8th International Symposium on Tilapia in Aquaculture 2008
1385
EXPERIMENTAL STUDIES ON NICKEL TOXICITY IN NILE
TILAPIA HEALTH
ABOU HADEED, A. H.1, K. M. IBRAHIM1, N. I. EL-SHARKAWY1,
F. M. SALEH SAKR2 AND S. A. ABD EL-HAMED.2
1- Faculty of Vet. Med. Forensic Medicine and Toxicology dept.
2- Central Lab. for Aquaculture Researches (Abbassa)
Abstract
Ths work was planned to investigate the toxic effect of nickel
chloride on health status of widely cultured fresh water fish tilapia
species. one hundred and twenty nile tilapia fish divided into 3
groups; the first group exposed to 1/5 lc50 (7.2 mg/l) of nickel
chloride for one week, the second group exposed to 1/10 lc 50 (3.6
mg/l) of nickel chloride for 8 weeks. the third group left as control.
the results showed respiratory disorder, abnormal swimming
behavior, rapid opercular movements and skin lesion besides white
discoloration of skin. blood parameters of tilapia species exposed to
1/5 lc50 of nickel chloride for one week revealed increase in rbcs
count, decreased hb, mch and wbcs count. tilapia fish which
exposed to 1/10 lc50 for 8 weeks showed increased rbcs count and
hb content and decreased mch and wbcs count. the liver and
kidney functions of tilapia fish exposed to 1/5 lc50 of nickel chloride
for one week and 1/10 lc50 of the same compound for 8 weeks
revealed increased alt and decreased ast and total protein. the
residual analysis of nickel fish tissues exposed to 1/5 lc50 and 1/10
lc50 of nickel chloride revealed increased residues in gills, liver and
muscles in different values depending on the used concentration
and time of exposure. the residue of nickel increased in the liver
more than gills and muscles. the histopathological investigations of
tilapia species exposed to nickel chloride revealed pathological
tissue alterations in the gills, liver, kidney, spleen, intestine. the gills
showed hyperplasia, edema and complete sloughing of the
secondary lamellae. the liver showed congestion of the central vein,
vacuolar degeneration of hepatocytes and periductal fibrosis. the
kidney showed alternative areas of activation and depletion of
hemopoietic elements and condensed glomeruli with edema in
bowaman’s capsule. in the spleen, depletion of large area of
hemopoietic elements and multiple melanomacrophag cells were
encountered while the intestine showed mucus cell metaplasia,
submucosal edema and round cell infiltration. it is concluded that
important trace metals including nickel altered physiological function
results, when one or m0re of these reach sufficiently high
concentration in cells.
INTRODUCTION
Metals are commonly found in the environment, they are present as a natural
elements or as a result of anthropogenic activities in different environmental media
such as air, water and soil, which constitute an important factor of exposure to animals
and human (Louis, 1993). Heavy metals are considered as one of the most important
1386
EXPERIMENTAL STUDIES ON NICKEL TOXICITY IN NILE TILAPIA
factors which affect fish population, reducing their growth, reproduction and/or survival
rate (Mohamed and Saleh, 1996 and Saeed, 2000). Nickel is one of the microelements
which occur in trace amounts in living organisms. It constitutes a potential hazard to
the enviornment media (air, water and soil). This is due to its extensive and wide
spread utilization in various industries, it is a common by-product of electroplating
industries, steel production, metal mining, smelting, refining,ceramic and processing
along with fuel combusation, and waste incineration activities. Effluents that spread to
streams, rivers and lakes may disrupt the integrity of the aquatic environment. Excess
of nickel contamination is a real hazard to aquatic ecosystems due to its persistence
and bioaccumulation (Atchison et al., 1987). In recent years, production of
electroplating factories contains high concentration of heavy metals, including high
concentrations of nickel
(Wong and Wong, 1990 and WHO, 1991) was sharply
increased.
