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The disposition of di-(2-ethylhexyl) phthalate (DEHP) and mono-(2-ethylhexyl) phthalate (MEHP) was studied in the rat. Three hours after a single oral dose of DEHP (2.8 g/kg), plasma concentrations of 8.8 +/- 1.7 micrograms/ml DEHP and 63.2 +/- 8.7 micrograms/ml MEHP were reached. MEHP levels declined with a half-life of 5.2 +/- 0.5 h. The ratio of the area under the plasma concentration-time curve of MEHP to that of DEHP was 16.1 +/- 6.1. When 14C-DEHP was administered, 19.3 +/- 3.3% of the radioactivity was excreted in the urine within 72 h, the rest being excreted in the faeces. The urinary excretion rate of total radioactivity declined with a half-life of 7.9 +/- 0.5 h. Single administration of MEHP (0.4 g/kg) resulted in plasma concentrations of 84.1 +/- 14.9 micrograms/ml 3 h after dosing; the half-life of MEHP was 5.5 +/- 1.1 h. Multiple dosing with DEHP (2.8 g/kg/day) for 7 consecutive days produced no accumulation of DEHP or MEHP in plasma.

Distribution of a single oral dose of methyl mercury (10 mg Hg/kg body weight) was followed from 90 min up to 120 h in plasma, erythrocytes, and brain of Japanese quails and rats. Significantly higher Hg concentrations were observed in plasma and brain of quails and red blood cells of rats. Blood/brain ratio decreased in quails from 6 to 2 at 24 h and 120 h respectively, whereas it increased in rats. Erythrocyte/plasma ratio in quails was about three times lower and averaged 54. The differences in Hg distribution were accompanied by a more than 3-fold higher acute toxicity in quails under adequate experimental conditions.

Six-week-old female albino rats were fed rat diet or human foods: meat, bread or milk--3 days before and 6 days after a single oral dose of 115m Cd. All animals were killed 6 days after administration and the radioactivity in the whole body and in the gut-free carcass were determined in a double scintillation counter. Gut retentions were calculated as the difference: whole body minus carcass. All animals fed meat, bread or milk had much higher body retentions than animals fed rat diet (whole body 4-5 times, carcass about 3 times and gut 10-14 times). Our results point out the importance of nutritional factors in metal metabolism and toxicity.

Hens were given a single oral dose (0.235 mg/kg) of tri-o-cresylphosphate (TOCP) during chronic n-hexane treatment (200 mg/kg daily, 5 days/week). They were compared with other animals treated only with n-hexane or only with TOCP. Animals treated with a higher TOCP dose (1 ml/kg) were used as positive controls. The animals treated with both n-hexane and TOCP showed rapid development of severe ataxia. The rate of the ataxia development was similar to that of the positive controls but with earlier onset of the first signs and with less loss of body weight. However, animals treated only with n-hexane, under the same conditions, showed only reversible weakness and sedative effects, and those treated only with TOCP showed slow and slight ataxia development. The n-hexane- and TOCP-treated hens showed axonal swelling with myelin retraction associated with Ranvier's nodes, which is characteristic of long hexacarbon exposure. Some internodal swellings were also observed but less frequently than the paranodal swellings. The time course of the ataxia development was similar to an organophosphorus-induced delayed neuropathy (OPIDN); however, the light microscopy observation more closely resembled hexacarbon neuropathy. The results suggest a potentiation effect of n-hexane and TOCP neurotoxicities which could be related to some human occupational neuropathies.

The effect of a single oral dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 10 microgram . kg-1, on the status of vitamin A (retinol) was studied in rats during an eight week period after administration. Retinol was determined spectrophotometrically after separation by means of high pressure liquid chromatography. In the liver of control animals the total storage and the concentration of retinol were found to increase linearly with time whilst in the TCDD-exposed animals both the concentration and total storage remained essentially unchanged. Differences in the storage levels were evident after 4 days, and after 8 weeks the treated animals had a total liver storage corresponding to about 30% of the controls. Retinol levels in serum were significantly higher in the treated animals after week 1 and 2.