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Pretreatment with nafenopin and pregnenolone-16-alpha-carbonitrile (PCN) decreased the acute lethal toxicity in mice induced by cerium chloride (12 mg/kg resp. 15 mg/kg). Treatment with nafenopin and PCN increased the relative liver weight. More cerium accumulated in the liver of nafenopin- and PCN-treated animals than in controls during the first hours after injection. After 14 days the amount of cerium in the livers of nafenopin-treated animals was significantly higher. The concentration of cerium as a percentage of the injected dose calculated per mg liver was lower during the first day in the nafenopin group and higher in the PCN group than in the control group. After 6 days cerium concentration decreased significantly less in the livers of the nafenopin group. Cerium concentration in the blood was significantly lower in the nafenopin group during the first day. Only small amounts of the injected cerium were excreted in the urine, and no difference between treated and untreated animals was found. The amount of cerium excreted in faeces was somewhat smaller in the nafenopin-treated animals during the whole experiment.

A number of drugs known to induce liver microsomal enzymes were studied with respect to their effect on the elevated liver triglyceride (TG) concentration and serum glutamic oxaloacetic acid transaminase (GOT) and glutamic pyruvic acid transaminase (GPT) activities induced by an i.v. injection of cerium in rats. Pretreatment with pregnenolone - 16 alpha - carbonitrile (PCN) and 2-methyl-2-[p-(1,2,3,4-tetrahydronaphth-1-yl)phenoxy]-propionic acid (nafenopin) decreased the liver TG concentration significantly. Spironolactone and phenobarbital pretreatment also decreased the TG level in comparison to controls, but the difference was not statistically significant. Both GOT- and GPT-activities in serum increased on the first day after cerium injection and reached a maximum after 3 days. All the drugs significantly reduced the elevated levels. After 7 days the activity was almost normal in all the surviving animals.

Acute intravenous toxicity and pharmacological properties of surface-active alkyltrimethylammonium bromides (C10-C20) were studied in female rats. The acute toxicity of the surfactants decreased with an increasing length of the alkyl chain length of 16 carbon atoms. Death appeared to be due to respiratory failure. The twitch responses of sciatic nerve-gastrocnemius muscle preparations were reversibly depressed at direct and indirect stimulation following intravenous injections of sublethal doses of C10-C14. Doses blocking the twitch responses of indirectly stimulated gastrocnemius corresponded to about half the LD50, and at these doses C10-C14 caused a transient decrease in respiratory rate. The C16 homologue caused respiratory arrest without affecting the twitch responses of gastrocnemius at relative low intravenous doses. Sublethal intravenous doses of C12-C20 caused, apparently due to vasodilatation, a transient fall in arterial blood pressure. The depressor response increased and the twitch response decreased with an increase in the length of the alkyl chain up to a chain length of 16 carbon atoms. Both the depression of skeletal muscle contraction and the vasodilatation is suggested to originate from a non-specific effect of the surfactants on muscle cells.

The sensitivity of male and female mice to Amanita virosa was compared. Dried, homogenized mushroom was given orally by stomach tubing at doses of 100, 200, 400 and 800 mg dried mushroom/kg body weight. Both in males and in females, the kidneys were the only organs showing macroscopical changes. The dose of 100 mg/kg caused renal damage in females, whereas in males the first signs of kidney damage were seen at the dose of 400 mg/kg. The renal lesions observed in the males were located in the cortex, while in the females they were limited to the outer stripe of the outer medullary zone. Testectomy diminished the nephrotoxicity of A. virosa in male mice and caused changes in the localization of renal lesions.