Protective Effects of Some Creatine Derivatives in Brain Tissue Anoxia

Perasso, Luisa; Lunardi, G.; Risso, Federica; Pohvozcheva, A. V.; Leko, Maria; Gandolfo, Carlo; Florio, Tullio; Cupello, A.; Буров, С. В.; Balestrino, Maurizio

doi:10.1007/s11064-007-9492-9

Cited by 26 publications

(38 citation statements)

References 46 publications

(64 reference statements)

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“…While some derivatives (e.g., Namidino-piperidine) were harmful, others (e.g., Cr-Mgcomplex acetate, PCr-Mg-complex acetate and Cr ethyl ester) showed interesting neuroprotective effects in hippocampal organotypic cultures (a model with disruption of BBB) (Perasso et al 2008;Adriano et al 2011). PCr-Mgcomplex acetate and another derivative, Cr benzyl ester, were also demonstrated to cross cell membranes without the help of the Cr transporter (Lunardi et al 2006).…”

Section: Creatine Derivatives For a Better Crossing Of Bbb?mentioning

confidence: 99%

Creatine and guanidinoacetate transport at blood‐brain and blood‐cerebrospinal fluid barriers

Braissant

2012

J of Inher Metab Disea

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While it was thought that most of cerebral creatine is of peripheral origin, AGAT and GAMT are well expressed in CNS where brain cells synthesize creatine. While the creatine transporter SLC6A8 is expressed by microcapillary endothelial cells (MCEC) at blood-brain barrier (BBB), it is absent from their surrounding astrocytes. This raised the concept that BBB has a limited permeability for peripheral creatine, and that the brain supplies a part of its creatine by endogenous synthesis. This review brings together the latest data on creatine and guanidinoacetate transport through BBB and blood-CSF barrier (BCSFB) with the clinical evidence of AGAT-, GAMT- and SLC6A8-deficient patients, in order to delineate a clearer view on the roles of BBB and BCSFB in the transport of creatine and guanidinoacetate between periphery and CNS, and on brain synthesis and transport of creatine. It shows that in physiological conditions, creatine is taken up by CNS from periphery through SLC6A8 at BBB, but in limited amounts, and that CNS also needs its own creatine synthesis. No uptake of guanidinoacetate from periphery occurs at BBB except under GAMT deficiency, but a net exit of guanidinoacetate seems to occur from CSF to blood at BCSFB, predominantly through the taurine transporter TauT.

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Section: Creatine Derivatives For a Better Crossing Of Bbb?mentioning

confidence: 99%

Creatine and guanidinoacetate transport at blood‐brain and blood‐cerebrospinal fluid barriers

Braissant

2012

J of Inher Metab Disea

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“…In vitro hippocampal slices were prepared as previously described [20]. Approval to conduct the experiments was obtained from the Italian ministry of Health in compliance with all animal care requirements that are requested by Italian law (law D.L.…”

Section: In Vitro Hippocampal Slicesmentioning

confidence: 99%

“…Anoxia was induced by replacing oxygen with nitrogen in the gas phase. Duration of the various treatments was chosen in agreement with our previous work with creatine, ouabain [5] and anoxia [20], and is shown in Figs. 3 and 4.…”

Section: Treatmentsmentioning

confidence: 99%

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A Novel Hypothesis About Mechanisms Affecting Conduction Velocity of Central Myelinated Fibers

et al. 2011

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The hypothesis that gap junctions are implicated in facilitating axonal conduction has not yet been experimentally demonstrated at the electrophysiological level. We found that block of gap junctions with oleammide slows down axonal conduction velocity in the hippocampal Schaffer collaterals, a central myelinated pathway. Moreover, we explored the possibility that support by the oligodendrocyte to the axon involves energy metabolism, a hypothesis that has been recently proposed by some of us. In agreement with this hypothesis, we found that the effect of oleammide was reversed by pretreatment with creatine, a compound that is known to increase the energy charge of the tissue. Moreover, conduction velocity was also slowed down by anoxia, a treatment that obviously decreases the energy charge of the tissue, and by ouabain, a compound that blocks plasma membrane Na/K-ATPase, the main user of ATP in the brain. We hypothesize that block of gap junctions slows down conduction velocity in central myelinated pathways because oligodendrocytes synthesize ATP and transfer it to the axon through gap junctions.

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“…Creatine is pivotally important in delaying ATP depletion during anoxia or ischemia through the creatine-phosphocreatine system [10,11]. Today, many athletes take a synthetic creatine powder supplement for performance enhancement.…”

Section: Introductionmentioning

confidence: 99%

The effect of an alkaline buffered creatine (Kre-Alkalyn®), on cell membrane behavior, protein synthesis, and cisplatin-mediated cellular toxicity

2015

Integr Mol Med

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Endogenous creatine is created in a stable, slightly alkaline, environment. It is reasonably efficacious in delivering ATP to its target in the body. Manufactured creatine is introduced orally into an acidic environment. A percentage is degraded in the stomach, or as a result of acidophilic bacterial exposure. In either case, a certain amount of orally ingested creatine never becomes available for ATP transport. Creatine supplementation, in and of itself, has been shown to influence endothelial permeability and cell surface reactivity to a modest degree, potentially interfering/blocking an inflammatory stimulus. In vitro endothelial cell adhesion experiments demonstrate that, as creatine concentrations increase, endothelial cell surface adhesion and permeability were both modified.Creatine does not cross the plasma membrane very well. Roughly 95% of creatine is released in close proximity to the muscle tissue and transported into the cell via a limited capacity creatine-transporter system. Recent reports have shown that an artificially created alkaline environment can influence cell membrane permeability and cell behavior. The alkalinity of soda has shown anti-proliferative effects on tumor cell lines. The ability of alkaline buffered creatine to produce micro-environmental remodeling, influence cell membrane behavior and impact cisplatin-mediated toxicity, are also examined in this paper.

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Protective Effects of Some Creatine Derivatives in Brain Tissue Anoxia

Cited by 26 publications

References 46 publications

Creatine and guanidinoacetate transport at blood‐brain and blood‐cerebrospinal fluid barriers

Creatine and guanidinoacetate transport at blood‐brain and blood‐cerebrospinal fluid barriers

A Novel Hypothesis About Mechanisms Affecting Conduction Velocity of Central Myelinated Fibers

The effect of an alkaline buffered creatine (Kre-Alkalyn®), on cell membrane behavior, protein synthesis, and cisplatin-mediated cellular toxicity

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