<i>β</i>‐amyloid decreases detectable endothelial nitric oxide synthase in human erythrocytes: a role for membrane acetylcholinesterase

Misiti, Francesco; Carelli-Alinovi, Cristiana; Sampaolese, Beatrice; Giardina, Bruno

doi:10.1002/cbf.2822

Cited by 16 publications

(8 citation statements)

References 36 publications

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“…Interestingly, amyloid beta protein (Aβ) has been identified in extraneuronal tissue, including RBCs and brain capillaries. Misiti et al very recently demonstrated that Aβ exposure results in a decrease in the immune staining of erythrocyte eNOS with concomitant alteration in RBC morphology, decreases in nitrite and nitrate levels, and alteration in membrane acetylcholinesterase activity [279]. The alteration in RBC morphology was reported to take place at just 10 μM Aβ concentrations.…”

Section: The Major Determinants Of Rbc Deformabilitymentioning

confidence: 98%

The Initial Common Pathway of Inflammation, Disease, and Sudden Death

Davidson¹,

Seneff²

2012

Entropy

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Abstract:In reviewing the literature pertaining to interfacial water, colloidal stability, and cell membrane function, we are led to propose that a cascade of events that begins with acute exogenous surfactant-induced interfacial water stress can explain the etiology of sudden death syndrome (SDS), as well as many other diseases associated with modern times. A systemic lowering of serum zeta potential mediated by exogenous cationic surfactant administration is the common underlying pathophysiology. The cascade leads to subsequent inflammation, serum sickness, thrombohemorrhagic phenomena, colloidal instability, and ultimately even death. We propose that a sufficient precondition for sudden death is lowered bioavailability of certain endogenous sterol sulfates, sulfated glycolipids, and sulfated glycosaminoglycans, which are essential in maintaining biological equipose, energy metabolism, membrane function, and thermodynamic stability in living organisms. Our literature review provides the basis for the presentation of a novel hypothesis as to the origin of endogenous bio-sulfates which involves energy transduction from sunlight. Our hypothesis is amply supported by a growing body of data showing that parenteral administration of substances that lower serum zeta potential results in kosmotropic cationic and/or chaotropic anionic interfacial water stress, and the resulting cascade.Keywords: inflammation; serum sickness; colloidal instability; interfacial water stress; bio-sulfates; Shwartzman phenomena; sudden death syndrome Glossary of TermsAnaphylaxis a severe, rapidly progressing, life-threatening, generalized allergic reaction. Biological equipoise a stable, non-equilibrium, dissipative system synonymous with life. Cholesterol sulfate (Ch-S)quantitatively the most important known sterol sulfate in human plasma where it regulates the activity of the serine proteases, in cell membranes where it has a stabilizing role, and in platelet membranes where it supports platelet adhesion. Coherence domain (CD)a water CD is a collection of liquid water molecules which oscillate in unison in tune with a self-trapped electromagnetic field at a well-defined frequency. The coherent oscillations produce an ensemble of quasi-free electrons, able to collect noise energy from the environment and transform it into high-grade coherent energy in the form of electron vortices. This high-grade energy may then activate biomolecules resonating with the water CD. Colloidal instabilitya property attributed to a colloidal suspension that develops when stabilizing repulsive steric and electrostatic forces between colliding particles are insufficient to prevent their natural tendency to aggregate into masses large enough to precipitate.Colloidal suspension a colloid that has a continuous liquid phase in which a solid is suspended in a liquid, e.g., our flowing blood. Exclusion zone (EZ)a glass-like, gel phase consisting of water CDs resonating in-phase, adjacent to hydrophilic surfaces, several hundred micrometers wide which excludes colloi...

