Date of Award:

5-1-1969

Document Type:

Dissertation

Degree Name:

Doctor of Philosophy (PhD)

Department:

Biology

Department name when degree awarded

Entomology (Insect Toxicology)

Committee Chair(s)

William A. Brindley

Committee

William A. Brindley

Committee

Datus M. Hammond

Committee

D. W. Davis

Committee

L. C. Ellis

Committee

J. T. Blake

Abstract

Median lethal concentration (LC50) parathion doses for 5th and 6th instar wax moth larvae (Galleria mellonella) were 152.309 ± 1.644 and 163.982 ± 1.115 microgram parathion per gram larval medium, respectively. Pretreatment of 6th instar larvae with sublethal doses of chlorcyclizine dihydrochloride, aminopyrine, or phenobarbital in the larval medium reduced the mortality due to parathion. Chlorcyclizine (0.5 gram/100 gram larval medium) decreased the toxicity due to the LC50 parathion dose for 6th instar larvae to 32, 20, 4, and 10 per cent mortality, when fed for 2, 4, 8, or 10 days, respectively. The 2-day pretreatment protection lasted only 24 hours whereas the longer times protected the larvae for up to 72 hours. Phenobarbital was somewhat more effective than aminopyrine. Both, however, offered protection against parathion if the time of exposure was increased. The data suggest that the protective effect is neither immediate nor permanent and that it depends upon the dosage and length of drug pretreatment. Chlorcyclizine, phenobarbital, or aminopyrine have been shown to induce microsomal drug metabolizing enzymes in mammals. Therefore, studies on wax moth gut homogenates were conducted before and after chlorcyclizine or phenobarbital treatment to 6th and 7th instar larvae to determine if the drugs induced microsomal enzymes or increased protein concentrations. In addition to total protein, activities of O-ethyl-O-p-nitrophenyl phenylphosphorothioate-detoxication (EPN-detoxication), p-nitroanisole O-demethylase, and Nicotinamide adenine dinucleotide phosphate-neotetrazolium reductase (NADPH2-NT-reductase) were determined. The present study revealed that chlorcyclizine or phenobarbital feeding caused induction of EPN-detoxication, p-nitroanisole O-demethylation, and NADPH2-neotetrazolium-reductase. The drugs also affected the protein content of the gut. EPN-detoxication and O-demethylase activities were induced to their maximum level after the fourth day of drug treatment and then declined. NADPH2-NT-reductase activity continued to increase to its maximum after the sixth day of chlorcyclizine exposure and then declined among 8-day treated larvae. Phenobarbital treated 6th instar larvae had the maximum NADPH2-NT-reductase activity after 4 days of pretreatment. Induction of EPN-detoxication and O-demethylase due to chlorcyclizine or phenobarbital was much less in 7th instar larvae than in the 6th instar larvae. On the other hand, NADPH2-NT-reductase activity was more significantly induced in 7th instar than 6th instar wax moth larvae. The data also suggested that inducing effect was dependent on (1) days of drug treatment, (2) type of the drug, and (3) the enzyme studied. These results, when considered with respect to the findings of others, indicate that drugs which induce enzymes in mammals may also induce enzymes in insects.

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