Environmental exposure to nickel occurs through inhalation, ingestion, and
dermal contact. The general population is exposed to high levels of nickel because it is
widely present in air, water, food, and consumer products. The general population is
exposed to nickel in nickel alloys and nickel-plated materials such as coins, steel, and
jewelry, and residual nickel may be found in soaps, fats, and oils (ATSDR 1997). In
aquatic systems nickel is adsorbed on clay particles of organic matter (algae, bacteria)
and invertebrates. Since invertebrates are major food resource for fish, they constitute
an important link in nickel transport chain to fish (Wong et al., 1991).Also it induce
decrease
in body weight of Oreochromis niloticus fish (El-Saieed and Mekawy
2001).Little studies have investigated nickel uptake in fish through aqueous and dietary
exposure. Further research investigating the exposure of fish to dietary nickel which is
needed to elucidate the potential impacts of chronic dietary nickelckexposure on natural
populations of fresh water fish (Ptashynski and Klaverkamp, 2002). Tilapia fish ere
selected as a research fish model because these fish were easily produced and
economically important. Fish are known by their tendency to localize significant
amounts of metals. They absorb metals from water through gills, skin and digestive
tract. Bioconcentration and biomagnificantion for heavy metals were previously
reported by many authors (Saeed, 2000). This study aims to describe the clinical signs,
postmortem lesions and histopathological changes due to nickel toxicity beside
estimation of alteration in hematological, biochemical parameters and bioaccumulation
and distribution of nickel in Nile tilapia organs.
ABOU HADEED, A. H et al.
1387
MATERIALS AND METHODS
Experimental design
A total number of 120 Tilapia fish (Oreochromis niloticus) were divided into 8
groups kept under optimal environmental condition. The groups were treated as
following:
Experiment 1: (short term exposure or acute intoxication)
This group contains 40 fish, divided into two subgroups, one of which kept as
control and the other group exposed to 1/5 LC5 (7.2 mg/L) of nickel chloride for
one week according to WHO (1991).
Experiment 2: (Long term exposure or sub chronic intoxication)
In this experiment 80 tilapia used where 40 of which were kept as control in 4 glass
aquaria and the other fishes were divided into 4 subgroups in 4 glass aquaria
containing 1/10 LC50 (3.6 mg/L) of nickel cholride for 8 weeks. The collected fish in
both acute and sub chronic toxicity were examined clinically using the methods
described by Lucky (1977) and Noga (1996).
II- Laboratory analysis:
a- Hematological investigations
Blood samples were taken from caudal vein of experimental Tilapia (20 fish)
after one week by syringe using heparin as anticoagulat (1000 unit/ml blood), from
both control and nickel exposed groups for acute and (32 fish) for subchronic
intoxication. 8 fish each two weeks (After 2, 4, 6 and 8 week) 0.5 ml blood was
used for determination of different blood parameters (erythroyctic count,
Hemoglobin concentration, leucocytic count ) (Lied et al., 1975).
b- Serum Biochemical analysis
Blood was collected in plain centrifuge tubes; centrifugated at 3000 r.p.m. for
15 minutes for serum separation for determination of serum transaminases and total
protein. Time of collection of serum and number of fish as in hematological
investigations
c- Histopathological examination
Specimens from the liver, spleen, gills, kidney and intestine (12 fish) were
collected from both control and treated fish one week from acute intoxication. The
same samples were taken at 2nd, 4th , 6th, 8th weeks from sub chronic (24 fish)
intoxicated fish for the microscopic changes.
The collected Tissue specimens were fixed in 10% buffered formalin solution.
Then, dehydrated in ascending concentrations of ethyl alchol, embedded in melted
paraffin wax, blocked in hard paraffin, sectioned at 4-5 microns and stained by
hematoxylin and eosin stain according to Carleton et al. (1967).
1388
EXPERIMENTAL STUDIES ON NICKEL TOXICITY IN NILE TILAPIA
d- Residual analysis
Muscle, gills and liver (5 g dry wt for muscle and gills and 1 g for liver) from
twenty eight fish of the control and treated fish after one week and 24 fish for
subchronic were kept frozen at -20ºC till analysis. Nickel was extracted according to
(Analytical Methods For Atomic Absorption spectrophotometry, 1982).
Statistical analysis
The data obtained in this study were statistically analysed using analysis of SPSS
(Independent sample test) according to Snedecor and Cochran (1969) for comparing
the different mean values with Duncan´s multiple range test by Duncan´s.
RESULTS AND DISCUSSION
Nickel compounds are known to be human carcinogens based on sufficient
evidence of carcinogenicity from studies in humans, including epidemiological and
mechanistic information, which indicates a causal relationship between exposure to
nickel compounds and human cancer. The findings of increased risk of cancer in
exposed workers are supported by evidence from experimental animals that shows that
exposure to an assortment of nickel compounds by multiple routes causes malignant
tumors to form at various sites in multiple species of experimental animals (Tenth
Report on Carcinogens 2002).
