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D Soltysiak-Pawluczuk

Publications and source records attributed to D Soltysiak-Pawluczuk.

5 recordsLinked to original sources
PubMed1992

Effects of thiol compounds on methotrexate uptake by murine lymphocytes from thymus and thymic lymphosarcoma.

The characteristics of methotrexate (MTX) uptake and the effects of exogenous sulfhydryl compounds (i.e. reduced glutathione and cysteine) on MTX accumulation in thymocytes and thymic lymphosarcoma cells has been studied. Significant differences in the rate and the extent of MTX uptake between normal and neoplastic cells were demonstrated. MTX accumulation was found to be more efficient in thymic lymphosarcoma cells as compared with parental cells. In the cells examined, MTX uptake was not affected by membrane impermeable GSH. In contrast, short-term exposure to cysteine revealed heterogeneity in MTX uptake systems between normal and neoplastic thymocytes. Thus, cysteine was demonstrated to enhance the rate and extent of MTX accumulation exclusively in thymic lymphosarcoma cells. The results obtained indicate that in neoplastic thymocytes biochemical changes had developed in the membrane redox state around the MTX uptake system. These alterations are chemically distinguishable by their characteristic response to cysteine. The findings suggest that the plasma membrane changes could be exploited for preferential enhancement of MTX uptake by neoplastic thymocytes.

Animals↗
PubMed1976

Effects of ionizing radiation and cysteamine (MEA) on activity of mouse spleen adenyl cyclase.

In mice X-irradiated with doses of 200 R and 400 R, there was a substantial increase in spleen adenyl cyclase activity; there was similar activation by MEA. In mice given MEA before irradiation, an additive effect of radiation and the radioprotective drug was observed. On the other hand, a dose of 800 R given either alone or after pre-treatment with MEA failed to elicit any change in cyclase activity. The results indicate the importance of the adenyl cyclase system in the response of cells to irradiation and action of MEA.

Adenylyl Cyclases↗
PubMedDate not supplied

Antiangiogenic effect of sulindac sulfide could be secondary to induction of apoptosis and cell cycle arrest.

BACKGROUND: The development of colon cancer is probably angiogenesis-dependent. Recently, sulindac sulfide was shown to possess anti-angiogenic activity. In the present work, the question of whether this activity reflects a specific interaction with angiogenesis or is secondary to the effect of sulindac sulfide on the survival of endothelial cells was addressed. MATERIALS AND METHODS: Endothelial and normal mouse fibroblast cell lines were incubated with non-steroidal anti-inflammatory drugs (NSAIDs), arachidonic acid (AA) and prostaglandin E2 (PGE2). Cell viability (survival), PGE2 synthesis, cell cycle and apoptosis were measured. Western blotting and semi-quantitative RT-PCR multiplex methods verified the changes in the levels of pro-apoptotic proteins and their expressions, respectively. RESULTS: Sulindac sulfide and celecoxib inhibited the survival of endothelial cells, whereas other NSAIDs were ineffective. In contrast to celecoxib, sulindac sulfide did not affect the survival of normal fibroblast cells. Both agents inhibited the production of PGE2 from AA and arrested the cell cycle in the S-phase. Moreover, sulindac sulfide activated caspases 3 and 8, decreased the levels of Bax and Bid proteins, caused cleavage of PARP and increased the expressions of the bax and caspase 3 genes. CONCLUSION: The results suggest that the anti-angiogenic activity of sulindac sulfide is secondary to the inhibition of endothelial cell survival resulting from cell cycle arrest and apoptosis.

Angiogenesis Inhibitors↗