Radioimmunoassay for serum levels of an anti-androgen TSAA-291 (Oxendolone) in rats.

A simple radioimmunoassay method was established to determine serum levels of a steroidal anti-androgen, TSAA-291 (Oxendolone, 16 beta-ethyl-17 beta-hydroxy-4-estren-3-one) utilizing ether-extract of serum. Using an antiserum raised against TSAA-291-3-oxime-BSA conjugate in a rabbit, a standard curve was obtained in the assay range from 30 pg to 12 ng/tube. Intra- and inter-assay coefficients of variation were calculated to be 11 and 21%, respectively.

Effects of dietary butylated hydroxytoluene on functional and biochemical properties of platelets and plasma preceding the occurrence of haemorrhage in rats.

Measurements of platelet-particle concentration, platelet haematocrit and mean platelet volume showed no significant differences between control rats and rats given 1.2% butylated hydroxytoluene (BHT) in the diet for 1 wk, but the platelet distribution width was significantly smaller in the rats fed BHT. By optical measurement, epinephrine-induced platelet aggregation was found to be significantly decreased in both the platelet-rich plasma and washed platelets of rats given BHT.

An improved method for labeling carboxyatractyloside by [3H]KBH4.

Carboxyatractyloside was labeled with [3H]KBH4 after oxidation of the primary alcohol of the glucose disulfate moiety by dicyclohexylcarbodiimide and P2O5 under anhydrous conditions in a dimethylsulfoxide medium. The 3H-labeled product was purified by DE 52 column chromatography followed by Cellulofine GCL 25 column chromatography. The final 3H-labeled product gave a single spot on a thin-layer chromatogram, and its Rf value was the same as that of authentic carboxyatractyloside.

Testicular atrophy induced by di-2-ethylhexyl phthalate: effect of zinc supplement.

The administration of di-2-ethylhexyl phthalate (DEHP) to young male rats was found to cause testicular atrophy and loss of testicular zinc. In an attempt to test the hypothesis that a cause and effect relationship exists between DEHP-induced loss of testicular zinc and testicular injury, zinc was coadministered (by ip injection or by dietary supplementation) with DEHP (po) for 10 days and organ weights and zinc concentrations were then measured. This testicular atrophy was not prevented by coadministration of zinc.

The metabolic profile of sodium o-phenylphenate after subchronic oral administration to rats.

We examined the metabolites of o-phenylphenol (OPP) in the urine of male and female rats dosed with 2% sodium o-phenylphenate (OPP-Na) in food from the age of 5 wk for 136 days. The urinary metabolites of OPP-Na produced during the 24 hr after OPP-Na feeding accounted for 55% of the dose in male rats and 40% in females. The main metabolites were OPP-glucuronide and 2,5-dihydroxybiphenyl (2,5-DHBP)-glucuronide.

The role of 2,6-di-tert-butyl-4-methylene-2,5-cyclohexadienone (BHT quinone methide) in the metabolism of butylated hydroxytoluene.

Male rats were fed 5.45 mmol/100 g diet butylated hydroxytoluene (BHT) or 2,6-di-tert-butyl-4-hydroxymethylphenol (BHT alcohol) in either a standard or purified diet for 1 wk, after which their livers were analysed for levels of unconjugated BHT metabolites and their blood clotting times were assayed. The BHT quinone methide, 2,6-di-tert-butyl-4-methylene-2,5-cyclohexadienone, was only found in appreciable concentrations (6-9 micrograms/g liver) in the livers of rats given BHT.

Metabolic studies in the rat with 2,4,6-tri-t-butylphenol: a haemorrhagic antioxidant structurally related to butylated hydroxytoluene.

Single oral doses of the haemorrhagic antioxidant 2,4,6-tri-t-butylphenol (260 mg/kg) were well absorbed in the rat. Peak blood levels of this compound were reached in 15-60 min. The blood elimination half-lives were 18.

On the mechanism of covalent binding of butylated hydroxytoluene to microsomal protein.

The structures of cysteine conjugates of 3,5-di-tert-butyl-4-hydroxytoluene (BHT) and the binding sites of BHT metabolites on microsomal protein were investigated by 13C nuclear magnetic resonance (13C-NMR) and gas-liquid chromatography/mass spectrometry. The cysteine conjugates of 2,6-di-tert-butyl-4-hydroxymethylphenol (BHT-alcohol) and 2,6-di-tert-butyl-4-methylene-2,5-cyclohexadienone (quinone methide), which are metabolites of BHT found in rat liver and specifically reacts with thiol compounds, were prepared as alcoholic aqueous solutions. The molecular structure of the cysteine conjugate of BHT-alcohol agreed completely with that of quinone methide in 13C-NMR spectra or mass spectra.

