Coordination-number dependence of magnetic hyperfine fields at (111)Cd on Ni surfaces.

Ferromagnetic Ni surfaces were investigated on an atomic scale using the perturbed angular correlation spectroscopy probe (111)Cd. A comprehensive set of data for magnetic hyperfine fields (B(hf)) at various probe sites is presented. A field variation from -7 T in Ni bulk to the surprisingly large value of 16 T at the adatom position on Ni(111) is observed.

Effect of rifampin, phenobarbital pretreatment, and acetylator phenotype on acetylisoniazid metabolism in the rabbit.

The metabolism of [14C]acetylisoniazid was studied in male New Zealand White rabbits. Pretreatment of the rabbits with the microsomal enzyme inducers rifampin and phenobarbital had little effect on acetylisoniazid metabolism. Rifampin appears to produce some inhibition of acetylation of the metabolite acetylhydrazine to diacetylhydrazine.

Metabolism of [14C]acetylisoniazid and [14C]acetylhydrazine by the rat and rabbit.

Male rats and rabbits were singly dosed with either 1-[14C]acetyl isoniazid (acetylisonicotinoylhydrazine, acetyl-INH, 200 mg/kg po) or 1-[14C]acetylhydrazine (50 or 100 mg/kg ip). Urine and expired 14CO2 were collected, and after 6 hr the animals were killed for the analysis of tissue 14C concentrations and covalent binding of 14C to hepatic protein. Rats excreted proportionately more 14C in urine and had lower 14C levels in their tissues compared to rabbits.

Isoniazid metabolism in the rabbit, and the effect of rifampin pretreatment.

The metabolism of 14C-isonicotinyl hydrazide (INH) (50 mg/kg, po) was studied in male New Zealand White rabbits and the effect on INH metabolism of pretreating the rabbits for 7 days with rifampin (100 mg/kg po per day) was also studied. The 14C-labelled metabolites were separated and quantitated by TLC and the unlabelled hydrazino metabolites by GLC. Absorption and elimination of INH was rapid since the peak blood 14C level was attained by 1 hr and the T 1/2 of elimination was 2.

Effect of analgesic nephropathy in women on the metabolism and excretion of 14C-acetaminophen.

Nephropathy due to excessive consumption of phenacetin-containing analgesic mixtures has been a problem in Canada. Following the withdrawal of phenacetin it seems probable that acetaminophen consumption will increase and this study investigated the metabolism of 14C-Acetaminophen in patients with nephropathy and in healthy women. The respective alpha T1/2s of excretion of Acetaminophen and its metabolites were 2.

Failure to observe pathology in the rat following chronic dosing with acetaminophen and acetylsalicylic acid.

Male Wistar rats were dosed daily by gavage for 200 days with either (1) aspirin, 200 mg/kg; (2) acetaminophen, 200 mg/kg; (3) aspirin and acetaminophen, 200 mg/kg of each; (4) aspirin and acetaminophen, 100 mg/kg of each or (5) vehicle alone. None of the treatments produced any marked signs of toxicity and no drug related deaths were observed. The full dose combination (3) did significantly reduce the weight compared to the control group (5).

Effect of subacute dosing and phenobarbital and 3-methylcholanthrene pretreatment on the metabolism of acetaminophen in rats.

The metabolism of 14C-ring-labelled acetaminophen was studied in male Wistar rats. Pretreatment with phenobarbital increased the initial rate of elimination of 14C from the blood and increased the amount of acetaminophen glucuronide excreted in the urine. Pretreatment with 3-methylcholanthrene did not significantly affect the rate of elimination from the blood and decreased the amount of acetaminophen glucuronide in the urine.