Mohamed, A. ElbeaJy; .t Bl . .. ISSN 1110-7219 127

EFFECT OF AMMONIA TOXICITY ON BIOCHEMICAL PARAMETERS AND TISSUE ALTERATIONS OF

NILE TILAPIA (0. NILOTICUS)

Mohamed, A. Elbealy; Eman, Zahran and Viola, H. Zaki Dept of lnternal medicine, mfecUous and nsh dlseases .

Fac. of vet . m~d. Mansoura u niversity

ABSTRACT

The effects of expOSf/res to sublethal ammonia concentrations on 0, l 1iloticus lVere

determined with respect to hlstology. The experiments were conducted for four weeks and with four different ammonJa concen trations / . 7, 8. 7, 17.4 and 34.8 mg / L total

ammonJa nItrogen (TAN).

Fish exposed to dJfferent ammonIa concenlrauons bad a sIgnIficant Increase In al­

most the bIochemIcal parameters recorded. In addition. p athologJc alteraUons were displayed in lh e g1l1s, lJver and kidney .

Keyw0rd6: Ammonia - Nile tJiapia fo. ntJotJcus) . Biochemical parameters - His­topaliJoJogy.

INTRODUCTION O. n Hoticus considered one of the most im­

portant aquacul ture species In Egypt. With tn ­

creas ing the demands for fish production: in­

tensification of tUapla culture has been

adopted. Fish reared under such conditions

are often exposed to various suessors. Ammo­

n(a Is one of those s lressors whiCh represent

a grea t slgnUlcance for its capabU lty to coun­

teract the Improved performance of the culti­

va ted s peCies (AJaJJJ. 2008). Un-Ionized form

of ammon ia (UIA) Is the most toxic form to

aqu aUc organisms as It can readUy dHfuse

through cell .mem branes and Is h ighly soluble.

In liquids (Smart 1978). S ub lethal UlA con­

centra tions are known to cause behav:loral ,

physiOlOgical , and h is tologic changes 1n ns h

and have several pOSSible mechanIsms of tox·

Icity. These mech~lsrns include cauSing wa·

MlU16oura, V.t. Med. J. (J2? - 14Q)

ter and mineral Imbalan ces. decreasing blood

pH. altering cardiac function , and affecting

ATP levels (Tomas8o 1994). Usual ly stress

a cts by Inhibiting certalJl metabolic process

(We1a ct al., 1981), Increase of AS'! (Aspar ­

tate aminotransferase) and ALT (Alanine ami ·

notransferase ) activities IS Ind ica tive of some

degree of tissue necros is (Nlle •• et al. , 1998)

or of Jiver dysfunction and leakage of these

enzymes [rom inj u red tissue to to blood (Salah

El-Deen, 1999). It's clearly observed that to·

tal protein and Lmm u noglobu lln was Ln hlblt ·

ed due to chronic exposure to s tressor. Hlgh

concentrations or increased durations of ex ·

posure to UIA may al so Increase s usceptlbJHty

to bacterial. fungal . and paraS itic d(seases

s uch as columnar ls saproiegn iosis (Carballo

et aI. 1996), and trlchodlnlasls as well as

higher mortalit ies.

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MohlHD.ed, A. EJbealy; et aI ...

Histological changes Include gtll hyperpla­

sia, hemorrhage. and telangiectasla. as well

as degenerative cbanges In the kidneys and

liver (TbW'stou. et aI .• 1978; Daud. et a1.,

1988).

Because of the possible effects on fish

heallli and survlval, ammonia accumulation

Is of particular concern in aquaculture. Therefore, the alms of this s tudy were to de­

termine (he effect of different UIA concentra­

tions on some biochemical parameter wuh

emphasiS on t issue alterations In Nne TUapla.

