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PubMedDate not supplied

Mistletoe (viscum album) lectins as cytokine inducers and immunoadjuvant in tumor therapy. A review.

Therapy of cancer with a Viscum extract has been carried out in Europe for over six decades in thousands of patients with uncertain advantages. This approach has been bedeviled by major problems such as variable composition of the extract, lack of knowledge of active component(s) and mechanism of action, to cite a few. However the recent standardization of Viscumin in terms of galactoside-binding lectin activity has allowed to clarify that it can act as powerful inflammatory mediator able to stimulate the immune system. Merits and demerits of this approach have been reviewed and although the active component has probably not unique immunoenhancing properties, it may be useful as an adjuvant in the biological therapy of cancer and it should not be ignored any longer. As usual, medical progress depends upon experimentation and not exclusively on intuition and emotion.

Adjuvants, Immunologic↗
PubMed1978

[Allergy and lectins: action between IgE-mediated histamine release and glycoproteins from Viscum album L. (mistletoe)].

Low-molecular constituents from Viscum album (toxic) release, in irritatively toxic manner, histamine from human leukocytes without destroying the cells (cytotox test). This histamine release is prevented by preincubation with viscum lectins. The viscum lectin blocks the Fc-portion of allergen-specific IgE against anti-IgE [125I]. Lectin also inhibits the allergen-specific histamine release from human leukocytes occurring through IgE; this can be demonstrated on leukocytes from patients with atopic extrinsic asthma. The inhibitory effect of lectin could also be due to a primary membrane effect, in addition to blockage of IgE.

Glycoproteins↗
PubMed1996

Immunotoxins containing A-chain of mistletoe lectin I are more active than immunotoxins with ricin A-chain.

Conjugates of anti-CD25 monoclonal antibodies against cell surface IL-2 receptor with MLIA and RTA were prepared and investigated. Both of the immunotoxins had high specific cytotoxic activity on target cells. The IC50 value of the anti-CD25/MLIA immunotoxin was 15-fold greater than that of the anti-CD25/RTA. Previous studies of the anti-CD5 immunotoxins with MLIA and RTA showed that the anti-CD5/MLIA IT was 80-fold more active than anti-CD5/RTA IT [Tonevitsky et al. (1991) Int. J. Immunopharmacol. 13, 1037-1041]. The surface hydrophobicity of the MLI A-chain was 4-fold higher than that of the ricin A-chain as estimated by binding with ANS. In model experiments with small unilamellar DMPC liposomes, MLIA but not RTA increased the turbidity of liposome suspensions at pH 4.5. Our results indicate that the greater cytotoxic activity of the MLI A-chain immunotoxin probably provided a higher surface hydrophobicity of the protein and the ability to interact with phospholipid membranes.

Anilino Naphthalenesulfonates↗
PubMed1990

Effect of phoratoxin B, a toxin isolated from mistletoe, on frog skeletal muscle fibres.

The effect of phoratoxin B on transmembrane potentials and currents of frog skeletal muscle was studied using intracellular microelectrode recording and double sucrose gap voltage clamp techniques. Phoratoxin B irreversibly depolarized the membrane. The depolarization was insensitive to tetrodotoxin, tetraethylammonium, 4-amino-pyridine, cesium, cadmium and D-600. In voltage clamp experiments, phoratoxin B induced an inward resting current (Irest) which did not inactivate. Irest was blocked by increasing the external calcium concentration in the Ringer solution; it was not blocked when Sr2+ replaced Ca2+. Analysis of the peak sodium current indicated that while both Ca2+ and Sr2+ screen membrane surface charges, Ca2+ bound and reversed the phoratoxin B induced Irest whereas Sr2+ did not. The inward Irest induced by phoratoxin B developed in the presence of external chloride and remained unchanged in the presence of bicarbonate. The data suggest that the depolarizing action of the toxin might be attributed to an increase in the non-selective leak current and that it might act as a detergent.

Animals↗
PubMed1992

Immunological mechanism of action of the tumor reducing peptide from mistletoe extract (NSC 635089) cellular proliferation.

A peptide isolated from the Viscum album extract (Iscador) has been reported earlier to the both cytotoxic and tumour reducing. Spleen cells from animals treated with a very small quantity of this peptide were found to have increased response to phytohaemagglutinin and Concanavalin-A, indicating that more mature lymphocytes are produced by the peptide administration. Moreover injection of the peptide at the lesion site produced infiltration of lymphocytes and macrophages and finally producing necrosis of the tumor. This peptide also stimulated macrophages in vitro and in vivo and activated macrophages were found to have cytotoxic activity towards L-929 fibroblasts.

Animals↗
PubMed2001

Immunotherapy of C3H/HeJ mammary adenocarcinoma with interleukin-2, mistletoe lectin or their combination. effects on tumour growth, capillary leakage and nitric oxide (NO) production.

Clinical application of interleukin (IL)-2-based immunotherapy of cancer has been limited by a major side-effect known as 'capillary leak syndrome', resulting from nitric oxide (NO) overproduction. A galactoside-specific lectin from Viscum album L. (VAA) has been reported to induce certain lymphokines and upregulate IL-2 receptors on lymphocytes. Present study was, therefore, designed to compare the effects of combination therapy with IL-2 (10(4) Cetus units/mouse, intraperitoneal (i.p). every 8 h, given as 5 day rounds per week, for one or two rounds) and VAA (1 ng/kg subcutaneous (s.c.), biweekly) with those of IL-2 or VAA therapy alone in C3H/HeJ female mice bearing s.c. transplants of a highly metastatic C3L5 mammary adenocarcinoma. IL-2 therapy alone reduced tumour growth and metastasis, but caused significant water retention indicative of capillary leakage in the kidneys after both rounds of therapy, whereas pleural effusion was only evident after the first round and not the second round. A sharp rise in the systemic NO levels after the first round, followed by a decline after the second round of IL-2 therapy suggested a causal relationship of increased NO levels to pleural effusion. A strong immunostaining for nitrotyrosine (a marker for the production of peroxynitrite) was noted in the renal tubules at the end of both rounds of therapy suggestive of a causal association of this toxic NO-metabolite with capillary leakage in the kidneys. Addition of VAA to IL-2 therapy had no effect on any of the above parameters. Unexpectedly, however, VAA therapy alone stimulated tumour growth as well as lung metastases. NO induction in the C3L5 cells by VAA was excluded as a possible reason for this stimulation. Present results suggest the need for exercising caution in the use of VAA as an immunoadjuvant in human cancer therapy.

Adenocarcinoma↗