The present study examined alterations in the protein pattern and histopathology of the hepatopancreas and gills of Macrobrachium malcolmsonii following exposure to Sevin, the commercial grade of carbaryl (1-Naphthylmethyl carbamate) pesticide. Juvenile prawns were exposed to sub-lethal concentrations 5.15 microg l(-1), 7.73 microg l(-1) and 15.47 microg l(-1) of carbaryl for 21 days. Samples were obtained from the hepatopancreas and gills of prawns. The concentration of buffer soluble protein in tissues of test prawns was significantly (p<2.5%) lower than the control. This suggests that proteins were utilized to generate energy in order to withstand carbaryl induced toxic stress. Polypeptide bands of different molecular mass (150-10 kDa) in tissues of test prawns stained less intensely than those in control. This indicates that carbaryl toxicity caused protein degradation in tissues of test prawns. The histology of the hepatopancreas and gills showed few marked pathological changes in prawns exposed to carbaryl. These include rupture of the basal laminae, abnormal infiltration/aggregation of hemocytes in the interstitial sinus of the hepatopancreas and in the hemocoelic space of gill lamellae, fused gill lamellae and necrosis like appearance both in the tubules of the hepatopancreas and gill lamellae. The structural alterations observed in the hepatopancreas and gills of the prawns suggest that carbaryl caused tissue damage in M. malcolmsonii. Protein degradation is a phenomenon in damaging tissues, and thus, under such condition the hepatopancreas and gills of test prawns would not perform their vital functions, which in turn ultimately affect the survival and growth of M. malcolmsonii. The changes noted in protein and histology of test prawns can be taken as biomarkers for monitoring pesticide pollution in aquatic environments. Since this species of prawn is a nutritious delicacy to human being, monitoring aquatic pollution by carbaryl is warranted.