Modulation of passive permeability by external ATP and cytoskeleton-attacking agents in cultured mammalian cells

Kitagawa, Toshikazu; Akamatsu, Yuzuru

doi:10.1016/0005-2736(83)90070-6

Cited by 11 publications

(8 citation statements)

References 34 publications

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“…This means that extracellular ATP may increase both cellular uptake and efflux at the same time. Interestingly, it was demonstrated that the ATP-induced permeability change was observed only when the intracellular ATP concen tration was reduced [23,41] . Recently, we have shown that the ATP-dependent transport proteins (ATP7A and ATP7B) are located close to the nucleus in sensitive and more peripherally in cisplatin-resistant A2780cis cells [40] .…”

Section: Discussionmentioning

confidence: 99%

“…A situation where more than half of the cell population failed to survive just by ATP treatment was not acceptable for the present set of experiments. Therefore unlike previous studies where ATP was used at concentrations in the millimolar range, we used concentrations which were lower than the estimated EC 50 values [21,[23][24][25][26] .…”

Section: Discussionmentioning

confidence: 99%

“…It was reported that ATP-induced permeability changes occur after a 1-to 24-hour treatment [23][24][25][26] . Therefore, we initially incubated the cells with various concentrations of ATP for 1 h/24 h, replaced the medium and then treated them with cisplatin.…”

Section: Discussionmentioning

confidence: 99%

“…Earlier studies indicated that extracellular ATP can increase the cellular accumulation of cytotoxic substances and can thereby increase the sensitivity of tumor cells towards those substances [23][24][25][26][27] . This study has been carried out to examine the potential to use ATP in addition to cisplatin to boost cisplatin activity in ovarian carcinoma cells.…”

Section: Discussionmentioning

confidence: 99%

“…Among the various other modes of action discussed, increasing the permeation of chemotherapeutic agents was cited as the main reason for sensitization of tumor cells by ATP [23][24][25][26][27] . The underlying mechanism is believed to be due to the interaction of ATP with the purinergic receptors on the cell surface, which opens the ion channels resulting in the rapid influx of Na + and Ca 2+ and efflux of K + and finally leading to membrane depolarization.…”

Section: Introductionmentioning

confidence: 99%

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Effect of Extracellular ATP on Cisplatin-Induced Cytotoxicity in Human Ovarian Carcinoma Cells

Rotte

Garmann²,

Buβ³

et al. 2010

Chemotherapy

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Background: Cisplatin resistance has been mainly associated with decreased cellular accumulation and increased intracellular glutathione (GSH) levels. ATP is known to increase the membrane permeability of cells and to decrease intracellular GSH levels. Our study aimed at using extracellular ATP to sensitize ovarian carcinoma cells towards cisplatin. Methods: The MTT assay was used to determine the EC₅₀ of cisplatin in the human ovarian carcinoma cell line A2780 and its cisplatin-resistant variant A2780cis. Intracellular platinum concentrations were determined using flameless atomic absorption spectrometry. Results: Preincubation and concomitant incubation with ATP did not alter the EC₅₀ of cisplatin. The presence of 100 µM ATP along with cisplatin decreased cell survival in A2780 but not in A2780cis cells. Extracellular ATP did not increase the cellular accumulation of cisplatin in both A2780 and A2780cis cells. Conclusion: The presence of extracellular ATP during treatment with cisplatin leads to additive cytotoxicity in the sensitive A2780 but not in cisplatin-resistant A2780cis cells.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Effect of Extracellular ATP on Cisplatin-Induced Cytotoxicity in Human Ovarian Carcinoma Cells

Rotte

Garmann²,

Buβ³

et al. 2010

Chemotherapy

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Growth inhibition of lung cancer cells by adenosine 5′‐triphosphate

Agteresch

Rooijen

Berg

et al. 2003

Drug Development Research

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Preliminary clinical data suggest that adenosine 5'-triphosphate (ATP) may inhibit lung tumor growth. Because studies of ATP on lung cancer cells are lacking, the aim of the present study was to explore effects of extracellular ATP on the growth and morphology of human lung tumor cells. Five human lung tumor cell lines derived from tumors with different cellular characteristics, i.e., a small cell carcinoma (GLC4), a large cell carcinoma (H460), a squamous cell carcinoma (H520), a mesothelioma (MERO82), and a papillary adenocarcinoma (H441), were exposed to 0, 0.5, 1, 2, and 3 mM ATP. Total cell numbers and dead or damaged cells were measured on days 1, 2, and 3. ATP induced a significant, dose-dependent growth inhibition in GLC4, H460, H520, and MERO82 cells. In contrast, H441 cells showed already maximal inhibition at 0.5 mM. Compared to untreated control cell lines, a significant growth inhibition (mean 7 SEM) of 65 7 5% (GLC4), 59 7 5% (H460), 45 7 5% (H520), 3872% (MERO82), and 55 7 8% (H441) was shown after 3 days incubation with 3 mM ATP. ATP also induced changes in morphology and attachment to the substratum. Although not demonstrated by the Trypan Blue exclusion test, on photographs it seems that ATP induces death of GLC4 and H460 cells at higher concentrations. In conclusion, in four out of five explored lung tumor cell lines, ATP induces a dose-dependent growth inhibition. Lung adenocarcinoma cells show already maximal inhibition at the lowest tested ATP dose. There is a relationship between growth inhibition and morphology changes. Drug Dev.

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Reciprocal effects of phenothiazines and naphthalene sulfonamides on the external ATP-dependent permeability change in Chinese hamster ovary cells

Kitagawa

Akamatsu

1985

Biochimica et Biophysica Acta (BBA) - Biomembranes

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Modulation of passive permeability by external ATP and cytoskeleton-attacking agents in cultured mammalian cells

Cited by 11 publications

References 34 publications

Effect of Extracellular ATP on Cisplatin-Induced Cytotoxicity in Human Ovarian Carcinoma Cells

Effect of Extracellular ATP on Cisplatin-Induced Cytotoxicity in Human Ovarian Carcinoma Cells

Growth inhibition of lung cancer cells by adenosine 5′‐triphosphate

Reciprocal effects of phenothiazines and naphthalene sulfonamides on the external ATP-dependent permeability change in Chinese hamster ovary cells

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