Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Schwartz, A.G. et al.

Suppression of 12-O-tetradecanoylphorbol-13-acetate-induced epidermal hyperplasia and inflammation by the dehydroepiandrosterone analog 16alpha-fluoro-5-androsten-17-one and its reversal by NADPH liposomes.

Dehydroepiandrosterone and related steroids produce cancer-preventive and other potentially important therapeutic effects in laboratory animals. These steroids are potent uncompetitive inhibitors of mammalian glucose-6-phosphate dehydrogenase, the first enzyme in the pentose phosphate pathway. Inhibition of this pathway could have profound effects on the supply of 5-carbon sugars required for nucleic acid synthesis as well as on the availability of nicotinamide adenine dinucleotide phosphate (NADPH) and the cellular redox state. NADPH is a source of reducing equivalents for the production of oxygen free radicals, which act as intermediate messengers stimulating mitogenesis and up-regulating the inflammatory response. Using a mixture of NADPH and cationic liposomes to facilitate uptake of the normally impenetrable dinucleotide, we found that intradermal injections of NADPH-liposomes reversed the anti-inflammatory and anti-hyperplastic effects of the dehydroepiandrosterone analog, 16alpha-fluoro-5-androsten-17-one, in mouse skin treated with 12-O-tetradecanoylphorbol-13-acetate, whereas similar treatment had no apparent effect on the anti-hyperplastic and anti-inflammatory effect of corticosterone.[1]

References

Suppression of 12-O-tetradecanoylphorbol-13-acetate-induced epidermal hyperplasia and inflammation by the dehydroepiandrosterone analog 16alpha-fluoro-5-androsten-17-one and its reversal by NADPH liposomes. Schwartz, A.G., Pashko, L.L. Cancer Lett. (2001) [Pubmed]

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