Clinical signs and post-mortem findings
The short term exposure of the fish to nickel chloride (7.2 mg/l) for one week the
exposed fish showed changes in their behavior as the fish were immobile, gathered
near the bottom and delayed reactions to light and sound. In the group exposed to 1/5
lc50 (3.6 mg/l) of nickel chloride along two months showed respiratory manifestation
characterized by surface swimming and white discoloration of the skin (photo 1) and
gasping. The Post-mortem examination revealed paleness of the gills, and kidney while
congestion in liver and distended gall bladder was apparent. The above-mentioned
clinical signs and post-mortem finding were more severe and prominent in fish exposed
to 1/10 Lc50 (3.6 mg/L) of nickel chloride for two months (photo 2).
The clinical symptoms recorded during our study were manifested by
respiratory disorders in fish exposed to nickel chloride along 2 months especially after
6th and 8th weeks. This could be attributed to the nickel nature as a respiratory toxicant,
causing decrease in arterial oxygen tension, an increase in arterial carbon dioxide
tension and a subsequent respiratory acidosis. The white skin lesion in the present
work is similar to these results observed by El-Saieed and Mekawy (2001). This pattern
ABOU HADEED, A. H et al.
1389
may be attributed to nickel and their water-soluble salts which are potent skin
senstizers induce skin irritation as studied by Menne, et al. (1982).
In the present study, the haemoglobin (Hb) value in fish exposed to 1/5 Lc 50 (7.2
mg/ L) for one week was decrease nonsignificantly and in fish exposed to 1/10 Lc50
(3.6 mg/L) of nickel chloride decrease significantly in 2nd week and increase
th
th
non
th
significantly in 4 , 6 and 8 weeks comparing with control (Table 1).
Table 1. Effect of nickel chloride on heamoglobin, erythrocyte count (RBCs) of Tilapia
fish after exposure to nickel chloride acute and subchronic for 8 weeks (Mean
± SE).
Time of
exposure
No. of
fish
group
Hb g/dl
RBCs counts x 106 µ
control
Acute
1st week
20
7.5±0.06 a
6.3±0.03 a
2nd week
10
7.63±0.32a
6.5±0.05 b
1.26±11.6 a
1.66±23.01 a
4th week
10
7.5±0.31 a
7.66±0.40 a
1.47±10.7 b
2.27±8.83 a
6th week
10
8.06±0.19 a
8.5±0.41 a
1.14±9.06 b
1.61±8.46 a
8th week
10
8.4±0.1 a
9.14±0.49 a
1.69±0.33 a
1.96±11.83 a
Sub
chronic
Sub
chronic
control
Acute
1.193±23.4 a
1.373±62.6 a
Means in the same row carrying different superscript are significant at P<0.05. a :increase, b:decreased
These results agree with that obtained by Sobecka (2001). The decrease of
hemoglobin
may be attributed to the destructive influence of nickel
on the cell
membranes of erythrocytes through binding of the toxicants with immunoglobulins or
through disturbance of the activity of erythrocyte enzymes, especially those responsible
for reduction of glutathione and thiol groups of proteins (Sun et al. 1985). According to
Kleczkowski et al. (1998), the excessive loss of glutathione, increased release of iron to
intracellular spaces, peroxidation, destruction of cell membranes, and release of metal
ions to the surrounding tissues should be attributed to free oxygen radicals. The effect
of the described processes is instability of hemoglobin, structural changes in
erythrocytes and increased susceptibility to hemolysis. Consequently, the pool of the
serum iorn from disintegrating erythrocytes increases,while the iron content in the
spleen decreases. In contrast to our results, Ptashynski and J. F. Klaverkamp (2002)
observed that, concentration of hemoglobin, value was unaffected between control and
treated lake white fish “Coregonus clupeaformis” and lake trout “salvelinus namaycush”
by exposure to nickel in diet 0, 10, 100 and 1000 µg for 10, 51, 104 days.
Agrawal et al. (1979) studied that, colisa fasciatus, a fresh water teleost, were
exposed for 90 hrs to 45 p.p.m nickel sulphate under static test conditions. The
treatment resulted in increase in hemoglobin value, this difference may be due to
variation in dose, and fish species and duration of treatment and time of adimstration.