MATERIALS AND METHODS ruh and aper1mcntal condition : ApparenU y heaJthy O. nUottcus wtth an av­

erage body weight of 120 ± 3 .6 g were ob­

tained from private farm at AJhamol. Kafr EI ­

sheikh Governorate. Fish were kept in full

glass aquaria measuring (100 x: 50 x 30 em)

and maJntained In aerated de-chlortnated

fresh water at 25 .t 20 e for 14 days prtor to

use In experiments . The tested fi sh were kept

for four weeks. Ammonia was s uppUed [rom

stock tank.s. Ammonium chJoride (NH4CI) was used as ammonia source . The ammonia con­

centrations were 1.7,8.7. 17.4 and 34.8 mg /

L TAN. The water (dechlorinated tap) In the

tanks was changed once every other day in

order to avoid the accumulation of toXlc me­

tabolites and decaying Cood. Fish were fed

with commercial diet (Alhamol ratton fac tory,

Kafer Elshtakh) contatnlng 30% crude protein at a daily rate of 3% of their body weight dur­Ing the experiment. Dally maintenance and cleaning of the fish tank of faeces was done .

The lotal ammonia concentrations (Compact photometer PF-ll , MACHEREY-NAOEL, sup­

phed wtth Ammonium 200 NANOCOLOR®

MIUl60UIS., Vet. Med. J_

128

tube tes ts kit - Germany), temperature (mer­

cury thermometer) and pH (electrochemically

USing a Radlo pH meter model 62) values were

measured daily in each tank. Pre-determined

total ammonIa concent,.atlon. pH and temper­

ature were used to UIA concentraUons ac­cording to Emmerson, et al .• (l976) (tablel):

Detennlnatton of TAN.

Determination of water temperature.

Determination of water pH.

FInding the multiplication factor using

water temperature and pH

Multiplying the TAN and the obtained

factor will result In UIA In mg/L.

2.2. B10chemJcal measurements: Fish were anesthetIzed with benzocaine

(200 mg/ L) and the blood samples were col­lected from the cauda] vein wit hout anti ­

coagulant for serum separatJon to be used In

measurLng blood chemIstry.

Blood samples of the tested fish were col­

lected at the time Interval of 0-7~14- 21 and

28 days. Activities of fAST). (AL T), total pro­

tein, albumln and globulLn were analyzed In

the blood samples by uSing CommercIal dtag~

nostic kits produced by Human GeseUschaft

fUr Blochemlca und diagnostic mbH. Germa­ny.

2.3. Hlatopathololllcal analysis for OWs, U- and kUlney oamplea:

o uts. liver and kJdney were fixed In Bou Ln's solution (Robert.. 2001) for hlstO!Oglcal ex­amination, dehydrated through graded series of ethanol solutions, cleared In xylene , and

embedded In paraffin. Five to six fJ.m thick sections were prepared from paraffin blocks

wtth a rotary microtome and were then

Vol. XIII, No.2, 2011

Mohamed. A. EJbesly; et aJ ...

stained with Hematoxylin and Eosin . Hlsto­

pathologlcal changes were examined under a

Ught microscope. MorphologlcaJ techniques

were performed accordJng to Karan, et a1.,

(1998).

RESULTS Biochemical analytic In..,.tlgatlon

The blochemJcal parameters of O.nUoUcus

exposed to sublethaJ concentraUon of 0 .1 mgl L of VIA under different exposure tune as

shown in Table (2) . Total protein showed a

slgntOcant Increase (P <0.05) (5.5 and 5 g/dl

at days 21 and 28 res pectively) from the con­

trol at day 0 (3.9 g/ dl). WhUe the gJobuJLns

showed Significance Increase (P < 0.05) (3.5 gl dl a t day 2 1) from the control at day a (2.1).

Tllapla showed a slgnlllcant Increase (P <

0 .05) in the concentraUon of ALT (36 and 45

VL) and AST (59 and 76 UL at days 21 aod

28 respectively) from the control at day 0 122

and 26).

The biochemical parameters of 0 . n11ou­

cus exposed to sublethaJ concentration of 0.5

mg/L of UIA under different exposure time

show in Table (3).Total protein showed a slg­

ntOcant Increase IP < 0.051 16.4 ,6.2.6.6 and

6.3 g/dl at days 7,14.21 and 28 respective ­

ly) from the control at day 0 (5. 4 g/dJ) .

