The toxicokinetics and bioavailability of[14C]paraquat were examined in rats which had received a single dose (11.6 μg/kg) of the herbicide by the iv, intragastric, dermal or pulmonary route. In the pulmonary route studies, rats were exposed to an aqueous solution or liquid aerosols of[14C]paraquat through a tracheal cannula or [14C]paraquat aerosols in a nose-only inhalation chamber. After intratracheal, intragastric, and dermal administration of[14C]paraquat to the rat, the average bioavailabilities were 0.45 ± 0.22, 0.12 ± 0.03, and 0.038 ± 0.027, which corresponded to 20.3 nmol, 5.4 nmol and 1.7 nmol of[14C]paraquat, respectively. Since the dose administered to the rat in the [14C]paraquat aerosol studies was unknown, the bioavailability for this exposure route could not be determined. However, about 27.5 nmol of[14C]paraquat was absorbed into the systemic circulation of the rat after inhaling [14C]paraquat aerosols through a tracheal cannula. [14C]paraquat administered to the rat iv was eliminated from the blood with a half-life of about 68 min. Urine and feces were the major excretion routes. The radioactivity absorbed into the systemic circulation of the rat was approximately equal to that excreted in the urine; about 23.8 nmol, 8.5 nmol and 1.5 nmol of[14C]paraquat were recovered from the urine of the rat after inhalation of[14C]paraquat aerosols in a nose-only exposure chamber, intragastric injection and dermal absorption of [14C]paraquat, respectively. Tissue distribution studies showed that the bulk of the [14C]paraquat administered to the rat by the inhalation and dermal routes remained at the sites of administration.

1. The LC50 and the uptake and elimination kinetics of 4-chlorodiphenyl ether (4-CDE), 2,4-dichlorodiphenyl ether (2,4-diCDE), 2,4,4'-trichlorodiphenyl ether (2,4,4'-triCDE) and 2,4,5,4'-tetrachlorodiphenyl ether (2,4,5,4'-tetraCDE) were examined in brook trout (Salvelinus fontinalis). The chlorinated diphenyl ethers (CDE) were administered in the water. 2. The 96 h LC50 of 4-CDE and 2,4-diCDE were 0.73 and 0.66 mg/l, respectively. The LC50 of 2,4,4'-triCDE and 2,4,5,4'-tetraCDE could not be determined since they were greater than the water solubilities of these chemicals. 3. Uptake of the CDE by trout was rapid; the uptake rate ranged between 2.4 and 48.9 micrograms/day. However, CDE uptake by trout did not reach a steady state at the conclusion of a 7 day exposure. In contrast, depuration of the CDE from trout was slow; the depuration half-lives of the CDE ranged between 3.9 and 63 days. 4. The toxicokinetics of the CDE in trout could be described by a one-compartment open model with zero-order absorption and first-order elimination. The CDE were taken up initially into the blood and liver of trout before they were redistributed to adipose tissue and muscle. 5. CDE are significantly bioaccumulated by fish from water; the model-predicted maximum body burdens of trout exposed to 100 micrograms/l CDE in water are 146, 316, 1381, and 930 micrograms/g for 4-CDE, 2,4-CDE, 2,4,4'-triCDE and 2,4,5,4'-tetraCDE, respectively.

1. Pyrene was administered i.p. as a single dose to trout (Oncorhynchus mykiss). Urine was collected continuously for 3 days and bile sampled at the end of this period. Pyrene metabolites in these biological fluids were identified by 1H-nmr spectrometry, glc-ms and hplc-ms. 2. 1-Hydroxypyrene was the major oxidation metabolite in the urine and bile. Small amounts of 1,6-dihydroxypyrene and a putative 1,8-dihydroxypyrene metabolite also were detected. Unchanged pyrene was not found in any of these biological fluids. 3. Both free and conjugated metabolites of pyrene were found in the bile and urine. The majority of the pyrene metabolites in the bile were conjugated with glucuronic acid or sulphate.

No abstract

14C‐ and 3H‐Labelled psilocin (4‐hydroxy‐N,N‐dimethyl‐tryptamine), the principal, active agent of hallucinogenic mushrooms, was synthesized from 2‐methyl‐3‐nitrophenol via 4‐benzyloxyindole. 14C‐Labelled potassium cyanide was reacted with 4‐benzyloxygramine (obtained from 4‐benzyloxyindole) to give 14C‐4‐benzyloxy‐3‐indole acetic acid, an intermediate for 14C‐psilocin synthesis. 3H‐Labelled lithium aluminium hydride was used to react with 4‐benzyloxy‐3‐indole‐N,N‐dimethyl‐glyoxylamide (obtained from 4‐benzyloxyindole) to give 3H‐4‐benzyloxy‐psilocin which was debenzylated to form 3H‐psilocin.