| Autor: |
Klein, Ami, Bruser, Barbara, Malkin, Aaron |
| Zdroj: |
Tumor Biology (Springer Science & Business Media B.V.); 1988, Vol. 9 Issue 5, p233-240, 8p |
| Abstrakt: |
We have shown prevoiusly that cortisol-sensitive lymphocytes (thymocytes) have a much lower capacity than cortisol-resistant cells to catabolize cortisol. We have also shown that sera of cancer patients (CPS) possess ethanol-extractable substance(s) which can inhibit the catabolism of cortisol by lymphocytes (CCL). Recently, we noted that unsaturated fatty acids can both inhibit CCL and modulate the sensitivity of lymphocytes to cortisol. In the present study, we attempt to identify the compounds responsible for CCL inhibition and to demonstrate that inhibition of CCL may make cortisol-resistant lymphocytes vulnerable to the steroid. The enzymes DNase, RNase, pronase and lipase were added to ethanol extracts of serum as a first step in our efforts to identify the nature of the inhibitors of CCL. Only lipase had an effect on the inhibition. In fact, lipase enhanced the inhibition of CCL. This finding correlates with our previous observations that unsaturated fatty acids are potent inhibitors of CCL. Examining the effect of ethanol extracts of CPS and normal serum on the vulnerability of lymphocytes to cortisol, we noted that ethanol extracts of normal serum had no significant killing effect, whereas an ethanol extract of CPS makes lymphocytes more sensitive to cortisol. Since the adsorbance of free fatty acids of CPS by defatted albumin reduced but did not eliminate the capacity of the serum to inhibit CCL, we assume that other compounds besides free fatty acids might also be involved in CCL inhibition and modulation of the sensitivity of lymphocytes to cortisol. Copyright © 1988 S. Karger AG, Basel [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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