C) and groups fed with MCD diet for 2 weeks (MCD2), 4 weeks (MCD4) and for 6 weeks (MCD6). After the diet, mice were sacrificied and AChE activity in liver and brain was determined spectrophotometrically. Hepatic AChE activity was higher in MCD2, MCD4 and MCD6 compared to control (p < 0.01), with most prominent increase in MCD6. AChE activity in hypothalamus was higher in MCD4 and MCD6 vs. control (p < 0.05 and p < 0.01, respectively), as well as in MCD6 compared to MCD4 (p < 0.01). In hippocampus, increase in AChE activity was shown in MCD6 compared to control (p < 0.01). In cortex and striatum, increase in AChE activity was noted in MCD6 compared to control (p < 0.05). Our findings indicate the increase of hepatic and brain AChE activity in mice caused by methionine-choline deprivation.

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Effects of adult-onset choline deprivation on the activities of acetylcholinesterase, (Na+,K+)- and Mg2+-ATPase in crucial rat brain regions

Cited by 9 publications

References 35 publications

Possible action of grape seed oil on brain toxicity induced by methomyl or imidacloprid of male rats.

Possible action of grape seed oil on brain toxicity induced by methomyl or imidacloprid of male rats.

Acetyl-CoA the Key Factor for Survival or Death of Cholinergic Neurons in Course of Neurodegenerative Diseases

Methionine-choline deprivation alters liver and brain acetylcholinesterase activity in C57BL6 mice

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