Peculiarities of metabolism of the microsporidia Nosema grylli during the intracellular development
A long adaptation of Microsporidia to intracellular development supposes the host-derived ATP dependence of merogony and sporogony stages. To prove this assumption the activities of ten carbohydrate and energy metabolism enzymes were compared in the microsporidia Nosema grylli intracellular stages a...
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Published in | Parazitologija Vol. 36; no. 6; p. 493 |
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Main Authors | , , |
Format | Journal Article |
Language | Russian |
Published |
Russia (Federation)
01.11.2002
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Subjects | |
Online Access | Get more information |
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Summary: | A long adaptation of Microsporidia to intracellular development supposes the host-derived ATP dependence of merogony and sporogony stages. To prove this assumption the activities of ten carbohydrate and energy metabolism enzymes were compared in the microsporidia Nosema grylli intracellular stages and mature spores. This species infects the fat body of crickets Gryllus bimaculatus. We have demonstrated lower activities of glycolytic enzymes, phosphoglucomutase and glucose-6-PhDH in the metabolically active meronts and sporonts than in the dormant mature spores. Low glycolysis level indicates that carbohydrate catabolism is not a principal mechanism of ATP supply in the N. grylli intracellular stages. Furthermore, we have not revealed a preferable expenditure of glycogen in comparison with triglycerides in infected cricket fat bodies. The N. grylli infection causes an equal reduction of glycogen and lipid content approximately in 2-3 times. Microsporidia have not mitochondria, Krebs cycle and electron-transport chain. Therefore they are not able to utilise fat reserves for ATP production. It seems to be proposed that microsporidia consume exogenous ATP which is produced by host cell metabolic system. The N. grylli infection provokes an increase of ATP content and ratio of ATP/ADP concentrations in cricket fat bodies approximately in 4 times. These data indicates a rise of host cell energy metabolism rate during the infection. |
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ISSN: | 0031-1847 |