Vitamin K content of liver and feces from vitamin K-deficient and butylated hydroxytoluene (BHT)-treated male rats.

Vitamin K content of liver and feces from male rats fed diets containing butylated hydroxytoluene (BHT) was estimated by a chick bioassay method to investigate the mechanism of BHT-induced decreases in the activities of vitamin K-dependent clotting factors. The concentration of vitamin K in the liver of rats receiving BHT was reduced as compared to that of control rats. Conversely, the concentration of vitamin K in the feces from rats receiving BHT increased more than that from control rats.

Effects of monoesters of O-phthalic acid on serum lipid composition of rats.

Male rats were administered diets containing monobutyl (MBP), mono-iso-butyl (MIBP), monooctyl (MOP) or mono-2-ethylhexyl phthalate (MEHP) for 1 week, and serum lipid compositions were determined. Non-esterified fatty acid was increased and triglycerides and total cholesterol were decreased in all monoester-treated groups. Fatty acid composition of triglycerides, cholesteryl esters and phospholipids showed similar alteration in the treated groups.

The mitochondrial glycine cleavage system: inactivation of glycine decarboxylase as a side reaction of the glycine decarboxylation in the presence of aminomethyl carrier protein.

Glycine decarboxylase, tentatively called P-protein, was inactivated when it was incubated with glycine in the presence of the aminomethyl carrier protein, called H-protein. The inactivation was accompanied by a spectral change in the P-protein as a pyridoxal phosphate enzyme; the spectrum became unusual, with a peak at 330 nm. The fluorescence emission spectrum of the inactivated P-protein showed a distinct peak at 390 nm when excited at 325 nm.

Toxicity of several phosphoric acid esters in rats.

JCL--Wistar male rats were fed a diet containing 0 or 0.5% of trimethyl phosphate (TMP), triethyl phosphate (TEP), tri-n-butyl phosphate (TBP), trioctyl phosphate (TOP), or tricresyl phosphate (TCP) for 9 weeks. Body weights in TMP- and TBP-treated rats were significantly lower than the control.

The mitochondrial glycine cleavage system: differential inhibition by divalent cations of glycine synthesis and glycine decarboxylation in the glycine-CO2 exchange.

The exchange of glycine carboxyl carbon with CO2 catalyzed by the combination of chicken liver glycine decarboxylase (P-protein) and aminomethyl carrier protein (H-protein) was markedly inhibited by various divalent cations, although extents of inhibition by individual metal ions varied considerably. Cu2+ and Zn2+, at 100 microM, inhibited the reaction almost completely, and the inhibitions by Co2+ and Ni2+ were also significant, while Mg2+ and Mn2+ did not appreciably affect the reaction. The inhibition by Zn2+ was competitive with both bicarbonate and H-protein and non-competitive with glycine.

Glycine cleavage system in ketotic hyperglycinemia: a reduction of H-protein activity.

Glycine cleavage activity was compared in the livers from three cases of ketotic hyperglycinemia (two cases of propionic acidemia and one case of methylmalonic acidemia) and three controls. In one case of propionic acidemia, glycine cleavage activity (5.2 nmole/mg protein/hr) was normal in the liver obtained at biopsy when the patient was well controlled by the treatment with low protein diet (0.

Effects of butylated hydroxytoluene (BHT) on the level of glutathione and the activity of glutathione-S-transferase in rat liver.

Oral administration of 500 mg/kg of butylated hydroxytoluene (BHT) daily for three days elevated the total glutathione (GSH) level and the activities of GSH-S-transferase for CDNB and DCNB and GSSG reductase in the rat liver. BHT-alcohol, which is a metabolite of BHT, also elevated the level or activity of these components. The induction of these components with BHT-alcohol was slightly less than that with BHT.

Defective glycine cleavage system in nonketotic hyperglycinemia. Occurrence of a less active glycine decarboxylase and an abnormal aminomethyl carrier protein.

The activities of then glycine cleavage system in the liver and brain of patient with nonketotic hyperglycinemia was extremely low as compared with those of control human liver and brain. The activities of glycine decarboxylase (P-protein) and the aminomethyl carrier protein (H-protein), two of the four protein components of the glycine cleavage system, were considerably reduced in both the liver and brain; the extent of reduction was greater in the H-protein. The activity of the T-protein was normal.