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R A Deitrich

Publications and source records attributed to R A Deitrich.

At least 91 records · Page 5Linked to original sources

Effect of hypnotics on mice genetically selected for sensitivity to ethanol.

It was previously shown that the rate of disappearance of blood ethanol was identical for two lines of mice selectively bred for differences in sleep-time after ethanol administration. The ED50 values for the loss of righting response with ethanol were significantly different at 3.64 g per kg for the SS line and 1.65 g per kg for the LS line. In the present study the mean sleep time is 367 sec for SS mice and 9342 sec for LS mice. The ED50 values remain essentially the same as previously reported. Unchanged LD50 values for ethanol, however, are not different at 4.8 g per kg for the SS and 4.5 g per kg for the LS line of mice. The ED50 value for loss for righting response following administration of methanol, butanol and t-butanol is approximately 2 fold greater for the SS line of mice than for the LS line. The ED50 values for sodium pentobarbital or ether in the 2 lines of mice for loss of righting response are virtually identical. In addition, the sleep-time values obtained after the administration of pentobarbital, chloral hydrate, trichloroethanol and paraldehyde are not significantly different. These data indicate that while the SS and LS lines of mice differ in central nervous system sensitivity to ethanol, methanol, butanol and t-butanol it is implied that they do no differ in central nervous system sensitivity to other hypnotic agents tested. Proof of this latter suggestion awaits determination of metabolic rates, and brain levels of these other depressants.

Animals↗

Genetic aspects of increase in rat liver aldehyde dehydrogenase induced by phenobarbital.

In the supernatant fraction of homogenized rat liver, the activity of aldehyde dehydrogenase that is dependent on nicotinamide adenine dinucleotide (E.C. 1.2.1.3) is increased up to tenfold after administration of phenobarbital for 3 days. The effect is genetically controlled and is inherited as an autosomal dominant characteristic. The mechanism is apparently unrelated to other druginduced increases in enzyme activity such as that which occurs in the hepatic microsomal systems for drug metabolism.

Animals↗