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PubMed1990

Intraperitoneally injected cultured mast cells suppress recruitment and differentiation of bone marrow-derived mast cell precursors in the peritoneal cavity of W/Wv mice.

Bone marrow-derived mast cell precursors form large mast cell colonies in methylcellulose and are designated as L-CFU-Mast. The effect of differentiated mast cells on recruitment and differentiation of L-CFU-Mast was investigated by using genetically mast cell-deficient WBB6F1-W/Wv mice. Giant granules of C57BL/6-bgJ/bgJ (Chediak-Higashi syndrome) mice were used as a marker to identify the origin of L-CFU-Mast and differentiated mast cells. Practically no L-CFU-Mast are present in the peritoneal cavity of WBB6F1-W/Wv mice. When bone marrow cells of WBB6F1(-)+/+ mice were i.v. injected, the concentration of +/+(-)type L-CFU-Mast increased in the peritoneal cavity of WBB6F1-W/Wv mice and became several times greater than that of nontreated WBB6F1(-)+/+ mice. This increase of L-CFU-Mast was suppressed by a prior i.p. injection of bgJ/bgJ-type cultured mast cells. The differentiation of the +/+(-)type L-CFU-Mast to morphologically identifiable mast cells was also suppressed by the i.p. injection of bgJ/bgJ-type cultured mast cells. The present results suggest that the suppression of recruitment and differentiation of L-CFU-Mast is a physiological function of differentiated mast cells.

Animals↗
PubMed1986

[Induction of activated macrophages by intraperitoneal injection of mitomycin C in mice and rats].

The local cellular response induced by i.p. injection of mitomycin C (MMC) was studied in C3H/HeN mice and ACI/N rats. MMC-induced peritoneal macrophages showed the maximum in vitro tumoricidal activity against 125I-UdR-labeled syngeneic tumor target cells 4 to 7 days after the i.p. injection of MMC at a single dose of 3 mg/kg and 1 mg/kg in mice and rats, respectively. The tumoricidal activity was dependent on the dose of mitomycin C injected and it was alos detectable against allogeneic and xenogeneic tumor target cells. In addition, these tumoricidal macrophages were found to have augmented functions of 2-deoxy-D-glucose incorporation and phagocytosis. Additional experiments excluded the possibility that the tumor cell cytolysis was the result of direct cytotoxicity of MMC that might have been incorporated into the peritoneal macrophages or of nutrient depletion in the medium during the cytolysis assay. Although the mechanism by which MMC injected i.p. induced the tumoricidal macrophages locally remained undetermined, in vitro production of macrophage-activating factor (MAF) from splenocytes cultured with concanavalin A was enhanced remarkably, following exposure of the spleen to MMC in vivo or in vitro, indicating the involvement of lymphokine in the induction of tumoricidal macrophages by MMC. Among other anticancer drugs, which were used at a dose of three-fifths of LD50, only adriamycin (7.5 mg/kg) was capable of inducing tumoricidal macrophages. A better understanding of the effect of anticancer drugs on macrophage tumoricidal activity may be useful in designing more effective local chemotherapy for cancerous peritoneal effusions.

Animals↗
PubMed1979

Carcinogenesis in rat esophagus by intraperitoneal injection of different doses of methyl-n-amylnitrosamine.

The carcinogenicity of methyl-n-amylnitrosamine in MRC-Wistar rats was determined after i.p. injection at a variety of dose schedules. After 6 weekly methyl-n-amylnitrosamine injections of 25 mg/kg or 12 weekly injections of either 12.5 or 25 mg/kg, the incidence of esophageal squamous cell papillomas was 85 to 100% and that of esophageal squamous cell carcinomas was 40 to 65%. With 12 injections, the mean survival time was 25 to 31 weeks. Treatment with 1 or 2 doses of 50 mg/kg produced a lesser incidence (less than 20%) of esophageal tumors, with a longer survival time of 67 to 77 weeks. One 85-mg/kg injection caused esophageal carcinomas in 5 of 7 rats. The treated groups also had squamous cell papillomas and carcinomas in the nasal cavity (up to 50% incidence) and trachea (up to 30% incidence). Hence, a 6- or 12-week treatment schedule was adequate for inducing esophageal tumors and could be used for studies on agents modifying esophageal tumor induction by methyl-n-amylnitrosamine.

Animals↗