Pathology of midgut gland-cells of Penaeus monodon postlarvae after Leucaena leucocephala feeding

Abstract

Leucaena leucocephala, one of the promising feed sources in aquaculture of tropical regions, induces drastic pathological alterations in the midgut gland ( = hepatopancreas) cells of Penaeus monodon postlarvae. After 28 d feedng on a formulated diet containing Leucaena wlth natural mimosine content, the most severely affected cell type is the R-cell, followed by F-cells B-cells are only rarely pathologically changed. Artificial reduction of mimosine content prior to &et formulation results in less severe signs of pathology. The course of cell injury suggests that the nucleus is one of the primary targets of Leucaena toxicity to midgut gland-cells. Pathology starts, in all cell types, with alterations In the fibrillar component of the nucleolus accompanied by fading of the nucleoplasm and cytoplasm. Thereafter, the heterochromatin of the cell nucleus is step-by-step decondensed. Obviously, structural components of the nucleolus organizer region are changed, thus leadlng to a cessation of rRNA synthesis and eventually of ribosome production. The simultaneous decondensation of the nuclear heterochromatin may cause disturbances of cell function and finally lead to cell lysis. Prawns may die of septicemia when high numbers of midgut gland epithelium cells are destroyed. From the cytoplasmic organelles, only the mitochondria and F-cell dictyosomes display disorders in the early stages of pathology. These alterations are probably nucleus-independent. The darkening of the mitochondrial matrix may be caused by depletion of oxidative phosphorylation due to enzyme inhibition, whereas the vacuolization of the Golgi-cisternae in F-cells is interpreted as cytoskeleton injury.