Ein, Zoot V4, 1900, bp. ERIE HISTOPATHOLOGICAL CHANGES UNDER LEAD EXPOSURE IN THE LIVER OF A FRESH WATER FISH, CHANNA PUNCTATUS (BLOCH) (Received May 4, 1990; Accepted October 20, 1990) B.S, Jha Department of Zoology, L.N. Mithila University, Darbhanga-846 004, India ‘The prescnt investigation deals with the hictopathological changes in the liver of the fish, Channa punctatus, following exposnre to a sublethal concentration (141.7 mg/1) of lead nitrate for 45 days. The important altcrations include liver cord disarzay, vacuolation of the cyto- plasm of hepatocytes, rupture of cell-membrane, necrosis of nuclei and clumping of the necrosed nuclei, Corresponding with heptic cellular damage, a significant (P< 0.05) dcurease in the HSI (from 1.69 + 0109 to 1.39 4 0.08) wae also recorded. Possible Feasous are discussed, The heavy metals pollute the aquatic onviro: Ament and induc ber of changes in fishes!~, They show stron fesuee ey ee 1g attraction to biological tissues and have become a subject of biological interest due to their bioaccumulative, immutable and non biodegradable properties. Much has been i i animals including fishes’-*, However, Published on metal toxicity to aquatic our knowledge about tl Pathological effect; s ‘ve poison", offects even at a tow dose”, to Indian Of lead. a cumulative poicom meagre It is in this pore freshwater fiche aro relatively 7 Fopective that th the histopathologi ‘ © present stu 3 ihe histopathological changes in the liver ofthe ti Sy "was undertaken to asses yosure ISM, Channa punctatus, under lead nitrateEffect of Lead on Liver of C, punctatus tu MATERIALS AND METHODS The fish were collected from the local fish ponds and were washed with 0.1% KMinO, solution to avoid any dermal infection. Healthy fish of 13.8, em (0.927) length and 29.2 g. (4:2.79) weight were selected and acclimatized to laboratory condi- tions in 40-litre glass aquaria for a fortnight. The fish were adjusted to natural photoperi- od and ambient temperature. Every day they were fed with goat liver ad (ibium. A batch of 40 fish was transferred each to the contrel and experimental tanks Equal volume of water was maintained in both the control and experimental tanks The experimental lot of fish was exposed to a sublethal concentration (141.77 mg/l) of lead nitrate for a period of 45 days. The lead salt was changed at every 96 hours. At the end of expo- sure period, the fish of both control and experimental groups were dissected in Ringer's saline, the liver was quickly removed and fixed in aqueous Bouin's, Carnoy and 10% neutral formalin fixatives tor optimum period of fixation. After proper washing, dehydration and cleansing, the tissues were embeddet paraffin wax. Serial sections af 6 tm were cut and stained with Heldenhain’s tron hemratuxylin~ eosin. RESULTS The most conspicuous pathological changee aro liver cord disarray, vacuo- lation of the cytoplasm of hepatocytes rupture of cell-membrane, blood-vessels and goneral necroeis (Figs. 1 and 2). The most severe and marked damage is ohserved at the level of nuclei which become highly necrosed and show clumping at intervals (rig.3). The damage in the central area is more severe than the perilobular area. Correspon- ding with hepatic cellular damage, a significant (P < 0.05) decrease in HSI (trom 7.69-£0.09 to 1.39 + 0.,8; Mean + SD) has also been recorded, DISCUSSION Similar to the present observations splitting, swelling, liquefaction, hypertrophy, Necrosis and vacuolation of the hapatic cells of several fishes exposed to phenolic ‘compounds have been reported by many workers’**. Kumar and Pant’ also reported ‘similar observations on liver of Puntius conchonius exposed to acute toxic levels of zinc and copper, Ram anu Sathyanesan® lave repo.ted hepatocyte degeneration, nuclearJha 118 } ntrol liver 2 1-Structure of Co: Figs, 1-3 of hepatocytes ‘owing clumping karyolysis of nuclei (x 400 ), eated liver sh c (x 400 ), 3-7, of the necrosed and marked vacu nuclei, ‘lationEffect of Lead on Liver of (:. fumelatus [to pyknosis and fatty necrosis in the liver of Channa punctatus treated with similar pesticide, chronically. However, contrary to the present findings, they have reported tumour formation close to the blood sinusoid, This difference may be due to the difference in the nature of toxicant and the period of expocure. The lesions developed in liver might be due to the cumulative action of lead nitrate and due to the direct access of the toxic blood to the nearby cellular structures of liver through the ruptured blood vessels. ACKNOWLEDGEMENTS The author is thankful to of Zoology, ratory faci Prof. S, Pandey, Head of the Department N. Mithila University, Darbhanga, for constant encouragement and labo- facilities and to the Directors of CDRI and ITRC Lucknow for library s. REFERENCES ‘Chauhan, T.P.S. Prakash, MM. Gupla, KC. and Verman, BR. (L9/¥). Comp. Physiol. Ecol, 4:59, Shatfi, S.A. (1979) Toxicology Letters, 31919. Saxena, O.P. (1981). Cur. Sci., 50 735. sae Shrivastava, A. and Pandoy, A.K. (1906), Zid, Js Zool, 14: 37. Doudoroff, P., Anderson, B.G., Burdick, G. Galtsoft, P.S., Hart, W.B., Patrick, R,, Strong. E, K., Surber, E, W, and Vonhorn, W.M. (1951). Sewage Ind. Wastes; 281 1380, Pant, SC., Kumar. , and Khanna, S.S. (1980) Comp. Physiol, Ecol, 5 146. Saxena, 0.P. and Parashari, A. (1983). J. Environ, Biol,, 4 : 91, Bengeri, K. V. and Patil, H.S. (1984), Bull, Pure & Appl. Seiyy 3A: 9 Coughlan, D. J., Gloss, S.P. and Kubota, J. (1986). Wate, Air and Soil Pole, 28: 265. 10. Sastry, K. 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