[Distribution studies of alpha-L-arabinofuranosidase already unstable at pH 7.0 (37 degrees C) in tumor-bearing mice in connection with its possible use to enhance the selectivity of the chemotherapy of malignant tumors].

Graffi et al. (1-3) had proposed the use of exogenous enzymes to toxify inactive transport forms of cancerostatic substances. For this purpose, the pH difference between normal tissues and the tumor was to be exploited, which can be essentially increased by the application of glucose and inorganic phosphate (5-7).

Temperature dependent pH-instability of some alpha-L-arabinofuranosidases.

In this paper are described alpha-L-arabinofuranosidases, partially purified from some moulds, with very high lability of their activity to weakly alkaline or neutral pH-values. This pH-lability strongly depends on temperature. The form of the inactivation curves suggests involvement of charge changes in this irreversible process.

[Experiments on the modification of the distribution of the activity of various alpha-L-arabinofuranosidases following i.v. application in tumor-bearing mice].

Graffi et al. have proposed the use of exogenous enzymes for selective cleavage of inactive transport forms of cancerostatic substances in tumor tissue. Enzymes appropriate for this purpose should, if possible, show also a certain enrichment in the tumor tissue.

[Pharmacokinetic studies of the activity of a pH-labile alpha-L-arabinofuranosidase following i.v. injection into tumor-bearing mice].

In order to increase the selectivity of tumor chemotherapy, Graffi et al. have proposed the application of xenogenic enzymes, which are able to split transport forms of carcinostatics under the pH-conditions in the tumor more vigorously than in the normal tissues. This paper describes the distribution within the body and elimination of the activity of the pH-labile alpha-L-arabinofuranosidase from G.

Increased incidence of lung metastases of sarcoma 276 bearing XVII/Berlin mice after total body irradiation and BCG.

Combined prophylactic treatment by total body irradiation and BCG produce an increase in lung metastasis incidence and pleural effusions in a syngeneic murine tumor model. The prophylactic effect of BCG on metastasis formation is abolished independently of the order of pretreatments. Several possible causative mechanisms underlying this phenomenon and the clinical implications are discussed.