WhUe the globulins showed significance In­

crease (P < 0.05) (5.3, 5.8 and 5.3 g/dl at

days 14, 21 and 28) from the control at day 0

(3.5). TUapla showed a s ignificant lncrease

(P<O.05) in the concentraUon of ALT (56,59,58

and 56 UL) and AST (98.105.112 and 123 UL

at days 7 ,14.21 and 28 respectively) from

the control at day 0(18 and 35). Whlle aJbu ­

min showed moderate decrease (P<0. 05) (l .5 ,

0.9, 1.0 and 1.01 g/dL at days 7 . 14,21 and

Mansoura, Vet. Med. J.

1;l9

28 respectively) from the control at day 0

( 1.9).

The bJochemicaJ parameters of O.nlloticus

exposed to sublethal concentration of 1.0

mg/L of UlA under dIfferent exposure time

show in Table (4). Total protein showed a

significant Increase (P<0.051 (8 and 8.3g/dl

at days 7 and 14 respec ltvely) from the

control at day 0 (5.4 g/d!) . While the globu­

lins showed significance Increase (P<0.05)

(7.1, 7.6 and 4 .1 g / dl at days 7. 14 and

21) from the control at day 0 (2.5) . TUapla

showed a s ignificant !ncrease (P<0.05) In the

concentration of AL T (59, 78 and 86 UL) and

AST (129 , 148 and 170 UL at days 7. 14 and

12 respecUvely) from the control at day 0 (30

and 48). WhIle albumin showed moderate

decrease (P<0.05) (0.9 g/dL at day 7) and

sever decrease (0 .7 and 0.3 g/dl at days 14

and 21 respectively) from the conlrol at

day 0 (2.0) .

The biochemical parameters of O,nUolicus

exposed to sublethaJ concenuaUon of 2.0 mgl

L of VIA under different exposure Bme s how

In Table (5). Total protein showed a significant

Increase IP < 0.05) (8.2 and 6.6 g/dl at days

7and 14 respectively) from the control at day

o (4.3 g/ dl). Whlle the globulins showed s lg­

nlflcance Increase IP < 0.05) (7.9 and 8.4 g/dl

at days 7 and 14 respectively) from the con­

trol at day 0 12.4). TUapla showed a signifi­

cant lncrease (P < 0.05) In the concentrat ion

of ALT (95 and 104 UL) and AST (165 and

187 UL at days 7 and 14 respectively) from

the control at day 0 (26 and 45) .WhUe albu­

min showed sever decrease (0.3 and 0.2 g/dJ

at days 7and 14 respectively) from the coo­

trol a t day 0 (1.9).

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Mohamed, A. E/bWy; ct al ...

IllatopathologlC8l alteration:

The histopathologic observattons for both

control and dtfferent sublethal ammonia cone.

exposed O,nUoucus with representative at ta­

ble (6) and tmages of the tissues displayed In ·

figs. Control IndJvlduaJs did not show any

histopathological changes In the tissues of

O.nilotlcus examined by the Hght m1croscope. Most differences between control and different

sublethal ammonia conc. matnly were found

in kidney. liver and giUs. In :the gills of O. nl­

loLicus shOwing moderate to sever prolifera­

tion of secondary lamellae besides congestion

of branchial branches at 1.0 mg/L UIA Fig. (lJ

and shoWing sever congestion of secondary la­

mellae With found cel1tnnltratJng their stroma

a( 2.0 mg/L UlA Fig. (2), Liver lesions consist­

ed of slight or minimal hemosiderosis and

nearly normal Hepatic architecture with s light

congestion of blood vessels at 0.5 mg/L UtA.

