Re: Cell death, radiation and oxidation 8 September 2004
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JamesJ Whitehead,
Treating myself in absence of access or co operation, member
4oA Josephine Avenue, London SW2 2LA

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Re: Re: Cell death, radiation and oxidation

Dear Eleni , The Perth Group, Nicholas, Editor and all

""The influence of alpha-lipoic acid (CAS 62-46-4) on the amount of intracellular glutathione (GSH) was investigated in vitro and in vivo. Using murine neuroblastoma as well as melanoma cell lines in vitro, a dose -dependent increase of GSH content was observed. Dependent on the source of tumor cells the increase was 30-70% compared to untreated controls. Normal lung tissue of mice also revealed about 50% increase in glutathione upon treatment with lipoic acid.

This corresponds with protection from irradiation damage in these in vitro studies.

Survival rate of irradiated murine neuroblastoma was increased at doses of 100 micrograms lipoic acid/d from 2% to about 10%. In agreement with the in vitro studies, in vivo experiments with whole body irradiation (5 and 8 Gy) in mice revealed that the number of surviving animals was doubled at a dose of 16 mg lipoic acid/kg.

Improvement of cell viability and irradiation protection by the physiological compound lipoic acid runs parallel with an increase of intracellular GSH/GSSG ratio.(208)

"This study demonstrates that (1) exogenously added GSH promotes the survival of IL-2-deprived activated T cells by influencing the GSH content of the cells; (2) intrinsic intracellular GSH levels are critical for activated T-cell survival; and (3) WI38-promoted survival of activated T cells leads to a concomitant rise in the intracellular GSH level of the cells, associated with factor(s) of greater than 30 kD. Taken together, these observations implicate GSH as a possible mediator in fibroblast- enhanced survival of activated T cells.

The apoptosis induced in activated T cells by the withdrawal of IL-2 in vitro is associated with a decrease in Bcl-2 expression12 (this study). As we have previously demonstrated, the continued presence of cytokines such as IL-2, IL-4, IL-7, and IL-15 (all of which signal via the -chain of the IL-2 receptor) promotes the survival of these cells via up regulation of Bcl-2 and subsequent cell proliferation.13 In contrast, fibroblast- promoted T-cell survival appears to be independent of Bcl-2, as Bcl-2 is not re-expressed in the rescued cells.12 This is also true for activated T cells rescued from apoptosis by the addition of exogenous GSH in vitro (this study)." (49).

Best Wishes

James J Whitehead

Long term survivor hiv/oxidative stress/aids member and Clinnical trials volunteer.

References :

49. Blood, Vol. 89 No. 7 (April 1), 1997: pp. 2453-2460. Upregulation of Intracellular Glutathione by Fibroblast-Derived Factor(s): Enhanced Survival of Activated T Cells in the Presence of Low Bcl-2. By Helena Hyde, Nicola J. Borthwick, George Janossy, Michael Salmon, and Arne N. Akbar >From the Department of Clinical Immunology, Royal Free Hospital School of Medicine, London; and the Department of Rheumatology, Birmingham University Medical School, Birmingham, UK. Taken from post headed SWEET TASTING MEDICINE THAT WORKS in the Alternative Therapies section on start Go Here for full artical with Graphs /89/7/2453


Influence of alpha-lipoic acid on intracellular glutathione in vitro and in vivo.

Busse E, Zimmer G, Schopohl B, Kornhuber B.

Abteilung fur Hamatologie und Onkologie, Johann Wolfgang Goethe- Universitat, Frankfurt/Main Fed. Rep. of Germany.

Competing interests: Lont term survivor hiv/oxidative stress / aids. researcher Continuum Magazine, member and