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R H Waring

Publications and source records attributed to R H Waring.

133 records · Page 8Linked to original sources
PubMed1968

Some metabolites of 1-bromobutane in the rabbit and the rat.

1. Rabbits and rats dosed with 1-bromobutane excrete in urine, in addition to butylmercapturic acid, (2-hydroxybutyl)mercapturic acid, (3-hydroxybutyl)mercapturic acid and 3-(butylthio)lactic acid. 2. Although both species excrete both the hydroxybutylmercapturic acids, only traces of the 2-isomer are excreted by the rabbit. The 3-isomer has been isolated from rabbit urine as the dicyclohexylammonium salt. 3. 3-(Butylthio)lactic acid is formed more readily in the rabbit; only traces are excreted by the rat. 4. Traces of the sulphoxide of butylmercapturic acid have been found in rat urine but not in rabbit urine. 5. In the rabbit about 14% and in the rat about 22% of the dose of 1-bromobutane is excreted in the form of the hydroxymercapturic acids. 6. Slices of rat liver incubated with S-butylcysteine or butylmercapturic acid form both (2-hydroxybutyl)mercapturic acid and (3-hydroxybutyl)mercapturic acid, but only the 3-hydroxy acid is formed by slices of rabbit liver. 7. S-Butylglutathione, S-butylcysteinylglycine and S-butylcysteine are excreted in bile by rats dosed with 1-bromobutane. 8. Rabbits and rats dosed with 1,2-epoxybutane excrete (2-hydroxybutyl)mercapturic acid to the extent of about 4% and 11% of the dose respectively. 9. The following have been synthesized: N-acetyl-S-(2-hydroxybutyl)-l-cysteine [(2-hydroxybutyl)mercapturic acid] and N-acetyl-S-(3-hydroxybutyl)-l-cysteine [(3-hydroxybutyl)mercapturic acid] isolated as dicyclohexylammonium salts, N-toluene-p-sulphonyl-S-(2-hydroxybutyl)-l-cysteine, S-butylglutathione and N-acetyl-S-butylcysteinyl-glycine ethyl ester.

Alkanes↗
PubMedDate not supplied

The metabolism and disposition of D-penicillamine in the DA-strain rat.

Radiolabelled [35S]-D-penicillamine was administered orally to DA-strain rats. After 72 hours approximately 65% of the dose was excreted with no significant differences between male and female animals. The major urinary product was inorganic sulphate with small amounts of D-penicillamine. Penicillamine disulphide, penicillamine-cysteine, S-methyl penicillamine and N-acetyl penicillamine were also found as metabolites. The female rat excreted significantly less sulphate (P less than 0.1) and more penicillamine disulphide (P less than 0.01) than the male. The residual radioactivity was found in the carcass, with slight concentration in the gut, skin, kidney, bladder and liver.

Animals↗
PubMedDate not supplied

Metabolism of phenothiazine in the guinea pig.

The metabolism of phenothiazine was studied in the guinea pig. In the adult animal after 24 hr, about 7% of the administered dose was found in feces, with traces of the sulfoxide and phenothiazone. Small amounts of all these compounds also were found in urine, with leucophenothiazone sulfate (approximately 12%) and a metabolite identified as phenothiazine N-glucuronide (approximately 22%). This latter compound was also present in bile. Both phenothiazine and its sulfoxide were retained in body tissues for a long time, about 85% of the dose being excreted after 7 days. In neonatal animals, phenothiazine, with up to 12% of the sulfoxide together with traces of leucophenothiazone, phenothiazone, and thionol was excreted in urine.

Aging↗
PubMedDate not supplied

The metabolism and elimination of S-carboxymethyl-L-cysteine in man.

The metabolism of 14C- and 35S-labeled S-carboxymethylcysteine (SCMC) has been compared. The majority of the dose appeared in urine in the first 24 hr; no activity was detectable in feces. Use of 25S-labeled compound gave small amounts of inorganic 35S-sulfate, whereas 14C-labeled material was degraded to give some [14C]urea. Peak excretion of the parent compound occurred first after administration of SCMC; metabolites requiring one chemical modification for their formation were maximally excreted 1-4 hr after the dose and those involving more metabolic processes appeared later (4-8 hr).

Biotransformation↗
PubMedDate not supplied

In vitro effect of the cysteine metabolites homocysteic acid, homocysteine and cysteic acid upon human neuronal cell lines.

Cysteine (CYS) is a non-essential amino acid which elicits excitotoxic properties via the N-methyl-D-aspartate (NMDA) subtype of the glutamate receptor. CYS levels are known to be elevated in association with neurological disease such as Alzheimers Disease (AD) and Parkinsons Disease (PD). We have previously reported studies investigating the toxicity of CYS and its major metabolite cysteinesulfinic acid (CSA) to human neuronal cell lines in vitro and in continuation of this we now report the toxicity of other compounds (Homocysteic Acid, HCA; Homocysteine, HCYS; and Cysteic Acid, CA) in the CYS metabolic pathway. Three cell lines, all of human origin and derived from separate discrete areas of the brain were used in the neurotoxicity assays. Lactate dehydrogenase (LDH) release was assayed as a measure of cell death. The cell lines investigated showed varying degrees of toxic responses which were the reverse of those seen when they were exposed to CYS or CSA. The SK.N.SH (Neuroblastoma) cell line, which exhibits a high toxic response to CYS and CSA, gave a low toxic response to HCA and CA while the TE 671 (Medulloblastoma) cell line, which exhibits a low toxic response to CYS and CSA, showed a high toxic response to HCYS, HCA and CA. However, the U-87 MG (Glioblastoma) cell line, which has a median toxic response to CYS and CSA, also has median response to HCYS, HCA and CA. These results show that toxic responses are cell-type specific for CYS and its metabolites and this may be reflected in the patterns of neurodegeneration observed in such diseases as AD and PD. HCYS is selectively toxic to medulloblastoma cells; this may explain why high HCYS levels result in neural tube defects in prenatal humans, where the same cell-type is involved.

Cell Line↗