Chronic Exposure to No-Effect Concentration of Diazinon Induced Histological Lesions in Organs of <i>Clarias</i> <i>gariepinus</i>

Abstract

In all parts of the world pesticides have been found in the aquatic ecosystem and scientific evidence has also shown that they can enter the food chain. Diazinon is an organophosphate pesticide, widely used in agriculture to control a wide variety of suckling and leaf eating insects and recently in fish culture to suppress some parasitic diseases; nevertheless, there is little study on its adverse effect on fish. In this study, seventy-two (72) apparently healthy catfish comprising adult and juvenile of both sexes were used to set up triplicate experimental groups of those exposed to culture water alone (control group), fish exposed to pre-determined no-effect concentration (0.405 ppm) of Diazinon (test group). The fish were exposed for 28 days and fish were sacrificed and organs harvested on days 21 and 28 to determine the effect of long-term exposure to diazinon on organ histology. Histological changes observed in diazinon-exposed catfish were hyperplasia and fusion of the gill epithelium, hyperplasia of mucoid producing cells and aggregation of melanin pigment in the skin. Histological lesions were also seen observed in other organs, including severe diffuse cellular swelling and fatty degeneration of the liver, interstitial congestion of the kidney, carbon deposit on the wall of the heart and multifocal haemorrhage. The water quality of the control was not significantly different from that of the test group throughout the experiment. The lesions detected in cells, tissue, or organs represent an integration of cumulative effects of physiological and biochemical stressors. The histological alterations observed in vital organ of fish show that exposure to “no-effect” concentration of diazinon induced structural damage in fish organs and are likely to affect the functionality of the organs. For example, the adverse effect on the gill might disrupt its feeding and oxygen uptake.