Tatsuyoshi Sugimoto

Inhibition of chitin biosynthesis by buprofezin analogs in relation to their activity controlling Nilaparvata lugens Stål

Abstract Buprofezin (Applaud, 2-tert-butylimino-3-isopropyl-5-phenyl-3,4,5,6-tetrahydro-2H-1,3,5-thiadiazin-4-one) strongly inhibited the [3H]chitin synthesis from N-acetyl- d -[1-3H]glucosamine in the brown rice planthopper, Nilaparvata lugens Stal. No inhibition was observed for [3H]-labeled protein biosynthesis from [5-3H]glucose or l -[3,5-3H]tyrosine but [3H]-labeled nucleic acid synthesis from [5-3H]glucose was weakly reduced by buprofezin. The lethal activity of buprofezin analogs related well to their inhibitory potency against chitin biosynthesis in N. lugens nymphs.

Inhibition of prostaglandin biosynthesis and oviposition by an insect growth regulator, buprofezin, in Nilaparvata lugens Stål

Abstract Buprofezin (2-tert-butylimino-3-isopropyl-5-phenyl-perhydro-1,3,5-thiadiazin-4-one) strongly suppressed the oviposition of Nilaparvata lugens Stal. An injection of prostaglandin E2 (10 pg/female) did not affect the egg-laying of untreated N. lugens at all, but significantly increased that of buprofezin-treated insects to produce a normal level of oviposition rate. Histological observation showed that the eggs accumulated in ovaries of the buprofezin-treated N. lugens were remarkably eliminated from the body after the prostaglandin E2 injection. [3H]Prostaglandin biosynthesis from [3H]arachidonic acid was also inhibited by 84% in the buprofezin-treated N. lugens female adults. The suppression of insect egg-laying by buprofezin should be attributed to the inhibition of prostaglandin E2 biosynthesis.

Determination of malotilate and its metabolites in plasma and urine

A method for the determination of malotilate (I), the corresponding monocarboxylic acid (II) and its decarboxylated product (III) in plasma is described. Plasma was extracted with chloroform spiked with internal standard. The residue, dissolved in methanol, was chromatographed on a reversed-phase column with a mobile phase of 60% acetonitrile and 1% acetic acid in water. The sensitivity limit for I, II and III was 50, 25 and 100 ng/ml of plasma, respectively. Compound I in the same plasma extract was also analysed by gas chromatography--electron-impact mass spectrometry. The base peaks m/z 160 for I and m/z 162 for internal standard (IV) were monitored; the sensitivity limit for I was 2.5 ng/ml of plasma. The determination of the metabolites of I, II and its conjugate (V), and isopropyl-hydrogen malonate (VI) in urine by high-performance liquid chromatography is also described. The limit of quantification for VI was 2.0 micrograms/ml, and the overall coefficient of variation of VI was 4.7%. The limit of quantification for II in urine was 0.5 micrograms/ml and that for V was 1.0 micrograms/ml as total II (II + V). The overall precision of the method was satisfactory. The method was used to determine plasma and urine concentrations in four dogs orally dosed with 100, 200 or 400 mg of malotilate.