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Section: The Major Determinants Of Rbc Deformabilitymentioning

confidence: 98%

The Initial Common Pathway of Inflammation, Disease, and Sudden Death

Davidson¹,

Seneff²

2012

Entropy

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“…Beside its presence in CNS, Aβ can be detected in platelets (Chen et al, 1995 ) and blood (Seubert et al, 1992 ), where it interacts with red blood cells (RBC). Our previous studies (Clementi et al, 2004 ; Misiti et al, 2012 ; Carelli-Alinovi et al, 2015a , 2016a ) suggest that Aβ is able to alter RBC metabolism. Other studies (Jayakumar et al, 2003 ; Mandal et al, 2003 ; Nakagawa et al, 2011 ; Lang and Lang, 2015 ), indicate that Aβ could impairs RBC functionality and integrity, enhancing abnormalities at the vascular level that could be responsible for AD (de la Torre, 2002 ).…”

Section: Introductionmentioning

confidence: 87%

Erythrocytes as Potential Link between Diabetes and Alzheimer’s Disease

Carelli-Alinovi

Misiti

2017

Front. Aging Neurosci.

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Many studies support the existence of an association between type 2 diabetes (T2DM) and Alzheimer’s disease (AD). In AD, in addition to brain, a number of peripheral tissues and cells are affected, including red blood cell (RBC) and because there are currently no reliable diagnostic biomarkers of AD in the blood, a gradually increasing attention has been given to the study of RBC’s alterations. Recently it has been evidenced in diabetes, RBC alterations superimposable to the ones occurring in AD RBC. Furthermore, growing evidence suggests that oxidative stress plays a pivotal role in the development of RBC’s alterations and vice versa. Once again this represents a further evidence of a shared pathway between AD and T2DM. The present review summarizes the two disorders, highlighting the role of RBC in the postulated common biochemical links, and suggests RBC as a possible target for clinical trials.

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“…The treated erythrocyte suspensions were centrifuged at 2500 rpm for 10 min, and the supernatants were separated from the pellets. NO concentrations were determined using NO kit instructions 52 (Nanjingjiancheng Biotechnology, Nanjing, China).…”

Section: = × Hemolysis Ratio Absorbance Of Each Tube Absorbance With ...mentioning

confidence: 99%

Comparative Study on the Protective Effect of Chlorogenic Acid and 3-(3-Hydroxyphenyl) Propionic Acid against Cadmium-Induced Erythrocyte Cytotoxicity: In Vitro and In Vivo Evaluation

Cheng

Song

Ding

et al. 2021

J. Agric. Food Chem.

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The metabolism of chlorogenic acid (CGA) through the intestinal tract was studied. As cadmium is a well-known toxic heavy metal, this study was carried out to investigate the comparative protective effect of CGA and its representative intestinal metabolite (3-(3-hydroxyphenyl) propionic acid, HPPA) against Cd-induced erythrocyte cytotoxicity in vitro and in vivo. We found that CGA and its intestinal metabolite appreciably prevented erythrocyte hemolysis, osmotic fragility, and oxidative stress induced by Cd. Also, we found that HPPA had a stronger protective ability than CGA against Cd-induced erythrocyte injury in vivo, such as increasing the ratio of protein kinase C from 7.7% (CGA) to 12.0% (HPPA). Therefore, we hypothesized that CGA and its microbial metabolite had protective effects against Cd-induced erythrocyte damage via multiple actions including antioxidation and chelation. For humans, CGA supplementation may be favorable for avoiding Cd-induced biotoxicity.

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β‐amyloid decreases detectable endothelial nitric oxide synthase in human erythrocytes: a role for membrane acetylcholinesterase

Cited by 16 publications

References 36 publications

The Initial Common Pathway of Inflammation, Disease, and Sudden Death

The Initial Common Pathway of Inflammation, Disease, and Sudden Death

Erythrocytes as Potential Link between Diabetes and Alzheimer’s Disease

Comparative Study on the Protective Effect of Chlorogenic Acid and 3-(3-Hydroxyphenyl) Propionic Acid against Cadmium-Induced Erythrocyte Cytotoxicity: In Vitro and In Vivo Evaluation

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