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Biomedical subjects

M Ring

Publications and source records attributed to M Ring.

At least 37 records · Page 2Linked to original sources
PubMed1988

Site-directed mutagenesis of beta-galactosidase (E. coli) reveals that tyr-503 is essential for activity.

By using the technique of site-directed mutagenesis we have succeeded in replacing tyr-503 of beta-galactosidase (E. coli) with a phe. A study of the kinetic and stability properties of this mutant enzyme (F-503 beta-galactosidase) showed that the loss in activity upon this change is due to the loss of a catalytic group (rather than a detrimental change in the enzyme's overall structure or a change in the enzyme's binding capacity). This confirms previous suggestions that this tyr residue is involved in catalysis.

Cloning, Molecular↗
PubMed1985

m-Fluorotyrosine substitution in beta-galactosidase; evidence for the existence of a catalytically active tyrosine.

The pH profiles of beta-galactosidase, having tyr replaced by m-fluorotyrosine, were compared to those of normal enzyme. The inflection point on the alkaline side was lowered about 1.5 pH units in the fluoro-enzyme, corresponding to the difference in the phenolic pKa values of m-fluorotyrosine and tyr. When glycosidic bond breakage was rate-limiting, the Vm at pH 7.0 was higher for the fluoro-enzyme. When hydrolysis was rate-limiting or when acceptors which made transgalactosylis rate-limiting were used, the Vm was lower for the fluoro-enzyme. This shows that a tyr in beta-galactosidase is a general-acid catalyst in the glycosidic bond breaking reaction and a tyr (probably the same one) is a general-base catalyst in the hydrolytic reaction.

Drug Stability↗
PubMed1983

What's in a name?

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Dental Technicians↗
PubMed1982

Evidence that alpha-methylepinephrine is an antihypertensive metabolite of alpha-methyldopa.

Several medullary cardiovascular relay nuclei contain high concentrations of epinephrine and phenylethanolamine-N-methyl transferase (PNMT), the enzyme which catalyzes the conversion of norepinephrine to epinephrine. Since alpha-methylnorepinephrine, a metabolite of alpha-methyldopa, has been shown to be a substrate for adrenal PNMT, we postulated that alpha-methylnorepinephrine would also be a substrate for central PNMT, resulting in the synthesis of alpha-methylepinephrine. Therefore, alpha-methylepinephrine could be an active metabolite of alpha-methyldopa. We have investigated this hypothesis. 1) The centrally-active PNMT inhibitor SKF-64139 attenuated the hypotensive response to alpha-methyldopa in spontaneously hypertensive rats at doses that had little effect on the hypotensive response to clonidine. 2) In radioligand binding studies, alpha-methylepinephrine was as potent as norepinephrine in competing for alpha 2-receptors, more potent than epinephrine, norepinephrine, or alpha-methylnorepinephrine in competing for beta-receptors, and less potent than epinephrine, norepinephrine, or alpha-methylnorepinephrine in competing for alpha 1-receptors. 3) Intracerebroventricular administration of methylepinephrine (1-40 micrograms) to Sprague-Dawley rats elicited profound hypotension and bradycardia. alpha-Methylepinephrine was more potent than epinephrine in lowering blood pressure. We conclude that alpha-methylepinephrine is a centrally active depressor agent and could therefore be an active metabolite of alpha-methyldopa.

Animals↗
PubMed1980

Cumulative alterations in rat behavior during continuous administration of LSD or mescaline: absence of tolerance?

Male hooded rats were observed for 6 days following implantation with slow-release subcutaneous pellets containing LSD, mescaline, or control vehicle solution. In animals housed in isolation cages, continuous hallucinogen administration resulted in a gradual increase in head twitches and catatonic postures which peaked 3--4 days after pellet implantation and then declined. In animals housed in social colonies, there were also delayed increases in behavior following hallucinogen-pellet implantation, but these principally involved social behaviors such as fighting by mescaline-treated animals and social grooming by LSD-treated animals. This finding of gradual and cumulative effects of continuous hallucinogen administration contrasts with the usual finding of a rapid tolerance to hallucinogens following repeated injections.

Animals↗
PubMed1979

Detection of environmental depigmenting substances.

We systematically screened the depigmenting capacity of several phenols, catechols and organic antioxidants. Clear-cut depigmentation was achieved with monomethyl ether of hydroquinone (MMH) and tertiary butyl catechol (TBC) using black guinea pigs and black mice as animal models. A goal was to establish a reliable in vivo method to demonstrate or to predict the depigmenting action of chemicals on mammalian melanocytes. There was no universal solvent or optimal body site, although all tested areas could be depigmented. Irritation induced by some vehicles and test materials produced false positive responses. False negative responses with known depigmenting chemicals were observed. Utilizing these observations, we propose a model for screening medicinal and industrial chemicals for depigmenting capacity.

Animals↗