SUMMARYUnusual swollen and branched cell forms were produced in a thymineless mutant of Escherichia coZi strain c by treatment with mitomycin C, and to lesser extents, by incubation without thymine and by exposure to ultraviolet light. In the case of mitomycin C treatment the morphological changes were accompanied at first by degradation of deoxyribonucleic acid (DNA), later by degradation of ribonucleic acid (RNA) and inhibition of protein synthesis, and throughout by inhibition of DNA synthesis and extensive loss in viability. Thymineless incubation prevented DNA synthesis and also resulted in extensive killing. Cultures incubated after exposure to ultraviolet light exhibited a small amount of DNA degradation and a lag in DNA synthesis. Upon prolonged incubation with mitomycin C or without thymine many of the abnormal forms became very enlarged and eventually lysed. No evidence of bacteriophage or bacteriocin could be detected in the treated cells.

A group of mutants of Neurospora crassa which require both isoleucine and valine have been described in a series of previous communications from this laboratory (WAGNER, SOMERS and BERGQUIST 1960; WAGNER, KIRITANI and BERGQUIST 1962;and KIRITANI 1962). These mutants were all found to be closely linked between the linkage group V markers Zys-1 (lysine-1, 33933) and sp

Ethanol, 1,3, and 5 g/kg, depresses the hydroxylation of amphetamine by the rat in vivo. At 5 g/kg, ethanol does not affect the hydroxylation of acetanilide or biphenyl in vivo. Amphetamine hydroxylation is unaffected by phenobarbitone or benzo[a]pyrene pretreatment but is depressed by pretreatment with 2-diethylaminoethyl-2,2-diphenylvalerate (SKF 525-A), 2,4-dichloro-6-phenylphenoxyethylamine (DPEA), and 2,4-dichloro-6-phenylphen~xy-NN-dieth~leth~lamine (Lilly 18947).We have reported previously that ethanol treatment markedly inhibits the hydroxylation of amphetamine by the rat in vivo (Creaven & Barbee, 1969). We have now made further investigations of this and other aspects of amphetamine hydroxylation in an attempt to determine the mechanism of this inhibition by ethanol and to elucidate the differences between amphetamine hydroxylation and that of other drugs. E X P E R I M E N T A L Materials and methodsMale Sprague-Dawley rats, 100 to 150 g, received intraperitoneal injections of ( f)-[2-14C]amphetamine sulphate 5 mg/kg (1 -6 mCi/mM), acetanilide (250 mg/kg in isotonic saline) or biphenyl (200 mg/kg in arachis oil). The animals were placed in metabolism cages and urine samples collected in flasks at 0 to 2' . Urinary pH was recorded and the urine frozen.Animals were pretreated with 1, 3, or 5 g/kg ethanol by stomach tube as a 25% solution (v/v) in water 30 min before the administration of amphetamine. Control animals received an equal volume of saline.Benzo[a]pyrene (2 mg/kg) and phenobarbitone (80 mg/kg) were administered intraperitoneally daily for three days; amphetamine was injected 24 h after the final dose. 2-Diethylaminoethyl-2,2-diphenylvalerate hydrochloride (SKF 525-A), 2,4-dichloro-6phenylphenoxyethylamine hydrochloride (DPEA), and 2,4-dichloro-6-phenylphenoxy-NN-diethylethylamine hydrobromide (Lilly 18947), 35 mg/kg, were injected intraperitoneally 45 min before the administration of amphetamine.Pyrazole (100 mg/kg in isotonic saline) and disulfiram (100 mg/kg in arachis oil) were injected intraperitoneally 15 and 30 min, respectively, before oral administration of 3 g/kg of ethanol. Amphetamine was injected 30 min after ethanol administration.Metabolites were identified by two-dimensional paper chromatography of urine to which authentic amphetamine andp-hydroxyamphetamine had been added. Chromatograms were developed in I-butanol-acetic acid-water (4 : 1 : 1 v/v) followed by 2propanol-ammonia-water (8 : 1 : 1 v/v) (Asatoor, Galman & others, 1965).

No abstract

No abstract