Fig. (3). and h emorrhage replacing necrotic

hepatocyted (lytic necrosis) at 1.0 mg/L UIA

Fig. (4) and narrowing of hepatic cords be­

sides sever congesuon of blood vessels at 2. 0

mg/ L UlA Fig. (5) .Whlle kidney of fish ex­

posed to sub lethal ammonia conc. displayed

slight or minimal congestion and nearly nor­

mal arch itecture at 0.5 mg/L UIA Fig. (6), and

necrotic renal tubular eplthel1um besides vac­

uolation of renal tubular epithelium a t 0.1

mg/L UlA Fig. (7) , and chronic lnfiammatory

ceUs in tnterstitial tissue With Hypercellularlty

in mesanglal cells Fig. (8).

RESULTS AND DISCUSSION ArrunonJa Is toXlc not only to Osh but also

to all aquatic anlmals especially In pond

aquaculture at low concentrations of dis­

solved oxygen. The toxic levels of unionized

ammonia for short term exposure usually are

MlUl6Oura. Vet. Jled. J.

190

repor ted to lie between 0 .6 and 2 mgIL. The

role of blood enzymes In monitoring and de­

tecting stress or disease has led to a growtng

concern in using them as biochemical Indica­

tors to Lrace envLconmental pollutants WU­• \lam (1997) and AdbAm <t aI. (1997, 1999).

Data of O. nlloucus in this study revealed

that the actMties of most serum enzymes

tAL T and AST) were significantly elevated in

response to exposure to ammonia experi­

ment's concentraUons. with a pOSitive correla­

tion between concentration and enzyme level

elevation, as AST Increased by more than 3

fold in comparison with zero time at 2 mg IL

UIA. The relation between fish IntOxication

and changes in both enzymes was earlier

studied by several authors. In a laboratory

controlled experIment. KraJuovtc"-OzreUc~

and KraJnovtc"-zreUc" (1992) recorded ele­

vated activities of ALT In the plasma of adult

gray mullets (Mugilavratus RIsso) exposed to

acute concentrations of CC14, phenol and cya­

nide. Similarly. Wteeer and Hlnterleitner (1980) reported increased aCtivities of ALT In

serum of rainbow trout In response to sewage

loading In flvers. Increased level of AST and

AL T 1n common carp after exposure to ammo·

rua may be due to the loss of Kreb's cycle wtth

the result that these enzymes compensate by

providing alpha ketoglutarate (Chatty. ct aI ••

1980 and Salah EI-DeCIl, 1999). The ob­

served changes could be also due to general­

Jzed organ system fallure due to the effect of

ammonia. Daa and yappBD (2004) found

that the fingerlings of (mrlgal . Clrrhlnus mrt ·

gala) showed Significant Increased AL T actiVI­

ty in the serum. braJ.n and gill at 4mgl L TAN.

The AST actiVity in the serum, brain and gLH

Vol XIII, No.2, 2011

Mohamed. A. Elbealy; et al ...

aJsa became significant at 8 mg/L TAN. The

Increase In the AL T and AST activity in the

serum may be attributable to the process of

either deamlnaUon or transam1naUon due to

the excess nttrogen In the organIsm. Total

protein levels were also affected by anunonla. exposure, whereas gIobulln increased slgnlfi­

canUy after 7 days of exposure to 2 mg /L UIA

but at the contrary. albumin was decreased

from 1.9±O. 1 g/dL to O.3±O,02 g/dL after 7

days of exposure to 2 rug /L VIA. The de­

crease recorded 1.0 total protein values may be

due to the severity of Ute s tressor . which

causes osmotic imbalance. Alkahem, et aI.,

(199B) attributed the reduction [n the pro­

teins to Its conversion to fuliUltng an In­

creased energy demand by nsh to cope with

detrimental conditions imposed by a taxi·

cant.

Concerning the effects of chrome ammonta

exposure on o. nlloUcus With respect to tis­

sue hi stology PersonLe Ruyett et aI .• (1998)

have s hown that NH3 entered fish Within 15

mtn exposure. The first effects of contami­nants us ually accurate cellular and subcellu­

lar levels, starUng from the first hour of con­

tamination (Metcalfe, 1998). Fl1s (1968).

reported that chronic ammonia exposure

might damage gills . Bver and kidney, which

may pred ispose the 6sh to numerous Infec·

Uons. In the present study, the Lmportant hiS ·

topathologlcal effects of chronic ammonia ex·

posure on the gills were proliferation of secondary lameUae and hyperemIa on epithe­lIum especially at 2.0 mg/L UlA. Gills are a

well known target organs In fish. being the first to react to unfavorable envlronmental

conditions. SeveraJ authors have reported

slmtlarlttes rations on the gills of different fish

MB.DJIOura. Vet. Mcd. J.

lSI

speCies exposed to ammonia (Mallatt, 1985).