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EXPERIMENTAL STUDIES ON NICKEL TOXICITY IN NILE TILAPIA
The RBCs count is highly affected by high concentrations and long time of
exposure to nickel. The increase of RBCS count started from the 1st week of exposure
till the end of the exposure time (Table 1).These results agree with that obtained by
Agrawal et al., (1979). This result may be attributed to that nickel induced hypoxia.
These finding are consistent with the mechanism of adenergically stimulated splenic
contraction to release supplemental erythrocytes into the circulatory system to increase
oxygen carrying capacity. This explanation agrees with Perry and Wood (1989).
The calculated blood indices MCH have a particular importance in describing
anemia in most animals (Coles, 1986). The decrease of MCH along the experimental
periods (Table 3) may be attributed to the disturbances in RBC S count and Hb content
and also to the exaggerated disturbances that occurred in both the metabolic and
hemopoietic activities of fish exposed to sublethal concentrations of pollutants (Mousa,
1996).
Table 2. Mean cells hemoglobin, leucocytic count (WBCs) of Tilapia fish after exposure
to nickel chloride either acute 7.2 mg/L (1/5 LC50) for one week or
subchronic 3.6 mg/L (1/10 LC50) for 8weeks (Mean ± SE).
Time of
exposure
No. of
fish
group
MCH (pg/cell)
WBCs counts x 103 µ
control
Acute
1st week
20
51.092±12.34a
38.8±0.519a
2nd week
10
54.49±7.925a
24.31±0.76b
35.00±6.928a
24.66±4.66a
4th week
10
52.55±4.67a
45.22±5.921a
34.66 ±6.35a
25.66±2.96a
6th week
10
70.133±13.39a
40.63±4.184a
36.33±6.64a
24.66±7.7 a
8th week
10
31.87±0.274a
31.6±3.62a
36.33±6.38a
31.33±11.62 a
Sub
chronic
control
Acute
33.66±5.811a
30.33±6.06a
Sub
chronic
Means in the same row carrying different superscript are significant at P<0.05. a :increase, b:decreased
The WBCS count decreased non significantly along the experimental periods
(Table 2). Such pattern agrees with the findings of Agrawal et al. (1979). Leucopenia
may be attributed to the inhibition of white blood cell maturation, their release from
tissue reservoir or occurrence of leucopoenia by an organism as a response to a stress
caused by toxic compounds which associated with allergic reaction (Sobecka 2001).
Moreover, nickel reduced the number of small lymphocytes may be attributed to
hindering of lymphopoiesis, induced by primary or secondary changes in hematopoietic
organs (Agrawal et al. 1979). The results of this work are conflicting with the results of
Nanda and Behera (1996) who found leucocytosis after long exposure of nickel to
catfish. Begeman and Rasteter (1979) noticed changes in some hemato-biochemical
parameters of heteropenustes fossilis (Bloch) after exposure to 40 ppm nickel (NiSO 4.
ABOU HADEED, A. H et al.
1391
6H2O) for 15 days. This contrast may be due to the different dose, or even due to
varied duration of treatment and time of administration.
Transaminases (ALT, AST) enzymes are frequently used to diagnose the
sublethal damage to the different organs as well as liver (Rojik et al., 1983 and
Benedeczky et al., 1984). Our results showed significant increase of the serum ALT
activities along the experiment (Table 3). While the serum AST activities showed non
significant decrease (Table 3). Our result agrees with Sobecka (2001). These change
attributed to the effect of nickel on the liver and kidney cells, which confirmed by our
histopathological study by the action of nickel and following cell damage, the
membranes become permeable and enzyme activity are found in the extra cellular fluid
and serum, so the highest activity of alanine amino transferes was recorded in the
serum of tilapia fish after one week exposure to nickel dissolved in water and in time
ALT, AST values decreased to drop below the value of control and only in the terminal
phase of the experiment it reached a level similar to the control (Sobecka 2001).
Table 3. Some biochemical analysis of Tilapia fish after exposure to nickel chloride
either acute 7.2 mg/L (1/5 LC50) for one week or subchronic 3.6 mg/L (1/10
LC50) for 8weeks (Mean ± SE).
