Several organotin compounds namely trimethyltin, triphenyltin and tributyltin are commonly used in plastic production, as pesticides and antifoulant paints. Among these compounds, triphenyltin is the least studied agent, especially its effects on histological system. This report describes in great details on the long term, low dose effects of triphenyltin hydroxide (TPTH) on the liver and kidneys of catfish (hybrid between Clarias gariepinus and Clarias macrocephalus ). Newly hatched catfish, approximately 1 month old, of both sexes were exposed to 1 and 3 ppb of TPTH for the period of 8 months. At the end of each month interval fish were killed by repid decapitation. Liver and kidneys were removed and processed for light and electron microscopic studies. For electron microscopic examination. Five stages of cellular change from normal to irreversibly injuried cells were used to describe the reaction patterns in liver and renal tubules produced by organotin. These were: Stage 1. Cells in the control preparation. The tubular structures were maintained throughout the period of the experiment. Stage 2. The characteristic of this stage was dilatation of the cisternae of the endoplasmic reticulum and of the nuclear envelope. Other organelles appeared to be normal. Stage 3. This stage comprised of the changes in Stage 2 plus contraction of the mitochondria. Stage 4. In addition to the changes of stage 3, This stage is characterized by swelling of some mitochondria. Stage 5. In addition to the changes seen in Stage 4,, there were numerousinterruptions in the continuity of the plasma membrane. All mitochondria were swollen. Some were ruptured and contained flocculent densities. Light microscopic findings of the liver revealed a variety of changes from mild to severe i.e. cellular swelling, fat droplet accumulation and necrosis. At both concentrations of TPTH used all of those changes were seen. The severity of changes were dependent either on the concentration of TPTH or on the duration of the examination. By electron microscopy, ultrastructure change of liver began to be observed earlier and composed of proliferation endoplasmic reticulum, nuclear envelope and ER dilated, parallel array and concentric lamella of ER cisternae, mitochondria contraction and swelling. Hepatocyte changes of stage 2 began at 2 months after exposure to 1 ppb TPTH and stage 3, 4 and final stage (stage 5) were seen in 4-6 month and at 7 month, most of hepatocyte injury are in stage 5. Focal cytoplasmic necrosis were seen. This similar alteration began earlier in 3 ppb TPTH treated liver. By light microscopy, kidney of this hybrid showed hydropic degeneration of the first and second proximal tubules at 3 ppb TPTH began at 1 month up to 7 month and more earlier than 1 ppb TPTH treated group which started at 3 month up to the end of experiment

hyaline droplets accumulation were first seen in the first proximal cells at the dose of 3 ppb TPTH in 3 month up to 7 month and more abundant than the lower dose that started at 1 month

tubular necrosis was first begun at 5 month up to 7 month of the 3 ppb TPTH group that showed more severely necrosis than the 1 ppb TPTH treated kidney. TPTH lppb. Tubules exhibiting stages 1-5 degeneration could be identified at the end of respectively various experimental intervals. Stages 2 and 3 were seen at the end of 1 and 3 months. Stage 4 was observed at the end of 5 months and stage 5 from 6 months onward but only in a few cells. TPTH 3 ppb. Again, various stages of degeneration from 1 to 5 could be identified. However, these changes occurred earlier. Stages 2 and 3 were seen just at the end of 1 month. By the end of 4 months, changes characteristic of stages 4 and 5 were seen. The degree of damage obviously more severe than in the group given TPTH 1 ppb. Conclusions. Chronic exposure of the catfish liver and renal tubules to TPTH an organotin compound a well known SH-group blocking agent, produced a similar sequence of ultrastructural changes to that observed in experiments involving a disturbance in cell membrane function. It is concluded that disturbance of the cell membrane may be either by inhibition of its function or by direct attack. The destruction of the SH-groups of the plasma membrane in the present study produced destruction of the cell membrane.