Redner and Stickney (1979), observed aneu­rysms, lamellar capillar congestion and hem­

orrhaging of Ttlapla aureus a n er acute (2.4

mg/ L UIA) and chIonlc (O.43-0.53 mg/L UtA)

exposure. Larmoyeux and Ptper (1973) de ­

termined aneurysms and fused lamella of rainbow trout (Sal mogalrdnerl) g.lll epItheLium

cells. Furlhermore. Kirk and Lewta (1993) re­

ported that the gills of the ralnbow trout ex-­

posed to 0.1 mg/L ammonia for 2 h exhibited deformation of the lamellae. Salin and Wllllot

(199l) observed tha t Siberian sturgeon (Ac(·

pencerbaert) (270 g) exposed to more than 60

mg/L of ammonia reveal a modification of the

epIthelium of the secondary lamellae and the

base of the filament Js s lightly turgescen t.

S1mUar results were also confirmed by Mltch·

ell and Cech (l98S) with channel catfish (Ic·

talurus punctatus). MaU.It, et aI .• (1986) with

common carp (Cyprlnus carpio) and Cardoso,

ct aI., (1996) With J.....ophlo stlurus alexandrl.

Necrotic hepatocytes and hydropiC degen · eraUons on the liver we re observed mainly a t

1.0 and 2 .0 mg/ L UlA, respecUveJy. As liver

being the main organ of various key metabolic

pathways, toXlc effects of ammonia usually

appear primarily In the liver. Ammonia can be

carrIed by the hepatic portal vein to the li ver

as a nu trient and cnter liver metabolic path­

ways (Kucuk, 1999). The most frequently en­

countered types of degenerative changes are those of hydropic degeneraUon. cloudy swell­

ing, vacuolIZation and focal necrOSiS on fish exposed to different kinds of contaminants

(Hawkes. 1980 and Hinton and Lauren, 1990). W8J8brot. et ai .• (1993) observed

clear Signs of LLver pathology tn g1Ithead sea­bream (Sparusauratus) after 20 days of expo-

Vol. xm. No.:I. :lOll

Mohamed. A. Elbesly; et Bl ...

sure to 13 mg/L TAN (0.7 mg/L UIA).

In the present study, kidney tissues dis­

played necrotic renal tubular epithelium and

hypercellularHy In mesanglal cells after being

exposed to dlfferent concentrations (0.5, 1.0

and 2.0 mg/LJ of VIA concentrations. The kId­

ney Is a one of the major organs of the toxic

effects. Thurston, et aI .• (1978) observed hy­

dropiC degeneration In the kidney of elltt throat trout after exposure to 0.34 mg/L UIA

and Larmoyeu:z and Piper (1978) determined

glomeruli congestion in kidneys of rainbow

trout after exposure to 0.8 mg/L VIA.

MaD80ura, Vet Med. J.

192

In conclusion, it's has been demonstrat­

ed that biochemical parameters of adult

O. nUoUcus were affected under sub le­thal exposure to ammonia tOXiCity. There­fore. it Is very tmportant that this water

quality stressor (arnmorua) be monitored

regularly and level should be controlled

through var10us management practlces

when necessary. If fish Js kept at the sub­

lethal value of ammonla, it can compro­

mlse its well-being by JeopardiZing its

Vol. XIII. No.2. 2011

Mobamed, A. EI1H:aly; ct aI ...

Table (1): Fraction of un-ionlzed ammonia in aqueous solutioll at dtfferent pH values and temperatures . Calculated from data in Emmerson, Cl 8 1.

