Author Topic: Trehalose, glutathione, Candida, brain function connection  (Read 7163 times)


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Trehalose, glutathione, Candida, brain function connection
« Reply #2 on: June 24, 2008, 05:14:08 PM »
I had previously posted a reply, really a question, but don't see it here, so I'll try again.  Not being a scientist, I can't interpret this article, which I find too technical.  My question is whether one can draw a conclusion from this article, one way or the other, as to whether the ingestion of trehalose would likely be a help or hindrance to someone who's dealing with systemic candida overgrowth.  Can anyone help put this article into layperson's terms?  Thank you for any insight you can provide!
« Last Edit: June 25, 2008, 01:23:03 AM by JC Spencer »

Offline JC Spencer

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Trehalose, glutathione, Candida, brain function connection
« Reply #1 on: May 12, 2008, 12:32:04 AM »
Comments by J. C. Spencer
With very little comment, let me simply reference this paper, present the abstract, and call it the trehalose - glutathione - Candida - brain function - connection.  Glutathione - or L-glutathione plays powerful roles in human cells, is a strong antioxidant, effects nutrient metabolism, and regulation of cellular events including gene expression, DNA and protein synthesis, cell growth, and immune response.  It is reported that Parkinson’s patients have a lower level of glutathione in the brain.  I do not believe supplementation of glutathione is a good idea because (1) the supplement may not penetrate the cell membrane and (2) some doctors believe supplementation may inhibit the cellular production of glutathione.  Acetylcysteine is the precursor to glutathione.  A medical doctor instructed me that supplementation with N-acetylcysteine (NAC) is an excellent means of boosting glutathione in the body.  I am told that NAC is rapidly absorbed after oral administration and reaches a maximum plasma level in 2-3 hours, with a half-life of about 6 hours. NAC readily enters the cell and is hydrolyzed to cysteine.

Here is the abstract on the trehalose - glutathione - Candida - brain function - connection.

Disruption of the Candida albicans ATC1 gene encoding a cell-linked acid trehalase decreases hypha formation and infectivity without affecting resistance to oxidative stress

Yolanda Pedreño1,2, Pilar González-Párraga1, María Martínez-Esparza3, Rafael Sentandreu2, Eulogio Valentín2 and Juan-Carlos Argüelles1

1 Área de Microbiología, Facultad de Biología, Universidad de Murcia, E-30071 Murcia, Spain
2 Departamento de Microbiología y Ecología, Universidad de Valencia, E-46100 Burjassot, Valencia, Spain
3 Departamento de Bioquímica y Biología Molecular B e Inmunología, Universidad de Murcia, E-30071 Murcia, Spain

Correspondence Juan-Carlos Argüelles

In Candida albicans, the ATC1 gene, encoding a cell wall-associated acid trehalase, has been considered as a potentially interesting target in the search for new antifungal compounds. A phenotypic characterization of the double disruptant  mutant showed that it was unable to grow on exogenous trehalose as sole carbon source. Unlike actively growing cells from the parental strain (CAI4), the null mutant displayed higher resistance to environmental insults, such as heat shock (42 °C) or saline exposure (0.5 M NaCl), and to both mild and severe oxidative stress (5 and 50 mM H2O2), which are relevant during in vivo infections. Parallel measurements of intracellular trehalose and trehalose-metabolizing enzymes revealed that significant amounts of the disaccharide were stored in response to thermal and oxidative challenge in the two cell types. The antioxidant activities of catalase and glutathione reductase were triggered by moderate oxidative exposure (5 mM H2O2), whereas superoxide dismutase was inhibited dramatically by H2O2, where a more marked decrease was observed in  cells. In turn, the mutant exhibited a decreased capacity of hypha and pseudohypha formation tested in different media. Finally, the homozygous null mutant in a mouse model of systemic candidiasis displayed strongly reduced pathogenicity compared with parental or heterozygous strains. These results suggest not only a novel role for the ATC1 gene in dimorphism and infectivity, but also that an interconnection between stress resistance, dimorphic conversion and virulence in C. albicans may be reconsidered. They also support the hypothesis that Atc1p is not involved in the physiological hydrolysis of endogenous trehalose.