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At least 217 records · Page 12Linked to original sources
PubMed1964

TYROSINASE INHERITANCE IN STREPTOMYCES SCABIES. I. GENETIC RECOMBINATION.

Gregory, Kenneth F. (Ontario Agricultural College, Guelph, Ontario, Canada), and Jay C. C. Huang. Tyrosinase inheritance in Streptomyces scabies. I. Genetic recombination. J. Bacteriol. 87:1281-1286. 1964.-Mutants derived from Streptomyces scabies strain A26 recombined with other derivatives of A26, but not with nine other strains of S. scabies nor with eight strains of other streptomycetes. Most of the spore progeny of heterogenomic mycelia formed from complementary diauxotrophic strains of S. scabies A26 were capable of forming tyrosinase (tye(+)), provided either of the parents was tye(+). About 99.8% of these spores carried the nutritional markers of either one or the other of the two parents. All recombinant classes between nutritional and streptomycin susceptibility markers were like-wise predominantly tye(+). We suggest that the tye(+) characteristic is carried in a small genetic unit, which is unlinked to most other genes and capable of replicating faster than the rest of the S. scabies genome.

Canada↗
PubMed1999

Tyrosine hydroxylase, aromatic L-amino acid decarboxylase and dopamine metabolism after chronic treatment with dopaminergic drugs.

Mice were treated with dopamine (DA) receptor agonist and antagonist drugs: Agonists: (+/-)-SKF 38393 ((+/-)-1-phenyl-2,3,4, 5-tetrahydro-(1H)-3-benzazepine-7,8-diol) [DA D1-like]; bromocriptine, [DA D2 selective]; quinpirole, [DA D2/D3 preferring]; (+/-)-7-hydroxy-dipropylamino-tetralin (7-OH-DPAT), [DA D3/D2 preferring], Antagonists: R(+)-SCH 23390 (R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4, 5-tetrahydro-1H-3-benzazepine), [DA D1-like]; and haloperidol, [DA D2-like]. All drugs were administered intraperitoneally, two injections daily 8 h apart for 30 days. Aromatic L-amino acid decarboxylase (AAAD) and tyrosine hydroxylase (TH) activity, protein and mRNA, as well as DA metabolism were followed with time thereafter in the nigrostriatal neurons. We observed that chronic administration of D1-like agonists had no effect on TH or AAAD activity, while D2-like agonists decreased AAAD, but not TH activity. Additionally, chronic blockade of DA D2-like receptors resulted in prolonged induction of TH and AAAD, while chronic blockade of DA D1-like receptors induced changes of AAAD only. Compared to TH the induction of AAAD was longer lasting. DA metabolism was altered by chronic administration of drugs acting on DA D2-like, but not DA D1-like receptors, and in general the patterns of change did not follow those for TH or AAAD. When studied 48 h after the last dose of the chronic haloperidol schedule TH displayed tolerance to acute drug challenge. At the same time interval, there was tolerance to the enhancing effects of haloperidol and SCH 23390 on DA metabolism. The induction of AAAD by haloperidol or SCH 23990 did not appear to develop tolerance after chronic administration. These observations complement existing knowledge, and provide novel information about AAAD that may have practical importance for Parkinson's patients on L-DOPA therapy.

Animals↗
PubMed1976

Lethality of tyrosine in mice: its potentiation by decarboxylase inhibitors and reversal byascorbic acid.

High doses of tyrosine were found to be lethal in mice. The lethality was potentiated by decarboxylase inhibitors which acted by elevating tissues tyrosine levels when given together with large amounts of tyrosine. The lethality of either tyrosine or tyrosine given in combination with decarboxylase inhibitors was found to be correlated with the elevation of tyrosine levels in liver. This toxicity does not appear to involve either tyramine or p-hydroxyphenylpyruvic acid formation. Ascorbic acid pretreatment afforded a marked protection against tyrosine toxicity. This compound was found to prevent the elevation of tissue tyrosine levels by stimulating p-hydroxyphenylpyruvic acid oxidase, increasing the urinary excretion and inhibiting the gastrointestinal absorption of tyrosine.

Animals↗
PubMed1984

Early changes in tyrosine hydroxylase and glutamate decarboxylase activity in the golden hamster striatum after intracerebral inoculation of the nigrostriatal system with scrapie agent (strain 263 K).

Unilateral inoculation of hamster substantia nigra (SN) with scrapie agent led to an early decrease in tyrosine hydroxylase (TH) activity in the corresponding striatum, which was detectable by the 5th day. This decrease was accompanied by an increase in glutamate decarboxylase (GAD) observed on the 20th day. Local phenomena related to administration of the agent were investigated by intrastriatal inoculation followed by local measurement of TH, GAD and choline acetyltransferase (ChAT) activities. A rise in GAD activity was observed 20 days later. The decrease in TH activity which occurred 5 days after inoculation of the substantia nigra with scrapie agent constitutes an extremely early indication in hamsters of the slow pathological processes at work: at clinical and behavioural levels, these can be detected at best only 80 days after the intracerebral inoculation.

Animals↗
PubMed1964

TYROSINASE INHERITANCE IN STREPTOMYCES SCABIES. II. INDUCTION OF TYROSINASE DEFICIENCY BY ACRIDINE DYES.

Gregory, Kenneth F. (Ontario Agricultural College, Guelph, Ontario, Canada), and Jay C. C. Huang. Tyrosinase inheritance in Streptomyces scabies. II. Induction of tyrosinase deficiency by acridine dyes. J. Bacteriol. 87:1287-1294. 1964.-Growth in minimal medium containing 1 mug of acriflavine per ml resulted in a large increase (up to 62%) in the frequency of tyrosinase-deficient (tye(-)) mutants in all of ten strains of Streptomyces scabies and eight unidentified streptomycetes studied. This increased frequency did not result from the selection of preformed mutants, since tye(-) clones were usually inhibited by lower concentrations of acriflavine than were tyrosinase-producing (tye(+)) clones, and no significant difference in mycelial yields occurred between the two types growing in a 1 mug/ml concentration of the dye. The mutations induced by X rays and acriflavine were either allelic or closely linked. This tye(-) phenotype was not caused by the production of an enzyme inhibitor, lack of a cofactor, or defect in the conversion of a protyrosinase to tyrosinase. Tye(-) mutants formed no detectable tyrosinase under a variety of conditions, including the presence of possible inducers. Mutants were able to oxidize glucose and succinate. The S. scabies tyrosinase was heat-labile (half-life at 59 C = 1.6 min) and not particle-bound. We conclude that acriflavine induces the loss of, or alteration in, a structural gene for tyrosinase production present as an extrachromosomal factor.

Acridines↗