Carcinostatic effect

Previous interest in the antitumor activity of fig (Ficus carica L.) fruit led to the isolation of benzaldehyde as a major active component (22). Its carcinostatic effect was attributed to selective inhibition of the uptake of nucleosides and carbohydrates, and the reduction of intracellular adenosine 5 -triphosphate level (23) However, benzaldehyde is an oilly liquid and only sparingly water soluble. Its instability in air and light presented considerable problems in the delivery and formulatioa Takeuchi et al (24) first prepared the complex with a-, p- and y-cyclodextrin. More importantly, the x-ray structure of a-cyclodextrin-ben dehyde 1 1 complex was subsequently determined (22). providing a woiking basis for uncovering its structure in solution. 

A carcinostatic effect, slowing the spread of metastases, is suggested by Russian research (duke 2). A comprehensive review of Russian studies is available. ... 

Gurtoo HL, Marinello AJ, Berrigan MJ, et al. 1983. Effect of thiols on toxicity and carcinostatic activity of cyclophosphamide. Semin Oncol 10(1 Suppl. 1) 35-45. 

The carcinostatic action of 8-azaguanine against the Ehrlich ascites tumor in mice was potentiated by 4-aminoimidazole-5-carboxamide, which exerted a synergistic effect by preventing deamination. The toxicity exerted by 8-azaadenosine in mice was traced to its 5 -triphosphate, which replaced adenosine triphosphate in the host s hepatocytes. Phosphatidylcholine liposomes were studied as a suitable vehicle for conveying 8-azaguanine to leukemic cells. ... 

Antimctabolite a compound so similar in structure to a metabolite that it occupies the same specific enzyme binding sites. This results either in inhibition of the enzyme or substitution of the A. for the metabolite in the reaction, possibly leading to incorporation of the A. into cell components. Both effects lead to metabolic disturbances or inhibition of cell division. Many A. are used therapeutically, e.g. analogs of purines and pyrimidines and folic acid antagonists are used as carcinostatic agents. 

Humoral immunity results from the interactions of antigen, macrophages, helper T-cells and B-cells the latter which produces the immunoglobulins antibodies. Cellular Immunity is a function of a number of cell types identified as macrophages, killer cells, and T-cells (l3miphocytes) of which there are functional subpopulations of lymphocytes. The evidence suggesting an effect on cellular Immunity by Se is supported by dinitrochlorobenzene (DNCB) hypersensitivity experiments, allograft rejection times, impaired microbicidal activity, insensitivity of lymphocytes to Se deprivation and carcinostatic activity. 

There are striking coincidences in effective Se levels between experiments of immunoenhancement and carcinostatic suppression when injected or ingested Se levels are compared. Data presented by Schrauzer (1976) for the reduction of mammary tumors in mice showing a dose-related effect of dietary Se can be superimposed with the dose-related enhancement of PFC and anti-SRBC antibodies in mice. Levels of dietary supplemented Se in animal experiments that were effective in immunoenhancement (Spallholz et al., 1973a) and tumor reduction (Schrauzer, 1976) were 1.25 and 2.0 ppm Se respectively. 

One way that selenium appears to act is as a non-specific stimulant of immune competent tissues and cells contributing to its anti-inflammatory, immunopotentiation and carcinostatic attributes. Additional data suggests other effects of Se upon cells of the immune system perhaps independent of GSHPx activity such as ubiquinone biosynthesis, (Coenz3one Q 10) which in turn affects host-defense mechanisms (Frost, 1975). A third possibility to explain the effects attributed to Se above is to propose that increases in levels of the selenium dependent enzyme glutathione peroxidase and perhaps other specific selenium-dependent functions in lymphocytes and macrophages is the reason for immunoenhancement. This subject has been addressed by Schauzer (1979) and is amplified here by the author. 

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