Toxicologic and marrow transplantation studies in rhesus monkeys given dimethyl myleran.

The hematologic and pathologic effects of single doses of dimethyl myleran (DMM) were evaluated in rhesus monkeys with and without the infusion of marrow. DMM 3 to 5 mg/kg produced severe but reversible myelotoxicity and no non-marrow toxicity. All animals given DMM 10 mg/kg died of marrow failure which was consistently reversed by the infusion of cryopreserved autologous marrow. At higher doses of DMM the protective effect of autologous marrow was less consistent due to increased gastrointestinal toxicity. Allogeneic engraftment was not achieved following administration of 10 mg/kg of DMM. In two animals receiving 15 mg/kg, proliferating allogeneic donor cells were present in recipient marrow seven days after marrow infusion.

Melioidosis in imported non-human primates.

In 1969, five cases of melioidosis in three separate outbreaks were diagnosed in nonhuman primates in the United States. In the first outbreak, two stump-tailed macaque monkeys (Macaca arctoides) developed signs of the disease approximately 6 months after purchase. A third animal, a chimpanzee (Pan troglodytes), probably acquired its infection from one of these monkeys. Two other unrelated cases involving a pig-tailed monkey (Macaca nemestrina) and a rhesus monkey (Macaca mulatta) were diagnosed. These monkeys had been imported 3 years and 6 months, respectively, prior to the recognized onset of their disease. These cases represent the first known occurrences of spontaneous melioidosis in nonhuman primates in the United States.

Potentiation of atherosclerotic lesions in rabbits by a high dietary level of vitamin E.

1. Two experiments were conducted to determine whether or not high dietary levels of vitamin E affect the development of atherosclerotic lesions in aortas of cholesterol-fed (5 g/kg diet) rabbits that were mechanically deendothelialized by balloon catheterization. 2. In the first experiment, the aortas of rabbits fed 2000 mg vitamin E/kg diet (i.e. 50-fold their nutritional requirement) for 8 weeks showed no gross morphological differences, either within or outside experimentally damaged areas, from those of rabbits fed the nutritionally adequate control level (40 mg/kg) of the vitamin. 3. In the second experiment, rabbits fed 10,000 mg vitamin E/kg diet (i.e. 250-fold requirement) for 14-15 weeks showed significantly greater endothelial loss and plaque formation at aortic sites outside of the mechanically damaged area than did controls. Plasma cholesterol levels were very high (9000-14,000 mg/l) and were not affected by dietary vitamin E level until 10-12 weeks when they were reduced moderately (18%). 4. It is concluded that very high levels of vitamin E can potentiate spontaneous atherosclerotic lesions, and it is suggested that this effect may depend on high cholesterol status.