The antitumour activity of Ganoderma lucidurn, called 'Ling-Zhi or holy mushroom' in Chinese traditional medicine, was investigated on intraperitoneally implanted Lewis lung carcinoma in syngeneic C57BL/6 mice. An aqueous extract of Ling-Zhi significantly increased the life span of tumour-implanted mice, when administered intraperitoneally alone or in combination with cytotoxic antitumour drugs (Adriamycin, fluorouracil, thioguanine, methotrexate, Cisplatin) or a synthetic immunomodulator (Imexon). The aqueous extract was not cytotoxic in cell cultures and the antitumour activity was abolished by pretreatment of mice with cyclosporine. The active principle(s) was found to be present predominantly in the ethanol precipitable fraction of the aqueous extract.
showed that a complex reagent containing molybdate, tungstate and phosphoric acid would react with proteins to yield a blue colour approximately proportional to the tyrosine and tryptophan content. Pressman (1943) defined some of the variables influencing colour yield. Herriott (1941) discovered that pretreatment with cupric ion greatly intensified the blue colour given by proteins and peptides, but had no effect upon the colour .yield from tyrosine. Lowry, Rosebrough, Farr & Randall (1951) further refined and systematized these observations into a practical method of protein assay which, because of its
A defined pollen extract of selected plants has been reported to possess some pharmacological activities on chronic prostatis or benign prostatic hyperplasia. This paper describes the antitumour potential of the watersoluble fraction (Cernitin T60) of pollen extract against Lewis lung carcinoma implanted intraperitoneally in syngeneic mice. Cernitin T60 was not cytotoxic in cell cultures at concentrations up to 2.5 mglmL, while it is significantly prolonged the life-span of mice carrying the tumour without any apparent side effects at 0.5 glkg. In addition, Cernitin T60 demonstrated beneficial therapeutic effects in an additive fashion on the life-span of mice when it was combined with standard cytotoxic antitumour drugs such as adriamycin, cisplatin, vincristine, methotrexate, fluorouracil, or thioguanine. The antitumour potential of Cernitin T60 was completely abolished by treatment with inhibitors of macrophage functions (2-chloroadenosine or carrageenan), but not with a T-cell inhibitor (cyclosporin A). Cernitin T60 appears to be a potent immunostimulator of macrophages.
The selective toxicity of antifolates for a variety of cancers can be improved, as illustrated by the combined administration of N0-methyltetrahydrofolate and methotrexate in tissue culture. When a variety of neoplastic cell types characterized by a deficiency of vitamin flisdependent N5-methyltetrahydrofolate methyltransferase (5- (18,19). It is clear that very specific "C1"-carrying tetrahydrofolates are uniquely required for the synthesis of thymidylic acid and the de novo synthesis of purines. The need for continued purine and thymidylic acid synthesis is directly related to the need for nucleic acid precursors (20) and is particularly apparent in dividing cells, since DNA replication is absolutely correlated with the rate of cell division (9,(21)(22)(23).The depletion of H4F absolutely prevents the biosynthesis of thymidylic acid and purines. Not only is DNA synthesis halted, but RNA synthesis, although somewhat protected by purine salvage mechanisms, is also seriously impaired. MTX, by its potent inhibition of dihydrofolic acid reductase, produces lethal H4F depletion in all mammalian cells. The cause of death in mammals is the profound effect on the most rapidly proliferating normal cells of the gut and hematopoietic system (24).The administration of N5-formyltetrahydrofolate (citrovorum factor, folinic acid, N5-CHO H4F, N5fH4F) circumvents the major MTX block by its conversion into the necessary "Cl"-carrying tetrahydrofolates through the following metabolic reactions:
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