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

  title={Effects of thiol compounds on methotrexate uptake by murine lymphocytes from thymus and thymic lymphosarcoma.},
  author={D Sołtysiak-Pawłuczuk and A Naciaźek-Wieniawska and Andrzej Danysz and Alina Czarnomska},
  journal={Cancer letters},
  volume={65 3},

Human galectin-1, -2, and -4 induce surface exposure of phosphatidylserine in activated human neutrophils but not in activated T cells.

Novel immunoregulatory contribution of galectins in regulating leukocyte turnover independently of apoptosis is suggested, indicating that galectin's effects are cell specific.

Cellular aspects of folate and antifolate membrane transport.

The physiological role of reduced folate carriers and folate receptors in normal and neoplastic cells is described regarding changes in transport activity and connection of transport systems with resistance to antifolates and cancer development.



Transport and metabolism of methotrexate in normal and resistant cultured rat hepatoma cells.

The results suggest that the cells become resistant as a result of a stable change in the transport system for MTX, but the mechanism of this process is not yet understood.

Kinetic correlates of methotrexate transport and therapeutic responsiveness in murine tumors.

Steady-state levels of drug accumulation in vitro reflected influx and efflux rates and were consistently correlatable with therapeutic responsiveness, and there was no significant difference in the extent to which folate and reduced 5-substituted folate derivatives compete with methotrexate for uptake in cells from all five tumors.

In vitro transformation induces abnormal protein thiol levels in rat liver cells.

Transformed cells exhibited an increased variability in cellular protein thiols which was most evident in G1 and S phase which implies early changes in redox state and/or modification of the amounts or types of sulphur-containing proteins in transformed cells.

Role of the glutathione redox cycle in acquired and de novo multidrug resistance.

These studies support a model of acquired and de novo multidrug resistance that includes alterations in both drug accumulation and the glutathione redox cycle.