No. of
Time of
exposure
fish
Serum ALT (U/L)
Serum AST (U/L)
Total protein (g/dI)
group
1st week
20
2nd week
10
4th week
10
6th week
10
8th week
10
control
Acute
18.00
±0.32b
Sub
control
Acute
25.40
23.40
±0.51a
±0.37a
chronic
Sub
control
Acute
20.60
2.41
2.10
±0.51a
±0.02a
±0.004a
chronic
Sub
chronic
17.60
22.60
24.30
22.40
2.31
2.19
±0.24b
±0.71a
±0.93a
±0.40a
±0.04a
±0.018a
16.80
20.40
25.40
23.80
2.51
2.21
±0.37
a
16.80
±0.37
a
17.80
±0.20
a
±0.24
a
20.60
±0.40
a
25.60
±0.40
a
±0.51
a
24.40
±0.51
a
27.20
±0.80
a
±0.32
a
21.20
±0.45
a
24.60
±0.68
a
±0.03
a
2.35
±0.02
1.99
a
2.31
±0.03
±0.06a
±0.02a
2.00
a
±0.03a
Means in the same row carrying different superscript are significant at P<0.05. a :increase, b:decreased
The quantitative determination of the total protein in the blood serum gives an
idea about the condition of the liver cells and consequently it is of vulnerable effect in
the diagnosis of the toxicity of fish. In the present study, serum total protein, of the
nickel exposed tilapia fish was non significantly decreased during the exposure period
(Table 3). This could be attributed to either a state of hydration or change in water
1392
EXPERIMENTAL STUDIES ON NICKEL TOXICITY IN NILE TILAPIA
equilibrium of the fish and/or disturbance in the liver protein synthesis. This disagree
with Gopal et al. (1997) who recorded that the exposure of Caprinus carpio to heavy
metal salts (Cu and Ni) at lethal and sublethal concentration induced an increase in
total protein from 2 to 20 hrs and followed by decrease. The difference may be
attributed to dose, or period of exposure.
In the present study the nickel chloride at 7.2 mg/L for one week and 3.6 mg/L
for 2 months showed variable degrees of congestion in the branchial blood vessels (fig.
1) and hyperplasia of secondary lameller epithelial cells (fig. 2 & 3) beside in severe
cases at 8th week complete sloughing of most secondary lamellae was seen. (fig. 4)
These results are coincided with those of obtained by El-Saeed and Mekawy (2001).
Roberts (1978) reported that, the epithelial hyperplasia was known as a protective and
defense mechanism of fish gills against harmful pollutants while sloughing of some
secondary lamellae may be due to the simple response to cellular necrosis. Congestion,
edema and hemorrhage in gill arch may be attributed to increase the permeability of
blood vessel, due to the destruction of cement substance connecting the endothelial
cells leading to escape of protein and consequently decrease the colloidal osmotic
pressure and extravasation of RBCs (Roberts, 1978). The congestion of branchial blood
vessels, may be due to the counter irritation and paralysis of vasoconstrictors of
stimulating vasodiltors (El-Saeed and Mekawy 2001).
The liver showed congestion of central veins and sinusoids (fig. 5), some
hepatocytes suffered from vacuolar degeneration besides inactivation of the pancreatic
acini (fig. 6). Most affected cases showed periductal fibrosis and newly formed bile
ductules (fig. 7 & 8). These results are in agreement with those obtained by El-Saeed
and Mekawy, (2001), The liver showed congestion of central veins and sinusoids (fig.
5), some hepatocytes suffered from vacuolar degeneration besides inactivation of the
pancreatic acini (fig. 6). Most affected cases showed periductal fibrosis and newly
formed bile ductules (fig. 7 & 8). These results are in agreement with those obtained
by El-Saeed and Mekawy, (2001), Ptashynski et al. (2001) and (Sobecka , 2001). The
inactivation of the pancreatic acini and the vacuolar and hydropic degeneration of
hepatocytes may be due to the irritation of toxic metabolites and impairment of
potassium sodium pump that disturb the ion exchange through the cell wall. The
periductal fibrosis and newly formed bile ductules may be due to the persistent of the
toxic effect for long time (sub chronic intoxication) which pointed out by fibrous tissue
proliferation (Atallah et al. 1997).
ABOU HADEED, A. H et al.
