Metabolic fate of [14C]endrin in bluegill fish

Bluegill absorbed 85% of 1 ppb of endrin from water within 48 hr under static exposure conditions. The absorbed radiocarbon was eliminated linearly with a half-life of about 4 weeks. Analyses of eliminated radioactivity revealed only conjugated metabolites. 12-anti-Hydroxyendrin and 12-syn-hydroxyendrin were tentatively identified by cochromatography using thin-layer chromatography/autoradiography and gas chromatography. These metabolites were also present as conjugates in the fish organs. Seventy-three percent of the absorbed radioactivity recovered from fish extracts was in the form of unchanged endrin.     

Melanin biosynthesis in Pyricularia oryzae: Site of tricyclazole inhibition and pathogenicity of melanin-deficient mutants

Tricyclazole (5-methyl-1,2,4-triazolo[3,4-b]benzothiazole) inhibits melanin synthesis in Pyricularia oryzae at concentrations less than 0.01 μg/ml. The primary site of inhibition in the biosynthetic pathway occurs between scytalone and vermelone. Accumulation of several metabolites derived from melanin precursors along branch pathways is associated with inhibition of melanin biosynthesis. At low tricyclazole concentrations (0.01–1 μg/ml), predominant accumulation of 2-hydroxyjuglone and 3,4-dihydro-3,4,8-trihydroxy-1-(2H)-naphthalenone (3,4,8-DTN) occurs as a result of the primary block between 1,3,8-trihydroxynaphthalene and vermelone. As the concentration of tricyclazole is increased from 1 to 10 μg/ml, flaviolin accumulation is markedly enhanced, whereas that of 3,4,8-DTN and 3,4-dihydro-4,8-dihydroxy-1-(2H)-naphthalenone is depressed, indicating possible secondary sites of inhibition in the main and branch pathways. Five melanin-deficient mutants of P. oryzae that phenotypically resemble the tricyclazole-treated wild-type strain were nonpathogenic or rarely infected two rice varieties. Three of the mutants studied were genetically defective in the melanin biosynthetic pathway at the site blocked by tricyclazole in the wild type. The wild-type strain converted both scytalone and vermelone to melanin; whereas the three mutants and the tricyclazole-treated wild type converted only vermelone to melanin. The data suggest a relationship between melanin biosynthesis and pathogenicity in P. oryzae.     

Comparative inhibition of the juvenile hormone esterases from Trichoplusia ni,Tenebrio molitor, and Musca domestica

Twenty-seven compounds were screened as potential inhibitors of juvenile hormone esterases. Of these compounds O-ethyl-S-phenyl phosphoramidothiolate provided the best inhibition for the cabbage looper, Trichoplusia ni (Hubner), and the yellow mealworm, Tenebrio molitor L., while the juvenile hormone esterases of the house fly, Musca domestica L., were best inhibited by a juvenoid carbamate (1-(m-phenoxy-N-ethyl carbamate)-3,7-dimethyl-7-methoxy-2E-octene). The inhibition patterns of T. ni and T. molitor are similar, while those of M. domestica are relatively different. Further studies on the juvenile hormone and α-napthyl acetate esterases of T. ni showed that they could be differentially inhibited. Diisopropyl phosphorofluoridate and an alkyl trifluoromethyl ketone selectively inhibit the hydrolysis of α-naphthyl acetate and juvenile hormone, respectively, while O-ethyl-S-phenyl phosporamidothiolate inhibits both enzymes. The juvenile hormone esterases of T. ni also appear to be unique enzymes that are selective for juvenile-hormone-like molecules. The in vivo inhibition of T. ni juvenile hormone esterases by O-ethyl-S-phenyl phosphoramidothiolate slows the in vivo hydrolysis of juvenile hormone and results in delayed pupation and malformed larvae that resemble larval-pupal intermediates. Thus, the esterases involved in juvenile hormone metabolism appear to be important in juvenile hormone regulation.     

Physiological actions of dinoterb,a phenol derivative: 2. Effects on isolated plant mitochondria and chloroplasts

Dinoterb, a contact herbicide, affects respiration and photosynthesis of mitochondria and chloroplasts. On mitochondria, at low concentrations, it acts as an uncoupler of oxidative phosphorylation; at higher concentrations, it inhibits the electron transport chains, probably before cytochrome c. On chloroplasts, dinoterb has a stimulatory effect on oxygen uptake in the reduced dichlorophenol-indophenol→methyl viologen couple; however, it is also an inhibitor of the Hill reaction and its site of inhibition is located before plastoquinone, near photosystem II.     

