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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↗
PubMed1978

Comparison of pseudorabies virus inactivated by bromo-ethylene-imine, 60Co irradiation, and acridine dye in immune assay systems.

Pseudorabies virus infections among animals, especially swine, have become prevalent in the United States in the past few years. The disease in swine is now economically important. Test systems and antigens are being developed for use in control and disease suppression efforts. Pseudorabies virus was inactivated by three methods: chemically, with bromo-ethylene-imine; physically, with 60Co irradiation; and chemically and physically, with 3,9-diaminoacridine dye followed by exposure to white visible light. The antigenicities of the preparations were determined in the presence of specific antibody in immunodiffusion tests and through immunoelectrophoresis. The latter technique permitted quantitation of either antigen or antibody. In the electrophoretic patterns, the antigenic mass in bromo-ethylene-imine preparations was estimated to be 42 mg/ml, the same as in the untreated control material. After 60Co irradiation, 22 mg/ml was present, in comparison with 50 mg/ml in the untreated control antigen. In contrast, 67 mg/ml was present in the acridine dye-light-treated preparation, in comparison with 58 mg/ml in the untreated control material. A possible explanation for the acridine dye-light-treated preparation values is that photodynamic inactivation interferes with viral maturation during the replicative cycle within cells, with a resulting production of a greater amount of antigen, at least some of which is in the form of defective particles.

Acridines↗
PubMed2001

Light sensitivity of the ciliate Tetrahymena vorax induced by the fluorescent dye acridine orange.

The ciliate Tetrahymena vorax is normally insensitive to light. However, after uptake of acridine orange, blue light evokes instant backward swimming. The dye accumulates mainly in posterior vacuoles, with half-maximal uptake after 1 min. Illumination for 10 s induced a depolarisation of approximately 15 mV lasting less than 2 s, followed by a sustained hyperpolarisation of approximately 20 mV. Deciliated cells displayed a similar response. The hyperpolarisation was linked to reduced membrane resistance, showed a reversal potential of approximately -55 mV and was blocked by 1 mmol l(-1) TEA. The rate of rise of electrically evoked Ca(2+)-spikes was reduced during the hyperpolarisation, which is compatible with elevated cytosolic Ca(2+) concentration. This suggests that the hyperpolarisation may be caused by activation of Ca(2+)-sensitive K(+) channels. The depolarisation was abolished in Ca(2+)-free medium, whereas the hyperpolarisation was unaffected. Illumination for 2 s, or prolonged stimulation restricted to the anterior part of the cell, induced depolarisation only. Illumination of the posterior part caused delayed hyperpolarisation with no preceding depolarisation. We conclude that the induced backward swimming is associated with Ca(2+) influx through anterior channels, while Ca(2+) released from intracellular stores activates K(+) channels responsible for the delayed hyperpolarisation.

Acridine Orange↗