1393
The kidney showed severe congestion, focal hemorrhage and hydropic
degeneration of renal tubules epithelium (fig. 9), alternative areas of activation and
depletion of hematopoietic element (fig. 10). Some glomeruli appeared contracted with
edema in the Bowman’s capsule (fig. 11 & 12). On the same side, this pattern agrees
with those obtained by Ptashynski et al., (2002) and Ptashynski et al. (2001). The
congestion and hemorrhage among the renal tubules may be due to increase in the
permeability and subsequently escape of the blood components especially RBCs out
side by diapedesis leading to focal hemorrhage under the influence of toxic metabolites
of nickel. Some glomeruli appeared contracted as a result of the pressure of edematous
fluid, which accumulated in the Bowman’s capsule (Ferguson, 1989). Areas of activation
of hematopoietic elements might be a general response due to the initiation of the
toxicity of nickel. The depletion may be long persistence of the toxic effect. The
hydropic degeneration may be due to the impairment of the electrolytes exchange
between the intracellular and extrcellular fluids (Roberts, 1978).
The spleen showed hyperplasia of melanomacraphages (MMC S) which
increased in number also become darker in color (dark brown) (fig. 13). Large areas of
depletion of hematopoietic elements were encountered (fig. 14). The number, size and
histological appearance of MMCs changed with age, season, state of nutrition and
outigenic exposure. The number and size of MMCs increase in the chronically sick fish,
old fish or excessive catabolism (Ferguson, 1989). The catabolism highly increased due
to persistence of stress.
The intestine showed sloughing of epithelil cell covering of villi. Severe mucus
cell metaplasia were noticed in fish treated with acute intoxication (fig. 15).The
submucosa showed edema , round cell infiltration and esinophilic granular cell in fish
exposed to chronic intoxication (fig. 16).
In this study, concentration of nickel residues were determined in the gills, liver
and muscle of treated fish either after acute or subchronic intoxication as shown in
(Table, 4) From data analysis, nickel had little capacity for bioaccumulation in the
muscles. Our results concise with the results obtained by El-Saieed and Mekawy, (2001)
in tilapia fish after one month of nickel exposure. This is confirmed by Seymore et al.,
(1996) and Vigh et al. (1996) who reported that, lowest nickel concentration occurred
in fat and muscle.
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EXPERIMENTAL STUDIES ON NICKEL TOXICITY IN NILE TILAPIA
Table 4. Residues of nickel (mg/kg, dry wt.) in the muscle, gills and liver sample of
Tilapia after exposure to nickel chloride either acute 7.2 mg/L (1/5 LC50) for
one week or subchronic 3.6 mg/L (1/10 LC50) for 8 weeks (Mean ± SE).
Time of
exposure
No.
of
fish
group
Muscle
control
Acute
0. 04
±0.01a
Gills
Sub
chronic
control
Acute
0.29
±0.02 a
1.31
±0.36a
Liver
Sub
chronic
control
Acute
0.65
±0.04 a
1.91
±0.2 a
Sub
chronic
1st week
20
0.04
±0.01a
2nd week
10
0.05
±0.02a
0.0 6
±0.02a
0.29
±0.06 a
1.22
±0.13 a
0.65
±0.04 b
1.91
±0.2 a
4th week
10
0.05
±0.02 b
0.0 7
±0.01a
0.30
±0.07 b
1.54
±0.25 a
0.65
±0.03b
2.38
±0. 2a
6th week
10
0.05
±0.01 b
0.0 9
±0.01a
0.32
±0.07 b
1.70
±0.38 a
0.66
±0.03b
2.77
±0.1a
8th week
10
0.05
±0.01 b
0.1
±0.01a
0.32
±0.08 b
1.68
±0.11 a
0.69
±0.04 b
1.91
±0.2 a
Means in the same row carrying different superscript are significant at P<0.05. a :increase, b:decreased
Our result revealed that liver and gill tissues showed higher nickel
concentrations than muscle tissues. This is in accordance with the results obtained by
Canli and Kalay (1998) in Cyprinus Carpio and Chandrastome regium caught at 5
stations on Seyhan river system. Moreover accumulation of highest amount of nickel
especially in the liver may be confirmed by the presence of severe hepatic lesions in
tilapia fish exposed to nickel chloride in the study provides an evidence that liver is an
important organ for accumulation. Also, the liver and kidney have a role in
accumulation, toxicity and detoxification of nickel in fish (Ptashynski and Klaverkamp,
2002).