Total hemolytic complement values in normal and diseased dog populations

The optimum conditions for handling and storage of canine sera for total hemolytic complement assays were assessed. Sera from 113 normal dogs and 217 clinical admissions to the University of Pennsylvania Veterinary Hospital were assayed for total hemolytic complement levels. Normal sera had a mean value of 185 CH50 units. Sera from animals with systemic lupus erythematosus and hemorrhagic gastroenteritis, had significantly lower mean levels of complement than the normal group. Sera from dogs with generalized demodectic mange, tumors, various inflammatory diseases, hypothyroidism, seborrhea, and rheumatoid arthritis had values significantly higher than the normal population.     

Experimental infection of calves with two strains of bovine virus diarrhoea virus: certain immunological reactions

Certain immunological responses of 4-6 month old calves experimentally inoculated with either cytopathic or non-cytopathic bovine virus diarrhoea virus (BVDV) were compared with those of uninfected control calves. The tests used to demonstrate the immunological responses were the transformation of lymphocytes by PHA mitogen, the percentage of lymphocytes with surface immunoglobulin, and the antibody titres induced by an intravenous inoculation of killed Brucella abortus. There were no significant differences between the two groups of calves and therefore, the mild experimental disease produced by BVDV did not appear to affect adversely the immunological response.     

Precocene II metabolism: Comparative in vivo studies among several species of insects,and structure elucidation of two major metabolites

Several species of insects, exhibiting varying responsiveness to the juvenile hormone antagonist precocene II (6,7-dimethoxy-2,2-dimethylchromene), were challenged topically with a tritiated preparation of the title compound. Metabolism of [³H]precocene II was subsequently examined by withdrawing hemolymph samples from treated animals at appropriate time intervals and characterizing the extractable radiolabel chromatographically. Quantitative (or qualitative) differences observed between the respective metabolic profiles were found not correlative with specimen sensitivity to precocene. Production of two heretofore unreported metabolites, identified by spectral and chemical means as O-β-glucosides of 6- and 7-monodemethylated precocene II, was demonstrated in both sensitive and insensitive species. No evidence for the presence of a hemolymphborne, biologically effective “activated metabolite” produced in vivo by precocene-susceptible insects could be found. The latter finding may well argue for in situ bioactivation of precocene at the target tissue(s) by these sensitive insects.     

In vitro metabolism of EPN and EPNO in susceptible and resistant strains of house flies

EPN is twice as toxic as EPNO to house flies from both the Diazinon-resistant strain and the susceptible strain. EPN and EPNO are also eight times more toxic to the susceptible than the resistant strain. This is due to the ability of the resistant strain to metabolize these compounds to a greater extent. Metabolism by the glutathione S-transferases present in the 100,000g supernatant is more extensive than that by the NADPH-dependent microsomal mixed-function oxidases. The glutathione S-transferases are the major route of metabolism for EPN and appear to be the principal mechanism conferring resistance. EPN was metabolized by the microsomal fraction via oxidative desulfuration to the oxygen analog, EPNO, and by oxidative dearylation to p-nitrophenol. EPNO was metabolized by the same system to p-nitrophenol and desethyl EPNO as well as to an unknown metabolite. The soluble fraction metabolized EPN to p-nitrophenol, S-(p-nitrophenyl)glutathione, O-ethyl phenylphosphonothioic acid, and S-(O-ethyl phenylphosphonothionyl)glutathione. The identification of the latter conjugate demonstrates a new type of metabolite of organophosphorus compounds. EPNO was metabolized by the soluble fraction to p-nitrophenol and S-(p-nitrophenyl)glutathione.     

The effect of some Frescon analogs on the aquatic snail,Lymnaea stagnalis: II. Correlation of neurotoxicity to Molluscicidal effectiveness

Although the molluscicide Frescon is a strong neurotoxin to the Lymnaea stagnalis central nervous system in vitro, it is probable that the exposure of the whole animal to this molluscicide fails to result in central nervous system abnormalities: Frescon does not appear to reach the brain in sufficient quantity to disrupt its normal activity. However, only those Frescon analogs found to be neurotoxic were molluscicidal, suggesting some related mode, if not site, of action. Frescon and its analogs may act by affecting excitable tissues other than the nervous system (e.g., the snail musculature) by altering certain functional and/or structural membrane properties.