Search PubMed⌕ Search

Biomedical subjects

R D Harbison

Publications and source records attributed to R D Harbison.

At least 109 records · Page 6Linked to original sources
PubMed1973

Rubratoxins.

Explore the source record for details and available documents.

Abnormalities, Drug-Induced↗
PubMedDate not supplied

Extraction and analysis of superoxide free radicals (.O2-) from whole mammalian liver.

Extraction of whole lobes of normal rat liver with dimethyl sulphoxide (DMSO) under N2 gives extracts which contain 5-10 mumol/l.O2- (50-100 nmol.O2- per 10 ml extract per 4 g liver; 1.25-2.50 nmol.O2- per millilitre per gram liver). Evidence for .O2- in the extracts is given by: (1) electron spin resonance signals (ESR), (2) differential pulse polarography (DPP), (3) chemiluminescence (CL), and (4) nitroblue tetrazolium reduction (NBT). All tests yield results identical with those obtained with authentic .O2-. Extraction of .O2- is enhanced by tetrabutyl ammonium ion, and is maximal at 1-3 min. These results raise the possibility that substantial amounts of .O2- are normally sequestered in protective membranous sites in vivo.

Animals↗
PubMedDate not supplied

The perturbation of hepatic glutathione by alpha 2-adrenergic agonists.

Single injections of epinephrine significantly lowered the hepatocellular levels of reduced glutathione (GSH) while producing small but significant elevations in serum glutamic-pyruvic transaminase (SGPT) activity. Hormones, i.e. glucagon and the corticosteroids, were also found to depress significantly hepatic glutathione. Based upon the agonist-antagonist studies performed, the hepatic GSH lowering effects of epinephrine appear to be mediated solely by alpha 2 receptors. Adrenergic antagonists with alpha 2 receptor blocking properties, phenotolamine and yohimbine, prevented the epinephrine-induced lowering of GSH while agonists with alpha 2 activity, clonidine and guanabenz, mimicked epinephrine's response. Antagonists with either alpha 1 or beta activity, i.e. prazosin, phenoxybenzamine and propranolol, did not prevent the epinephrine-induced lowering of hepatic GSH. Contrary to these findings antagonists with either alpha or beta receptor blocking activity significantly reduced the epinephrine-induced elevations in SGPT activity. Thus, there was no apparent relationship between the elevation of SGPT activity and the reduction in hepatic glutathione levels. It is concluded that the therapeutic administration of these compounds, or physiologic responses to stress or pain, may exacerbate the hepatotoxicity of compounds detoxified by GSH or alter important glutathione-mediated hepatocellullar processes.

Adrenergic alpha-Agonists↗