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.
Val. xm. No.2. 2011
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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