Biomedical subjects
Publications and source records attributed to M J Thompson.
An ecdysone 20-hydroxylase enzyme system that converts alpha-ecdysone to 20-hydroxyecdysone was prepared from the midgut of the tobacco hornworm prepupa. This partially purified enzyme is NADPH dependent and is localized in the mitochondrial fraction of the midgut tissue.
Several C11 to C15 amides and amines that disrupt growth in certain insects showed high nematicidal activity in direct contact tests. Two amides and 9 amines killed Panagrellus at 5-10 ppm. Of these, 1 amide and 3 amines killed Meloidogyne larvae at 20 ppm.
26-Hydroxyecdysone is the predominant molting hormone in 24- to 44-hour-old embryonated tobacco hornworm eggs, accounting for approximately 80% of the ecdysones present at this stage of development. This molting hormone was previously shown to be the major ecdysone present in 48- to 64-hour-old embryonated eggs of this insect. During both of these periods of embryonic development in the hornworm 20-hydroxyecdysone is a minor component, in contrast to its presence as the major ecdysone in the hornworm during certain stages of post-embryonic development.
The expression of resistance to u.v. irradiation mediated by R factor R46 has been studied in strains deficient in excision repair and recombination repair. The R factor protected wild-type bacteria and also wild-type cells in which repair had been inhibited by the substitution of bromouracil for chromosomal thymine. It increased the survival of strains defective in the endonucleolytic (uvr), repolymerizing (pol) and joining (lig) stages of the excision repair process. Recombination deficient bacteria mutant at the recB or recC loci were protected by R46, but the R factor had little effect on the survival of a recA strain or a recA recB double mutant. R46 increased the survival of cells that had been treated with chloramphenicol before u.v. irradiation, but did not protect cultures treated with chloramphenciol after irradiation. It is concluded that R46 confers resistance to the lethal effects of u.v. irradiation by a mechanism that is independent of excision repair. Resistance appears to be mediated by an inducible gene product, which is possibly a nuclease and dependent on a functional host recA gene for expression.
As a possible more rapid test of lymphocyte reactivity to phytohaemagglutinin (PHA) than the standard estimation of thymidine uptake after 72 hours (T72), uridine uptake after 24 hours (U24) was studied in a total of 96 individuals. No reliable correlation between the two estimations was found in 29 outpatients showing a wide range of reactivity to PHA nor in 30 healthy control subjects nor in 16 pregnant subjects. Conflicting reports have appeared in the literature as to whether lymphocyte reactivity to PHA is normal, depressed or enhanced in pregnancy. Our group of pregnant subjects showed a significant depression of both U24 (P less than 0-01) and T72 (P less than 0-02) results as compared to normal female controls. Cultures of semipurified lymphocytes prepared by gradient centrifugation on a further 21 normal control subjects showed no better correlation between U24 and T72 results than the above unpurified-leucocyte cultures.
Makisterone A is the predominant ecdysone in the 96 +/- 4-hour-old embryo of the large milkweed bug and it is the first molting hormone with a C-24 alkyl substituent of the side chain to be isolated and identified from an insect. In addition, unknown compounds that may represent other C28 ecdysones were detected in very low concentrations. The milkweed bug could well possess a biosynthetic-metabolic pathway for C28 molting hormones instead of or in addition to known pathways for the C27 ecdysones.
Radiolabeled sterols, 14C-cholesterol, 14C-cholestanol, 3H-stigmasterol, 3H-stigmastanol, and 3H-sitosterol, were fed to larvae of the Mexican bean beetle, Epilachna varivestis Mulsant, bu coating soybean leaves. Free sterol and sterol ester fractions from treated insects were isolated and analyzed, and in each case nearly 30% or more of total radiolabeled sterols retained by the insect were found in the sterol ester fraction after 8 days. delta5-Dietary sterols were readily reduced to stanols, and C29-stanols thus produced were dealkylated to cholestanol. Significant amounts of labeled lathosterol were formed from delta5-C29 sterols; little, if any, radiolabeled cholesterol was detected in insects fed either of the labeled delta5-phytosterols, stigmasterol or sitosterol. Sterol metabolism of this insect thus differs considerably from that found for most phytophagous insects.
Several new branched and straight chain secondary and tertiary amines were shown to have inhibitive effects upon development and metamorphosis and the delta-24-sterol reductase system in larvae of the tobacco hornworm similar to those previously observed with a number of azasteroids. Certain of the amines which are related structurally to compounds with juvenile hormone activity in insects also blocked development and metamorphosis in three other species of insects. These compounds are lethal or inhibit development in all larval stages and thus differ in action from compounds with juvenile hormone activity where the principal effect is to block the penultimate or ultimate molt.
A number of azasteroids and other nitrogen containing steroids with a modified nucleus or side chain were prepared and tested for their inhibitory effects on the growth and development of several species of insects. Structure-activity studies showed that compounds with a structurally related steroid nucleus and side chain were approximately equal in inhibitory activity for a particular species. The replacement of the tertiary amino group in the side chain of the 5beta-steroid with other nitrogen substituents, such as nitro, cyano, acetylamino, or a quaternary ammonium salt, resulted in a considerable loss of inhibitive activity in the tobacco hornworm or the yellowfever mosquito. However, certain modifications of the azasteroid nucleus resulted in compounds that still retained high biological activity. As a result, a compound was synthesized that lacked the A and B rings of the steroid nucleus and that inhibited insect growth, molting, and metamorphosis and the delta24-sterol reductase enzyme system of the tobacco hornworm.
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