The present study also showed that the concentration of nickel in the tissues
increased with exposure time especially in liver and gills. Pane et al. (2003) concluded
that, accumulation of nickel in various tissues of water born fish sampled at 117 h after
exposure to 11.6 mg Ni/L. nickel accumulated significantly in the heart, stomach,
kidney, intestine and gill. This contrast may be due to different dose, or even due to
varied duration of treatment and time of exposure.
ABOU HADEED, A. H et al.
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EXPERIMENTAL STUDIES ON NICKEL TOXICITY IN NILE TILAPIA
ABOU HADEED, A. H et al.
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EXPERIMENTAL STUDIES ON NICKEL TOXICITY IN NILE TILAPIA
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7. Benedeczky, I., P. Biro and Z. S. Scaff. 1984. Effect of 2,4-D containing herbicide
(Diconirt) on ultrastructure of Carp liver cells Biol. Szeged, 30:107-115.
8. Canli. M., O. and M. Kalay. 1998. Levels of heavy metals (cd, pb, cu, cr and Ni) in
tissue of cyprinus carpio, Barbus capito and Chondrostoma regium from the
seyhan River, Turkey. Tr. J. oF Zoology (22)149-157.
9. Carleton, H. M., R. A. Drury, E. A. Willingtion and H. coneron. 1967. Carleton
Histological techniques. 4th Ed., oxford univ. Press, N4, Toronto.
10. Coles, E. H. 1986. Veterinary Clinical pathology .W. B . Saunders Philadelphia, pp:
10-42.
11. El-Saieed, M. E. and M. M. Mekawy. 2001. Nickel Toxicity in Oreochromis niloticus
fish J. Egypt Soc. Toxicol. 24:47-54.
12. Ferguson, H. W. 1989. Systemic pathology of fish. Iowa state University press,
Ames, Iowa 50010.
13. Gopal V., S. Parvathy and P. R. Balasubramanlian. 1997. Effect of heavy metals on
the blood protein biochemistry of the fish cyprinus carpio and its use as
Bioindicator of pollution stress. Environmental Monitoring and Assessment, 48
(2): 117–124.
ABOU HADEED, A. H et al.
1399
14. Kleczkowski, M., W. Klucinski, E. Sitarska and J. Sikora. 1998. Oxidative stress and
selected factors of antioxidative state of animals. Med. Wet. 54(3):166-171. (In
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15. Lied, E., Z. Gzerde and O. R. Braskhan. 1975. “Simple and rapid technique for
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669-701.
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18. Menne,T., O. Borgan and A. Green. 1982. Nickel allergy and hand dermatitis in
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19. Mohamed, W. and G. l. Saleh. 1996. Effect of copper and zinc pollution on growth
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‫‪ABOU HADEED, A. H et al.‬‬
‫‪1401‬‬
‫التأثير السمى للنيكل على صحة أسماك البلطى‬
‫على حيدر أبو حديد‪ ،1‬خلود إبراهيم‪ ،1‬نبيلة الشرقاوى‪ ،1‬صالح فتحى صقر‪ 2‬وسماح عطية‬
‫‪2‬‬
‫طب بيطرى الزقازيق‪ ،‬المعمل المركزى لبحوث األسماك بالعباسة‬
