Olusola A. ADEYEYE, B. Moses OKOT-KOTBER
Department of Biological Sciences, Duquesne University,
Pittsburgh, PA 15282, USA.
Feeding com earworm larvae on a diet supplemented with L-azetidine-2-carboxylic acid AZC results in cuticular lesions and significantly reduced hemolymph levels of dopamine and N-ß-alanyidopamine (NBAD) by at least two- to three-fold. The levels of N-acetyidopamine (NADA) are reduced to a lesser extent. The correlation of cuticular lesions and tanning/sclerotization failure with deficiency in hemolymph NBAD suggests that L-azetidine-2-carboxylic acid has an inhibitory influence on the mechanisms involved in dopamine metabolism, and/or NBAD synthesis, transport or catabolism. Further studies reveal that catecholamine levels are much higher (approx. 100-fold) in the gut than in the frass; there is a two-fold increase in the excretion of dopamine and ß-alanine by larvae that fed on AZC-supplemented diet. The levels of DOPA and dopamine present in the guts of pupae with tanning failure are, respectively, two- and seven-fold the levels found in control pupae. These results indicate that the deficiency in hemolymph NBAD of larvae that fed on AZC- fortified diets is not caused by inoreased catabolism of NBAD. Rather, it is likely due to a reduction in the acylation of dopamine to NBAD. Thus, the cuticular lesions that are caused by feeding on AZC very likely are caused by a defective 13- alanyidopamine synthetase.