الفهرس 
Cover Page Title in EnglishOnly 14 pages are availabe for public view
 |  | from | 118 |  |  |
| | | from | 118 | | |
Abstract
A total number of 402 of apparently healthy Nile tilapia were divided into three experiments; 126 fish were classified into 7 equal groups namely GPs 1,2,3,4,5,6 and 7 given daily 0, 0.2, 0.4, 0.6, 0.8, 1.0 and 1.2 mg/L mercuric chloride, respectively to determine the LC50-96h. Physiochemical parameter of chlorine-free taps water were {PH = 7.4, Hardness = 15 mg/L, Chloride = 0.0233 ppt, Dissolving organic matter = 19 mg/L, Ammonia = 0.09 mg/L, Salinity = 0.219 ppt, Sulphate = 150 mg/L, Nitrite = 0.20 mg/L and alkalinity = 85 mg/L}. The LC50-96h of mercuric chloride in Nile tilapia was 0.774 mg/L.
Regarding the acute experiment; 60 fish were classified into two equal group, control group and treated group that exposed to 0.4 mg/L (1/2 LC50). Water and toxic material renewed daily for 7 days. While, in chronic experiment; 90 fish divided into an equal three groups as the following control group, HgCl2 group that exposed to 0.0774 mg/L (1/10 LC50 HgCl2) and HgCl2 + vitamin C group that exposed to 0.0774 mg/L + 500 mg L-ascorbic acid/Kg diet. Water and toxic material renewed every day for 8 weeks and also diet was daily provided at 3% of body weight and divided on two parts over the day.
Gills, hepatopancreas, kidney, spleen, brain and intestine were collected daily in the acute experiment to describe the associated pathological lesions, while weekly collection of the pervious mentioned organs was carried in the chronic experiment to describe the pathological changes. Besides histopathology was determined quantitatively by mathematical calculation of lesion indices, blood sampling collected at 2nd, 4th and 8th weeks for some hematological investigations and Serum separation was done for clinico-biochemical determination.
Clinically, the affected fish in both experiments suffered from respiratory and nervous manifestations while in HgCl2 + vitamin C group exhibited only respiratory manifestations.
Internally, there was congestion of the internal organs. The gills exhibited dark red spots alternative with another pale area. Gallbladder distended with greenish bile. On the other hand, the HgCl2 + vitamin C group showed only congestion of the internal organs.
Mortality % in case of acute mercuric chloride toxicosis is 20 %.
(1): Microscopical examination:
The gills suffered from congestion in branchial blood vessel, telangiectasis, lamellar necrosis, edematous separation of surface epithelium of secondary lamellae from capillary beds, proliferation of the epithelial lining at the base of the secondary lamellae resulting in fusion of some secondary lamellae and filamentous clubbing beside mucus cells in primary lamellae these results observed in acute and chronic experiments. The gill arch exhibited edema, congestion, hemorrhage and EGCs infiltration in acute experiment while hemorrhage and EGCs infiltration in chronic mercuric chloride group.
The hepatopancreas showed acute cellular swelling, fat degeneration of the hepatocytes, perivascular EGCs infiltration, activation of MMCs, hemorrhage and congestion of blood vessels these results observed in acute and chronic experiments. Moreover, necrosis of hepatocytes and pancreatic acini were noticed especially at chronic mercuric chloride group.
The renal lesions consisted of congestion, acute cellular swelling, hyaline degeneration in the tubular epithelium, hyaline cast in the lumen of renal tubules, hemorrhage, activation of MMCs and tubular necrosis in acute and chronic experiments.
The spleen showed activation of melanomacrophage centre (MMCs), depletion in white pulp, dilatation of blood sinusoids (telangiectasis) (acute experiment) and apoptosis of lymphocytes with infiltration of tingible-bodies macrophages (Starry sky appearance) (chronic experiment).
The intestine exhibited congestion and EGCs infiltration in acute experiment while hyperplasia of the goblet cells in acute and chronic experiment.
The brain lesions were congestion of the blood vessels beside pyknotic and depletion of Purkinji cell in the cerebellum in acute experiment. Moreover, there was perivascular edema and perivascular cuffing especially at chronic HgCl2 group while there was congestion only in HgCl2 and vitamin C group.
(2)- Quantitative histopathological assessment:
The most affected organ by mercuric chloride toxicosis were gills > posterior kidney > hepatopancreas > spleen > intestine > brain. Besides the lesions in case of group containing vitamin C were less in degree and severity.
(3): Hematological and biochemical studied:
• WBCs count, RBCs count, Hb and PCV were significantly decreased in mercuric chloride treated fish when compared with the group containing vitamin C and control.
• AST, ALT, alkaline phosphatase and glucose were significantly increased in mercuric chloride treated fish when compared with the group containing vitamin C and control. On the other hand total protein and albumin showed a significant decrease especially at the end of chronic experiment.