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Microsomal metabolism of DDT is more active in housefly strains showing resistance to DDT. Susceptible as well as resistant strains produce two fairly polar metabolites in vitro (metabolites 2 and 3), and a water-soluble metabolite (metabolite 1). Resistance to DDT in one of the strains studied (Fe) is apparently brought about by the production of large amounts of metabolite 1 in vivo and not by DDT-dehydrochlorination. DDT-dehydrochlorination can explain resistance per se in two strains (P2/sel and DS), but additional degrees of resistance are given in the P2/sel strain by microsomal enzyme activity. The two strains (Fc and P2/sel) which employ microsomal oxidative enzymes show induction of microsomal enzymes upon DDT pre-treatment. This enzyme induction by DDT is accompanied by an increase in the rate of incorporation of C14-labelled uracil into total RNA. It is suggested that cross-resistance between DDT and pyrethrum (with associated resistance to naphthalene) may be related to microsomal enzyme induction. Zusammenfassung BIOCHEMISCHE UNTERSUCHUNGEN AN DER INSEKTIZID-RESISTENZ VON MUSCA DOMESTICA Der mikrosomale DDT-Stoffwechsel ist starker bei Hausfliegenarten, die Resistenz gegen DDT aufweisen. Sowohl die empfindlichen wie die widerstandsfahigen Arten bringen in vitro zwei annahernd polare Metabolyte (Metabolyt 2 und 3) und einen wasserloslichen Metabolyten hervor (Metabolyt 1). Die Resistenz gegen DDT bei einem der untersuchten Stamme (Fe) wird vermutlich durch das Zustandekommen grosser Mengen von Metabolyt 1 in vivo und nicht durch DDT-Dehydrochlorination verursacht. Die DDT-Dehydrochlorination an sich erklart die Resistenz bei zwei Stammen, P2/sel und DS, doch wird die Resistenz bei P2/sel noch durch mikrosomale Enzymtatigkeit erhoht. Die Stamme Fe und P2/sel, bei denen mikrosomale Oxydationsenzyme zur Wirkung kommen, weisen nach DDT-Vorbehandlung eine Induktion der mikrosomalen Enzyme auf. Gleichlaufend mit dieser Induktion der Enzyme durch DDT erfolgt eine grossere Aufnahme von C14-markiertem Uracyl in die RNS. Es wird vermutet, das die “cross-resistance” zwischen DDT und Pyrethrum (und gleichzeitiger Resistenz gegen Naphthalin) in Zusammenhang mit der mikrosomalen Enzyminduktion stehen konnte.

Excerpt To the editor: Superficial soft tissue infection is usually treated on an outpatient basis by incision and drainage with or without accompanying antibiotic therapy. Many investigators have ...

A NUMBER of otherwise pharmacologically inactive compounds are known to prolong sleep induced by barbiturates in mammals1. The most widely investigated of these is ‘SKF 525A’ (2-diethylaminoethyl 2,2-diphenylpentanoate), which prolongs the action of barbiturates and other drugs by inhibiting liver microsomal enzymes which degrade a wide variety of drugs1. When applied to insects, ‘SKF 525A’ synergizes pyrethroid insecticides and antagonizes the toxicity of the organophosphorus poison, malathion2. In these respects, ‘SKF 525A’ mimics the action of commonly used insecticide synergists such as piperonyl butoxide2. Although piperonyl butoxide and other chemically related synergists have been included in insecticide formulations for many years, their effects on drug activity in mammals have not been examined. In this communication the effects of two insecticide synergists on the hypnotic action of barbiturates are described.

As part of a wider investigation into the causes of insecticide resistance in a strain of house flies (Musca domestica), which show resistance to both DDT and the pyrethroids1, specifically labelled (14C)-pyrethrin I has been used to examine penetration of this insecticide into these insects.