Biochemical stress responses in tissues of the prawn Macrobrachium malcolmsonii on exposure to endosulfan

This study was conducted to investigate the induction of biochemical stress responses in Macrobrachium malcolmsonii following exposure to endosulfan and to determine the most sensitive parameter of endosulfan-induced stress in this species of prawn. Intermolt juvenile prawns were exposed to three sublethal concentrations of endosulfan (10.6, 16.0, and 32.0 ng/L) for a period of 21 days. Samples were taken from the hemolymph, brain, hepatopancreas, gills, and muscle of respective prawns from each test and control group on 1, 8, 15, and 21 days of exposure. The content of glutathione S-transferase (GST) was found to be higher in test prawns than in controls. This suggests that there was an activation of a mechanism to detoxify endosulfan. However, the toxic effects of endosulfan were not fully neutralized, and, hence, there was evidence of impairments in various biochemical mechanisms. Biphasic alterations were noted in phosphatases and in lactate dehydrogenase (LDH) levels in tissues of rest prawns. The concentration of soluble protein in the hemolymph was found to be elevated, whereas this declined in other tissues of test prawns in comparison to controls. Elevation in the level of total free amino acid and decline in DNA and RNA levels in test prawns were recorded. Endosulfan toxicity resulted in breakdown of various polypeptides in tissues of test prawns. Thus, protein denaturation appeared to be one of the manifested toxic effects of endosulfan. The content of acetylcholinesterase (AchE) declined in test prawns. This reflects the disturbances of basic metabolic activities in test prawns. The grade of endosulfan-induced biochemical stress responses in rest prawns was in the order phosphatases > LDH > GST > protein denaturation > AchE. The present investigation records that endosulfan severely impairs various biochemical and physiological mechanisms in M. malcolmsonii and hence poses a threat to its survival, growth, and maturation. (C) 2001 Academic Press.