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© 1996 Oxford University Press

research-article

Effects of chemopreventive selenium compounds on Jun N-kinase activities

Victor Adler, Matthew R. Pincus 1, Scott Posner, Pramod Upadhyaya 2, Karam El-Bayoumy 2 and Ze'ev Ronai 3

Molecular Carcinogenesis Program, American Health Foundation Valhalla, NY 10595
1Department of Pathology and Laboratory Medicine, Veterans Affairs Medical Center 800 Poly Place, Brooklyn, NY 11209 Dept. Pathology, SUNY Health Science Ctr Brooklyn, NY
2Division of Cancer Etiology and Prevention, American Health Foundation Valhalla, NY 10595, USA

3To whom correspondence should be addressed

Activation of Jun-N-kinases (JNK) is stimulated by diverse agents including UV-irradiation, heat shock, tumor necrosis factor and osmotic shock. In the present study we have elucidated the effect of the organoselenium chemopreven-tive agent l, 4-phenylenebis(methylene)selenocyanate (p-XSC), on UV-mediated JNK activation. Using mouse fibroblasts as a model cell system we found that low concentrations (1–10 µM range) of p-XSC did not affect JNK activity, yet were capable of potentiating JNK activity when administered prior to UV-irradiation. While higher doses of p-XSC have minimal effect on JNK activation, when combined with UV, there is a dose-dependent decrease in JNK activation. Similar to its effects on JNK, p-XSC is a potent inducer of src-related tyrosine kinases.p-XSC mediated changes in JNK activation correlate with its ability to potentiate the association of JNK with p21ras, in a manner similar to that we have previously observed with GTP or sodium vanadate. That p-XSC can modulate JNK activities points to a possible mechanism by which it contributes to the cell's ability to cope with stress.


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