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The effects of juvenile hormone on mitrochondrial [sic] metabolism in the Indian meal moth, Plodia interpunctella (Hubner)

Author: Donald Elliott Firstenberg
Publisher: 1975.
Dissertation: Thesis (Ph. D.)--University of Florida, 1975.
Edition/Format:   Thesis/dissertation : Thesis/dissertation : Manuscript   Archival Material : EnglishView all editions and formats
Database:WorldCat
Summary:
Investigation into the effects of synthetic H. cecropia juvenile hormone (methyl-10, ll-epoxy-7-ethyl-3, 11-dime thy 1- trans 2, trans 6-tridecadienoate) on mitochondrial metabolism in larvae of the Indian Meal moth, Plodia interpunctel la (Hiibner) revealed that juvenile hormone affected citrate cycle oxidations, electron transport, heme synthesis and cytochrome synthesis. Juvenile hormone inhibited all NAD-linked  Read more...
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Additional Physical Format: Online version:
Firstenberg, Donald Elliott, 1946-
Effects of juvenile hormone on mitrochondrial [sic] metabolism in the Indian meal moth, Plodia interpunctella (Hubner)
1975
(OCoLC)821011663
Material Type: Thesis/dissertation, Manuscript
Document Type: Book, Archival Material
All Authors / Contributors: Donald Elliott Firstenberg
OCLC Number: 38046388
Notes: Typescript.
Vita.
Description: x, 109 leaves : ill. ; 28 cm.
Responsibility: by Donald Elliott Firstenburg.

Abstract:

Investigation into the effects of synthetic H. cecropia juvenile hormone (methyl-10, ll-epoxy-7-ethyl-3, 11-dime thy 1- trans 2, trans 6-tridecadienoate) on mitochondrial metabolism in larvae of the Indian Meal moth, Plodia interpunctel la (Hiibner) revealed that juvenile hormone affected citrate cycle oxidations, electron transport, heme synthesis and cytochrome synthesis. Juvenile hormone inhibited all NAD-linked oxidations in the citrate cycle of isolated mitochondria. However, the f lavoprotein-linked oxidation of a-glycerophosphate was not affected by juvenile hormone while succinate oxidation was stimulated. NADH oxidation in vitro by aged and uncoupled mitochondria was also inhibited by juvenile hormone. Experiments using ferricyanide to artificially accept electrons from NADH dehydrogenase indicated that juvenile hormone prevented electron transport at the nonheme iron level of complex I in the electron transport chain. Further experiments revealed that the inhibition was noncompetitive. These results indicated that the inhibition of NAD-linked oxidations in the citrate cycle was due to the effects of juvenile hormone in the electron transport chain. Inhibition of NAD-linked substrate oxidations in the citrate cycle could result in an increase in cytochrome synthesis by a mechanism involving synthesis of malats from pyruvate and the reversal of reactions in the citrate cycle. Inclusion of juvenile hormone in the diet of the larvae resulted in an increase in the concentration of mitochondrial cytochrome. However, this stimulation was dependent upon some factor associated with the larval molt. The concentration of juvenile hormone at the beginning of an instar affects the mitochondrial cytochrome concentration within that instar. The results of the cytochrome analyses indicated that the hypothetical mechanism of control of cytochrome synthesis had a second level of control associated with the molt. Since cytochromes are composed of heme and apoprotein, the effects of juvenile hormone on the synthesis of just the heme portion of the molecule was investigated. Inclusion of juvenile hormone in the diet stimulated de novo heme synthesis, but this effect was immediate and therefore presumably direct. The data suggest a metabolic mechanism for juvenile hormone controlling insect growth and development by determining the maximum capacity of cellular energy production. Energy production levels may be limited by the concentration of electron transport chain components.

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