( 1975)

Table (2)~.''8iochemica l parameters of examined adu lts OnilOlicus (n=28) after 0, 7 14, 21 and 28 days of exposure to 0.1 mgfL unionized ammonia concentration.

~ Total Albumin Globulins ALT

Protein (gldL) (g/dL) (U/L) Days (gldL)

0

7

14

2 1

28

3.9 ± 1. 8 ± 2. 1 ± 22 ±

0.2 1 0. 1 0.18 1.8

4.1 ± 1.7 ± 2.4 ± 28 ± 0.3 1 0.9 0.2 1.9

4.9 ± 1.8 ± 3.1 ± 35 ±

0.33 0.)2 0.22 2.5

5.5 ± 2.0 ± 3.5 ± 36 ±

0.39' 0.18 0.2 1'" 3.0*

5.0 ± 1.6 ± 3.4 , 45 ±

0.4* 0.1 0.2 3.1* Results are mean values ± standard error of three replicates.

'" Statistically significant (p < 0.05) differences . "'* Highly statistically significant (p < 0.005) differences.

AST (U/L)

26 ±

1.8

35 ± 2.1

37 ±

2.6

59 ± 3.9"

76 ±

5.8**'

133

MIW6Ount. Vc~ Med. J . Vol. XlII, No.2. 2011

Mohamed. A. Elbealy; et aI ...

Table (3): Biochemical parameters of ex.amined adults o.niloticus (n=28) after 0, 7 14, 21 and 28 days of exposure to 0.5 mgIL unionized ammonia concentration

I~ Total

Albumin Globulins ALT AST Protein

Days (g/dL) (gldL) (gldL) (UlL) (UIL)

0 5.4 ± 1.9 ± 3.5 ± 18 ± 35 ±

0.35 0.11 0.19 1.2 0.22

6.4 ± 1.5 ± 4.9 ± 56 ± 98 ± 7

0.42· 0.1 • 0.28 3.9* 0.75"

14 6.2 ± 0.9 ± 5.3 ± 59 ± 105 ±

0.43'" 0.05 '" 0.37· 5.0· 0.8S·· 6.8 i 1.0 ole 5.8 ± 58 ± 11 2 ±

21 0.48- 0.06 " 0.42'" 4.7- 9.S"

28 6.3 ± 1.01 + 5.3 ± 56 ± 123 ±

0.49" 0.08 • 0.4 1" 4.9· 10.2" Results are mean values ± standard error o f three replicates .

• Stali srica lly significa m (p < 0.05) d ifferences .

•• Highly statistically significant (p < 0.005) difTerences.

T a ble (4): Biochemica l pa rameters of examined adullS o.niloticus (0""28) after 0, 7 14, 2 1 and 28 days of exposure to 1.0 mgIL unioni zed ammonia concentration.

I~ Total

AJbumin Globulins Days

Protein (gldL) (gldL)

(gldL)

0 4.5 ± 2.0 ± 2.5 ±

0.33 0. 17 0. 15

8.0 ± 0.9 ± 7.1 ± 7

0.56" 0.07 * 0.54*

14 8.3 ± 0.7 + 7.6 ±

0.6' 0.04** 0.6*

4.4 :i: 0.3 ± 4.1 ± 2 1

0.33 0.0 11 ** 0.28*

28 , , .. .. --

Results nre mean values ± standard error of three rephcates . .. Stati sticall y sig.njficont (p < 0.05) differences . .. Highl y statisricall y signi ficant (p < 0.005) differences.

J Fisbes di d not survived to this point

ALT AST (U/L) (UIL)

30 ± 48 ±

2.4 3.1

59 ± 129 ±

4.7* 10.2**

78 ± 148 ± 6.1* 11.2**

86 ± 170 ± 5.4* 15**

" ,

-- --

194

MlUl6oura, Vet Med. J. Val. XIII, No.3. 3011

Mohamed, A. I!.lbeaIy; .t oJ ...