‫وجوووع صر وور الريكوول بعركيووز صووالة يووة البي ووة ي ووكل ‪.‬ط و ار كبي و ار صجيدووا ويرج و ارع ووا وجوووع‬
‫لالسووع‪.‬عاماا الواسووعة المععووععث يووة كليوور مووخ ال ووراصاا و‪ .‬و ووا‬
‫ووراصة ال ووجب وي‪.‬وور الريكوول مووخ‬
‫م‪.‬ج اا عجك ال راصاا إلى البحار واألردار والعر والم ارف محعلا ض ار ار صجى األحياء الما ية‬
‫ية هذا العمل عم عراسة عألير الريكل صجى‬
‫حة اسماك البجطة المرزرصة ية المعمول المركوزل لبحووث‬
‫اللروث السمكية بالعباسة وععج‪.‬ص رعا ج هذ العراسة كما يجة‪:‬‬
‫لقع أجريا العجربة صجى ما ة وص روخ سمكة مخ اسماك البجطة مقسمة إلى لالث مجامي‬
‫عم ععرض‬
‫المجموصووة األولووى مووخ األسووماك ‪ 5/1‬الجرصووة الر ووي مميعووة لمووعث ‪ 7‬أيووام وععوورض المجموصووة اللاريووة مووخ‬
‫األسووماك إلووى ‪ 10/1‬الجرصووة الر ووي مميعووة لمووعث لماريووة أسووابي صجووى الع ووالة وعركووا المجموصووة اللاللووة‬
‫كضووابطة وبمالح ووة األسووماك المعرضووة لجرصوواا م‪.‬عج ووة مووخ الريكوول كارووا ال ووورث المرضووية يووة‬
‫أص وراض عر سووية ملوول احووعالا طريقووة العوووم وزيوواعث حركووة طوواء ال‪.‬يا وويم م و‬
‫دووور إ وواباا ججعيووة صجووى‬
‫األسووماك أ دوورا الرعووا ج رقووص يووة أوزاخ جسووم اسووماك البجطووة يووة األسووماك المعرضووة ل‪.‬م و‬
‫العركيز المميا عملجا‬
‫ورث العم ية األسماك المعرضة ل‪.‬م‬
‫وورث‬
‫و لع وور‬
‫العركيز المميا رقص ية (الديموججووبيخ‬
‫و معوسوور عركيووز الديموججوووبيخ و صووعع كووراا الووعم البيضوواء) و زيوواعث يووة صووعع ك وراا الووعم الحم وراء أمووا‬
‫األسوماك المعرضوة لع ور العركيوز المميوا أ دورا رقوص يوة الديموججووبيخ و معوسور عركيوز الديموججووبيخ‬
‫ورقووص يووة صووعع كوراا الووعم البيضوواء أ دوورا ال حوووص الدسووعوبالوجية ألسووماك البجطووى لجعركيوزاا م‪.‬عج ووة‬
‫م ووخ كجوري ووع الريك وول وج وووع عخيو وراا بال‪.‬يا وويم والحج ووة والحب ووع والطح ووا ا واألمع وواء عراوح ووا م ووا ب وويخ احعق وواخ‬
‫وارع وا أوعيموى يوة ال‪.‬يا وويم مو عجمو ل‪.‬اليوا الووعم و احعقواخ يوة مع وم األوصيووة العمويوة و‪.‬ا وة الوريووع‬
‫المركزى ية الحبع م عحوخ يجواا عا‪.‬ول ‪.‬اليوا الحبوع وعجيوي يوة القروواا الم ارريوة وعموعع ل‪.‬اليوا الطال يوة‬
‫وكذلك وجع باألمعاء ارع ا أوعيمى وزياعث ية ال‪.‬اليا الحأسية البيضواء وعموعع يوة ال‪.‬اليوا المبطروة لجورقوة‬
‫ال‪.‬يو ووومية وععركووز وسووقو األو ارق اللارويووة لج‪.‬يا وويم ويووة الحجووة وجووع احعقوواخ وبعووض افرزيووة وارع وا‬
‫أوعيمووى واضوومحالا لمكوروواا الووعم وكووذلك وجووع بالطحوواا عحووالر لمركووز الميالروماحرويووا والعووى زاعا يووة‬
‫الحجم والععع وزياععه ية عث الجوخ الوذل مواا إلوة البروى الوعاحخ أ دورا رعوا ج اف‪.‬عبواراا البيوكيميا يوة‬
‫يووة اسووماك البجطووة العووة عووم ععريضوودا ل‪.‬م و‬
‫العركيووز المميووا لمووعث ‪ 7‬أيووام و األسووماك المعرضووة لع وور‬
‫العركيووز المميووا إلووى زيوواعث يووة امرزيموواا المر مووة لو ووا ي الحبووع والحوول‪ ALT,‬ورقووص يووة‬
‫‪AST,Total‬‬
‫‪ 0 protien‬ألبعوا رعووا ج عحجيوول ال‪.‬يا وويم والحبووع والعضووالا المعرضوة لعركيوزاا م‪.‬عج ووة وجوووع بقايووا لجريكوول‬
‫ية هذ األرسجة ععراسب م عركيز الريكل ية الميا ويعرث الععرض لدا حيث البا زيواعث العركيوز يوة الحبوع‬
‫صخ ال‪.‬يا يم صخ العضالا‬