Single IP injection of high dose (LD 10) of methyl-CCNU administered to sexually mature male mice resulted in severe inhibition of spermatogenesis and reduction in testicular wet weight, without significant changes in plasma testosterone levels, and with hyperplasia of the interstitum, including Leydig cells, in the testis. These effects were temporary, spermatogenesis and testiculer weight recovered 50 days after treatment. Mating of the treated males with normal females demonstrated absolute sterility at 20 days and full recovery at 50 days after treatment. Administration of a single lethal dose (38 mg/kg, LD70) of methyl-CCNU to immature (25 day-old) male mice also caused severe but temporary inhibition of spermatogenesis, and mating of mice which survived the treatment and reached sexual maturity, with normal females, resulted in 80 to 100% pregnancies at 40 and 70 days after treatment, respectively. Three repeated injections of 30 mg/kg (at 10 day intervals) of methyl-CCNU to 15 day-old male mice resulted in inhibition of spermatogenesis without alteration in plasma testosterone. Ninety days after this treatment, only 40% of matings with normal females resulted in pregnancies. Female mice treated once with 20 mg/kg of methyl-CCNU, 3 days before or 7 days after mating with normal males, showed complete failure to complete pregnancy-resorption of the embryos was demonstrated in those female mice treated 7 days after mating. After a second mating trial with these two treated groups, performed 40 to 55 and 42 days after the first trial, respectively, 80 and 86% of the females delivered offspring. However, average litter size was reduced to 4 in the second group, as compared to 8 in untreated mice. There were no apparent birth defects in the offspring of methyl-CCNU treated male or female mice.

Animals↗

PubMedDate not supplied

Red cell osmotic fragility in experimental murine leukemia.

Explore the source record for details and available documents.

Animals↗

PubMedDate not supplied

Effect of lymphoproliferative disease virus and of niridazole on the in vitro blastogenic response of peripheral blood lymphocytes of turkeys.

Turkeys inoculated at 5 weeks of age with lymphoproliferative disease (LPD) virus developed typical lesions in the spleen, thymus, and pancreas. The in vitro blastogenic response of peripheral blood lymphocytes to the mitogens phytohemagglutinin and concanavalin A was drastically (up to 90%) suppressed in the inoculated turkeys 1 to 4 weeks postinoculation compared with uninoculated controls, and even at 11 weeks the response was about 50% inhibited. A lethal (about LD33) dose of antihelminthic drug niridazole, 100 mg/kg given each day for 3 days to 4-week-old turkeys, caused a transient inhibition of the blastogenic response within 32 days of treatment, which was less pronounced than that observed in turkeys inoculated with LPD virus, whether pretreated with niridazole or not. Virus-associated reverse transcriptase activity in the plasma was significantly higher in the turkeys pretreated with niridazole, and LPD lesions developed to the same extent in the untreated and treated groups, as determined 9 weeks post virus inoculation. A sublethal dose of niridazole, 50 mg/kg given each day for 4 days, did not suppress the blastogenic response to mitogens at any time determined (starting 10 days post-treatment) and did not affect the pathogenesis of LPD and the viremia. Body weights were significantly decreased by virus infection and by treatment with lethal doses of niridazole.

Animals↗