TOXICITY OF TAMARIND (Tamarindus indica) SEED HUSK TO Oreochromis niloticus (LINNAEUS 1758) AND Clarias gariepinus (BURCHELL 1822) JUVENILES

Abstract

In the present study, juveniles of Oreochromis niloticus and Clarias gariepinus were exposed to tamarind seed husk powder in other to determine the tamarind seed husk’s toxicity to the species at both acute and chronic exposures. Oreochromis niloticus were exposed to acute concentration of 1.2, 1.4, 1.6, 1.8 and 2.0mg/l of tamarind seed husk powder and chronic doses of 0.02, 0.04, 0.06, 0.08 and 0.10mg/l of tamarind seed husk powder while Clarias gariepinus were exposed to acute concentration of 3.0, 3.5, 4.0, 4.5 and 5.0mg/l of tamarind seed husk powder and chronic doses of 0.05, 0.12, 0.20, 0.30 and 0.42mg/l of tamarind seed husk powder. Both experiments had control that served as reference. Effects of tamarind seed husk powder were measured using behavioral, phytochemical, haematological and histopathological indices. Results of the acute toxicity test showed tamarind seed husk powder was toxic to the species in a dose-dependent manner. The active ingredients and their composition in plant part (Seed husk) as well as 96 hours acute toxicity (LC50) on Oreochromis niloticus and Clarias gariepinus juveniles were investigated. The values of the tamarind seed husk powder established for Oreochromis niloticus and Clarias gariepinus were 1.52mg/l and 3.78mg/l respectively. Data obtained from this investigation were subjected to simple percentages and analysis of variance (ANOVA) at 0.05% level of significance. The phytochemical screening showed that tamarind seed husk contains saponins, steroids, flavonoids, terpernoids, tannins, alkanoids and cardiac glycosides. Most importantly, tamarind seed husk induced hyperactivity at acute level of exposure. Significant (P<0.05) hematological changes observed at both acute and chronic exposure include anaemia, leukocytosis, proteinanaemia and lymphocytosis. Histological changes observed in gills include attenuation and clubbing at the tips of the primary lamellae, mild congestion in the cartilage, gradual degeneration of the primary lamellae, blanketing, rupture with hemorrhages, intense cellular necrosis, blood congestion, oedema, epithelial lifting and hyperplasia of epithelial cell. Changes in liver exposure include mild congestion of the sinusoids, pyknosis of the nuclei, perivascular cuffing around the central vein, aggregation of nuclei, fibrosis, rupture of hepatocytes, disarrangement of hepatic cord, bile pigment disintegration, eosinophilic granules in the cytoplasm and cytoplasmic vacoulation. Changes in the kidney of exposed fish include granular degeneration, hyaline droplets, mild damage of renal tubules, gramerular oedema, cellular hypertrophy, haemorrhages, bacterial colony, fat droplets, vacuum, tuber necrosis and dilation of Bowman;s space. Behavioural responses were excess mucus secretion and apathy, air gulping, loss of balance, barbell deformation, discoloration, fin deformation, erratic swimming behavior and hanging vertically in water column. The study revealed that tamarind seed husk was moderately toxic to Oreochromis niloticus and Clarias gariepinus juveniles and affects behavior, haematology and histology of some vital organs in fish. Plants products - primarily tamarind seed husk is quickly accumulated by aquatic biota and causes adverse effects. Contamination of aquatic environment by toxic plants whether as a consequence of acute or chronic events constitute additional stress for aquatic organisms. Tamarind seed husk accumulation by organisms has resulted in adverse effects ranging from reduced growth, impaired reproduction and death.