| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 1978232 | Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology | 2006 | 9 Pages |
Abstract
The metabolic effects of methotrexate in perfused livers are similar to those exerted by hormones acting through Ca2+-dependent mechanisms. The aim of the present study was to determine whether the effects of methotrexate are mediated by a direct action on cellular Ca2+ fluxes. Methotrexate did not affect the ATP-dependent 45Ca2+ uptake by mitochondria, microsomes and inside-out plasma membrane vesicles and Ca2+ efflux from plasma membrane vesicles. However, methotrexate was able to stimulate 45Ca2+ release from preloaded microsomes. The amount of Ca2+ released by methotrexate was similar to that induced by IP3. Methotrexate could be acting through the capacitative calcium entry mechanism.
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Authors
Clairce L.S. Pagadigorria, Fernanda Marcon, Ana M. Kelmer-Bracht, Adelar Bracht, Emy L. Ishii-Iwamoto,