Re: Stop The Thyroid Madness Newsletter

[Guest guest]

interesting synchronicity regarding oxalates....i was going to post this a

couple of days ago!

the information is from the files in the trying_low_oxalates group (i hope

it is ok to have copied it) ...the link to the group is here:

Trying_Low_Oxalates/

Listmates,

Candida is killed by releasing excess calcium intracellularly which is

taken up by their mitochondria, probably inducing cell death.

This increase of calcium can occur by various means, like having nystatin

punching holes in the cell membrane, but oxalates, by binding that calcium,

may prevent cell death.

This may explain the relationship between having high oxalates and being

less able to defend against candida.

6: J Antimicrob Chemother. 2004 Sep;54(3):603-8. Epub 2004 Jul 28.

Release of calcium from intracellular stores and subsequent uptake by

mitochondria are essential for the candidacidal activity of an N-terminal

peptide of human lactoferrin.

Lupetti A, Brouwer CP, Dogterom-Ballering HE, Senesi S, Campa M, Van Dissel JT,

Nibbering PH.

Department of Infectious Diseases, C5-P, Leiden University Medical Center

(LUMC), P.O. Box 9600, 2300 RC Leiden, The Netherlands.

OBJECTIVES:

Earlier studies showed that mitochondrial damage is a hallmark of

the candidacidal activity of an N-terminal peptide of human lactoferrin,

further referred to as hLF(1-11). Since uptake of Ca(2+) by mitochondria may be

essential for their activation, the aim of this study was to define the role of

Ca(2+) in killing of Candida albicans by the hLF(1-11) peptide.

METHODS:

The effect of compounds interfering with Ca(2+) homeostasis on the

hLF(1-11)-induced candidacidal activity, changes in mitochondrial membrane

potential, and

reactive oxygen species production were evaluated using a killing assay,

rhodamine 123

staining, and 2',7'-dichlorofluorescein diacetate, respectively. The increase in

cellular Ca(2+) content was measured using (45)Ca(2+).

RESULTS:

Our results revealed that Ruthenium Red, which inhibits the mitochondrial

Ca(2+)-uniporter

and the voltage-sensitive Ca(2+) release from internal stores, blocked (P<0.05)

the hLF(1-11)-induced candidacidal activity as well as changes in the membrane

potential of mitochondria, and reactive oxygen species production.

Oxalate, which precipitates Ca (2+) in intracellular organelles, decreased

(P<0.05) the

peptide-induced changes in the membrane potential of mitochondria, reactive

oxygen species production, and candidacidal activity.

Furthermore, the Ca(2+) ionophore ionomycin combined with high CaCl(2)

concentrations enhanced the

hLF(1-11)-induced candidacidal activity. (Nystatin is also a calcium ionophore.)

Moreover, hLF(1-11) caused an influx of Ca(2+) from the extracellular medium

into C. albicans reaching a three-fold

increase at 2 h, whereas no increase was found in unexposed cells. In agreement,

the Ca(2+)-chelator EGTA blocked the

peptide-induced candidacidal activity.

CONCLUSIONS: Ca(2+) release from intracellular stores, probably through

subsequent mitochondrial Ca(2+)

uptake, is essential for the hLF(1-11)-induced candidacidal activity.

PMID: 15282237 [PubMed - indexed for MEDLINE]

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