Table (5): Biochemical parameters of exami ned adul lS O.nilOlicus (n=28) after 0, 7 14, 21 and 28 days of exposure to 2.0 mglL unionized ammonia concentration

Parameter Total PTotein Albumin Globulins (gldL) (gldL) (gldL)

Days

0 4.3 ± 1.9 ± 2.4 ±

0.32 0.1 0. 17

7 8.2 ± 0.3 ± 7.9 ±

0.7"'" 0.02 ...... 0.52**

14 8.6 ± 0.2 ± 8.4 +

o.n " O.O lu 0.6 1 II<*"

21 , , , .. .. ..

28 ; ; J .. .. ..

Resull s a(e mean values ± standard error of three replicates .

.. Statistically signifi cant (p < 0.05) di fferences .

.. Highly statistically significant (p < 0.005) differences. J Fishe.s did not survived to this point

ALT AST

(U/L ) (UIL)

26 ± 45 ±

2.0 3.3

95 ± 165 ±

8.0"· 11"'*

104 ± 187 ,

8.7 .... J4.5 u , ; .. .. , ; .. ..

T able (6): Histopathologic observations fo r both contro l and different sublethal ULA cone (mglL) exposed 0 niloticus '

Tiss ue and histopathology Control 0.1 0.5 1.0 2.0

Hyperemia · · + ++ ++

Gills proliferation of secondary lamellae · · · + ++ Congestion of branchial branches · · · + +++

Liver bydropic degeneration · · + ++ +++

necroti c nepatocyred · · · + ++

Kjdney necrotic renal tubular epithelium · · · + ++

hypercellularity in mesangial ce lls · · + ++ +++

195

MlUJ6oura, Vet. Met!. 01. Vol. XIII, No. :J, :JOIl

Mohamed. A. Elbealy; .t aI ...

Figure 1: Section of gUls of O.nUotlcus

exposed to 1.0 mg/ L UlA

shOwing moderate to severe

prol1feratton of secondary la­

mellae (arrow) and conges.

Uan of branchial branches

(arrow head) .

Figure 2: SecUon of gills of O.nUotlcus

exposed to 2.0 mg/ L UIA

show1.ng sever congestion of

secondary lamellae (arrow)

with Round cell Infiltrating

their stroma (thick arrow).

Man60ura. Vet. Med. J.

196

FtJUrC S: Section of Uver of O.nfloticus

exposed to 0.5 mg/ L UlA

showtng ~lIght or mLnlmal

hemosIderosis {acrow).and

nearly normal Hepatlc archI­

tecture wtth slight conges­

tion of blood vesse1s (arrow

head).

FIgure 4: Section of liver of O,ntloUcus

exposed to 1.0 mg/L UlA

shOwing hemorrhage necmt­

Ie hepatocyted (lytiC necro­

siS).

Vol. xm. No. Z. ZOl1

Mohamed, A. E/beaJy; et aI ...

P'1gure 5: SecUon of lIver of O.n11oucus aposed . to 2 .0 mg/ L UIA

showing replacing narrowing

of hepaUc cords (thln arrow)

and sever conge.stlon of

blood vessels (thick arrow).

FIgure 8; Section of kidney of

O.ntloUcu$ exposed to 0 .5

mg/L UIA shOWing slight or

minimal congestion and

nearly . normal architecture

(arrow).

MIHlAoura, Vet. Met! J.

197

Ftgure 7: Sectlon of kidney of

O .nlloUc us exposed to 1.0

mg/ J.. UlA showing necrotic renal tubular epltheUum

(tnln arrow) and vaculatlon

of renal tubular epithelium

(thick arrow).

Ftgure 8: Section of kidney of

O.nUoticus exposed to 1.0

mg/ L UIA shOWing chronic

inflammatory ceUs In Inter ·

sUtiai Ussue (thin arrow)

with HyperceUularUy In me·

sangJai cells (lhlck arrow).

Val. XIII. No.:J, :JOIl

MohlUD.ed. A. Elbealy: .t al ...

health.

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·1 .' 'wl <.! .r-~ <.! ••

Man6oura. Vet. Met!. J.

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