CHANGES IN CATECHOLAMINE LEVELS IN THE GUT AND FRASS OF THE CORN-EARWORM, HELICOVERPA-ZEA INDUCED BY DIETARY L-AZETIDINE-2-CARBOXYLIC ACID

Citation
Bm. Okotkotber et Oa. Adeyeye, CHANGES IN CATECHOLAMINE LEVELS IN THE GUT AND FRASS OF THE CORN-EARWORM, HELICOVERPA-ZEA INDUCED BY DIETARY L-AZETIDINE-2-CARBOXYLIC ACID, Insect biochemistry and molecular biology, 27(5), 1997, pp. 431-438
Citations number
26
Categorie Soggetti
Entomology,Biology
ISSN journal
09651748
Volume
27
Issue
5
Year of publication
1997
Pages
431 - 438
Database
ISI
SICI code
0965-1748(1997)27:5<431:CICLIT>2.0.ZU;2-L
Abstract
Several studies have shown that a plant-derived lower homologue of pro line, L-azetidine-2- carboxylic acid (AZC), fed to larvae of the corn earworm, Helicoverpa tea, induces toxicity leading to an array of deve lopmental defects including incomplete pupal cuticular sclerotization or tanning. Destabilized cuticular tanning has recently been shown to be correlated with a deficiency in a hemolymph catecholamine, N-beta-a lanyldopamine (NBAD) (Okot-Kotber and Adeyeye, 1995). Analysis of gut and frass catecholamine contents has revealed that an AZC-supplemented diet induces a two-fold increase in the excretion of dopamine (DA) an d beta-alanine. Also, more 3,4-dihydroxyphenylalanine (DOPA) was excre ted in this group than in the controls, although overall, less DOPA wa s detected than DA in both cases. Four catechols of unknown structure, designated FC1, FC2, FC3 and FC4 according to their relative chromato graphic retention times, were found in frass extracts,vith relatively higher levels in the AZC-treated larvae than in the controls. Three of these; FC1, FC2 and FC3 were also found in the diet, but FC4 was dete cted only in frass. Gut tissue catecholamines were much higher (by app roximately 100 fold) than found in the frass. Approximately two-fold h igher DOPA and seven-fold higher DA concentrations were detected in th e guts of pupae with incomplete tanning, that had developed from AZC-t reated larvae, compared to the controls. It appears, therefore, that t he deficiency in NBAD observed in the hemolymph of AZC-fed larvae is l argely caused by a slower rate of acylation of DA into NBAD, which res ults in the accumulation of DA in the gut. The data suggests that ther e is a defective beta-alanyldopamine synthetase in the AZC-treated ins ects rather than an increased catabolism of NBAD. (C) 1997 Elsevier Sc ience Ltd.