In U-937 promonocytes, misteltoe lectin I increases basal (Ca2+)i,enhances histamine H1- and complement C5a-receptor-mediated rises in(Ca2+)i, and induces cell death.

Journal/Book: Naunyn-Schmiedebergs-Arch-Pharmacol 1997 Feb, VOL: 355 (2), P: 190-7,ISSN: 0028-1298.. 1997;

Abstract: Mistletoe lectin I (ML I) from *Viscum* album inhibits cell growth andinduces apoptosis (programmed cell death) in several cell types. Becauseincreases in cytosolic Ca2+ concentration ((Ca2+)i) constitute a signalfor the induction of apoptosis, we studied the effects of ML I on basal(Ca2+)i, receptor-mediated rises in (Ca2+)i and cell viability, usinghuman U-937 promonocytes as model system. Treatment of U-937 cells withML I (30-100 ng/ml) significantly increased basal (Ca2+)i. ML I (10-30ng/ml) enhanced histamine-induced rises in (Ca2+)i up to five-fold. Theeffect of histamine was inhibited by clemastine but not by famotidine,indicative for its mediation via H1-receptors. ML I additionallyenhanced the stimulatory effect of complement C5a on (Ca2+)i, whereasthe effect of ATP was unaffected. ML I did not induce responsiveness ofU-937 cells towards a bacteria-derived chemotactic peptide. ML I up to10 ng/ml did not affect cell viability and growth of U-937 cells. ML Iat 30 ng/ml moderately inhibited cell growth and reduced cell viability.At 100 ng/ml, ML I was strongly cytotoxic. Our data support the viewthat Ca2+ plays a role as intracellular signal molecule in the inductionof apoptosis and point to an accelerating role of H1- and C5a-receptorsin the regulation of this process. Author.

Keyword(s): ANTIGENS-CD/ PH (physiology)

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