Experimente zur Anaerobiose der Krebszellen

Warbürg, Otto; Gawehn, Karlfried; Geissler, August-Wilhelm; Kayser, D.; Lorenz, Susanne

doi:10.1007/bf01485244

Cited by 17 publications

(8 citation statements)

References 4 publications

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“…In a later paper they corrected this to say that the inhibition was not present when the experiment was performed in the dark (40). Furthermore, when the riboflavin was added to the culture medium and irradiated with 452-nm light and cells were then added after irradiation, the inhibition still took place.…”

Section: Discussionmentioning

confidence: 99%

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Effect of Near-Ultraviolet and Visible Light on Mammalian Cells in Culture II. Formation of Toxic Photoproducts in Tissue Culture Medium by Blacklight

Stoien

Wang

1974

Proc. Natl. Acad. Sci. U.S.A.

133

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Near-ultraviolet radiation was found to be lethal for mammalian cells in Dulbecco's modified Eagle's medium without serum or phenol red. Irradiation of the cells with near-ultraviolet light while the cells were in phosphate-buffered-saline abolished the lethal effect. When only the medium was irradiated followed by the addition of unirradiated cells and serum, the cells were still killed. The photoactive components of the medium for this effect were riboflavin, tryptophan, and tyrosine. When riboflavin was deleted from the medium being irradiated and added later, almost no killing was detected. Irradiation of salt solution of riboflavin and tryptophan or riboflavin and tyrosine, resulted in cell killing. Little Irradiation of Cells. The light sources used in this study were two General Electric F15T8 BLB integral filter blacklight tubes with emission in the 300-to 420-nm range peaking at 365 nm (12). Light exposure was carried out in covered Falcon 3002 60-mm dishes placed approximately 20 cm below the light source. The lids of these dishes exclude light below 300 nm (6). Exposure intensity was 4 sW/mm2 at the cell surface, as measured by a Blak-ray meter J-221 (Ultraviolet Products, Inc.). Temperature was monitored and regulated to avoid any effect due to heating by the light source. The cells were trypsinized and plated in medium containing serum but no phenol red, 18 hr before exposure to blacklight. Twenty minutes before irradiation, the medium was removed and replaced with either 3.5 ml of phosphate-buffered saline containing NaCl, KC1, Na2HPO4, and KH2PO4; or MEM free of both phenol red and serum. The dishes were placed in the exposure chamber under 10% CO2 for 20 min before the light was turned on. At various intervals, dishes were removed from the light and kept in the dark in the same chamber. After the last dishes were removed from the light, serum was added to all dishes.Irradiation of Medium or Medium Components. Exposure conditions were similar to those of the last section except that no cells were present and only the aqueous solutions of medium components were exposed. The basic mixture (BaM) employed, to which other components were selectively added, contained NaCl, KC1, CaC12, MgSO4, NaH2PO4, Fe(NO3)3, glucose, inositol, cysteine, and glutamine. For the determination of the medium components responsible for photoproduct formation, other ingredients were added to BaM: (1) aminoacid solution (AA) containing arginine, isoleucine, leucine, lysine, methionine, threonine, valine, glycine, and serine; (2) vitamin solution (Vit) containing nicotinamide, thiamine, choline, D-pantothenic acid and pyridoxine; (3) one or more of the following compounds: histidine, phenylalanine, tryptophan, tyrosine, and riboflavin. After irradiation, the missing MEM ingredients and serum were added to the dishes fol-

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Section: Discussionmentioning

confidence: 99%

“…The possibility that these metabolites were of photochemical origin has not been investigated. Warburg has stated that patients on high B-vitamin diets should exercise caution by wearing sunglasses in direct sunlight (40). Zigman has indicated that such caution should be exercised by all (8).…”

Section: Discussionmentioning

confidence: 99%

Effect of Near-Ultraviolet and Visible Light on Mammalian Cells in Culture II. Formation of Toxic Photoproducts in Tissue Culture Medium by Blacklight

Stoien

Wang

1974

Proc. Natl. Acad. Sci. U.S.A.

133

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“…The mechanistic staging of carcinogenic cellular processes includes profound alterations of normative mitochondrial function ( 26 – 29 ), notably dependence on aerobic and anaerobic glycolysis, aberrant production and release of lactate, and metabolic downregulation of mitochondrial oxidative processes according to the classic theory promoted by Warburg et al ( 30 ). The primacy of cancer as a mitochondrial metabolic disease has been proposed ( 31 – 33 ), in marked contrast to widely espoused theories supporting the causative role of multiple somatic mutations in the etiology and persistence of numerous types of cancer.…”

Section: Mitochondrial Heteroplasmy and Cancermentioning

confidence: 99%

Mitochondrial DNA heteroplasmy in human health and disease

Stefano¹,

Kream²

2016

Biomedical Reports

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The biomedical literature has extensively documented the functional roles of genetic polymorphisms in concert with well-characterized somatic mutations in the etiology and progression of major metastatic diseases afflicting human populations. Mitochondrial heteroplasmy exists as a dynamically determined co-expression of inherited polymorphisms and somatic mutations in varying ratios within individual mitochondrial DNA genomes with repetitive patterns of tissue specificity. Mechanistically, carcinogenic cellular processes include profound alterations of normative mitochondrial function, notably dependence on aerobic and anaerobic glycolysis, and aberrant production and release of lactate, according to a classic theory. Within the translational context of human health and disease, the present review discusses the necessity of establishing critical foci designed to probe multiple biological roles of mitochondrial heteroplasmy in cancer biology.

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“…The fact that the effect of glyceraldehyde, usually DL, has been studied on a variety of systems, and as an inhibitor of tumour growth (e.g. Warburg, Gawehn, Geissler & Lorenz, 1963;Bennett & Cannon, 1966), makes it of value to have more knowledge of the metabolism of the compound itself. Landau & Merlevede (1963) examined the initial reactions involved in the metabolism of D-GA and L-glyceraldehyde by rat liver.…”

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confidence: 99%

The metabolism of d-glyceraldehyde by the lens

Heyningen

1969

Biochemical Journal

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1. The metabolism of d-glyceraldehyde by the lens was examined. 2. When low concentrations of d-[U−14C]glyceraldehyde were incubated with lens extracts there was no incorporation of the label into protein; more than two-thirds of the labelled metabolites consisted of glyceric acid and glycerol, their relative proportions depending on the species. Lactic acid, a phosphate, glutathione–glyceraldehyde compounds and a neutral compound were also formed. 3. When high concentrations of d-[U−14C]glyceraldehyde were incubated with lens, extensive incorporation of the label into protein occurred and the protein became yellow–brown. This coloured protein did not exhibit the fluorescent properties shown by the brown proteins of human cataractous senile lens, or of naphthaquinone-treated lens. 4. Evidence that d-glyceraldehyde is formed by the lens was sought but not found.

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Experimente zur Anaerobiose der Krebszellen

Cited by 17 publications

References 4 publications

Effect of Near-Ultraviolet and Visible Light on Mammalian Cells in Culture II. Formation of Toxic Photoproducts in Tissue Culture Medium by Blacklight

Effect of Near-Ultraviolet and Visible Light on Mammalian Cells in Culture II. Formation of Toxic Photoproducts in Tissue Culture Medium by Blacklight

Mitochondrial DNA heteroplasmy in human health and disease

The metabolism of d-glyceraldehyde by the lens

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