NO-ergic neurons of the cervical nucleus of the rat brain in normal conditions and after administration of opiates.

Histochemical reactions for NADPH-diaphorase (NADPH-d) were used to study the dynamics of NO synthesis activity in the cervical nuclei of the rat brain after i.v. administration of morphine hydrochloride.

[NO-ergic rat brain commissural neurons in the norm and during opiate administration].

Using histochemical reaction demonstrating NADPH-diaphorase (NADPH-d), the dynamics of NO synthesis was studied in the rat brain raphe nuclei following intravenous injection of morphine hydrochloride. In normal conditions NADPH-d activity was demonstrated in neurons of all raphe nuclei. Acute and chronic administration of morphine in different doses (0.

Dynamics of NADPH diaphorase activity in raphe neurons during chronic treatment with opiates.

Systemic administration of diacetylmorphine considerably reduced the number of NADPH diaphorase-positive (NO-synthesizing) neurons in rat brain raphe nuclei. This effect was blocked by naloxone. In animals with the withdrawal syndrome NO-ergic activity in raphe neurons increased and surpassed the normal.

[Bleomycetin antitumor activity in relation to solid mouse tumors].

The antitumor activity of bleomycetin or bleomycin A5 was studied with respect to sarcoma 180, Garding-Passey melanoma, cervical carcinoma CC-5 and lymphosarcoma L10-1. Bleomycetin showed a high selective effect on the solid form of sarcoma 180. Its activity against Garding-Passeys melanoma and cervical carcinoma CC-5 was lower.

[Antitumor activity of bleomycetin against ascitic tumors in mice].

When used intraperitoneally in doses of 18.0-0.006 mg/kg daily bleomycetin inhibited th growth of lymphadenosis NK/Li by 90-100 per cent.

[Antitumor activity of the components of a carminomycin complex].

The antiblastomic activity of the carminomycin complex components was studied with respect to 8 strains of transplantable tumors of mice: lymphosarcoma L10-1, prestomach cancer OZh-5, sarcoma 180, lymphoid leucosis L 1210, lung bronchogenic cancer RL, lymphodenosis NK/LI, Ehrlich carcinoma and Garding-Passy melanoma. It was shown that components I, II and III possessed almost the same high antiblastomic activity and the same optimal administration schemes should be used for them. The scheme consisted of two-fold administration of the drug at intervals of 96-120 hours.

[Preparation of dihydrocarminomycin and a comparison of its antitumor activity with the activity of carminomycin].

A dihydro derivative of karminomycin was prepared using chemical reduction with potassium boron hydride. When dihydrokarminomycin was administered intravenously to healthy albino mice in a single dose it practically showed the same toxicity as karminomycin. However, unlike the latter dihydrokarminomycin induced the death of the animals at later periods of time.

[Antitumor activity of carminomycin antibiotic used orally].

Antitumor activity of karminomycin used perorally was studied with respect to 3 strains of mouse transplantable tumors, i. e. one ascitic strain of lymphadenosis NK/LI and two solid strains of lymphosarcoma L10-1 and sarcoma 180.

[Cross resistance in tumor cells and staphylococci with respect to anthracycline-group antineoplastic antibiotics].

The variants of the tumor cells of Fisher lymphadenosis, strain L-5178 and Staph. aureus resistant to rubomycin simultaneously became partially less sensitive to adriamycin. Sensitivity to karminomycin in the rubomycin resistant strains did not practically change as compared to the sensitivity of the initial strains.