Biochemical and Histopathological Effects of Aflatoxin on ...

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in gross hepatoma in 44 <strong>of</strong> 117 fish after 12 months <strong>and</strong> in 50 <strong>of</strong> 88 fish in 16 months. Other trout fed crystalline aflatoxin Bb the most toxic fraction, at 0.5,2.0 or 8.0 ppb had gross tumours after 12 months in 37 <strong>of</strong> 116, 45 <strong>of</strong> 115 <strong>and</strong> 52 <strong>of</strong> 121 fish, respectively (Ashley et ai, 1964; Halver, 1967). 2.9. Acute aflatoxicosis Halver (1967) reported most rainbow trout force fed crude aflatoxin at 1, 3 or 5mg/kg body weight in single dose or Img/kg body weight daily for 5 days were moribund by day 10 <strong>and</strong> only six fish survived in the groups fed Img/kg body weight daily for 5 days. All fish had gross multiple haemorrhagic areas in liver <strong>and</strong> adjacent viscera. Moribund fish had dark skin, nearly white gills, indicative <strong>of</strong> severe anaemia, <strong>and</strong> were listless. Death usually occurred in less than 24 hours after symptoms appeared. Additional experiments using the more potent aflatoxin B1 force fed to trout resulted in similar pathology <strong>and</strong> showed that B] is approximately 10 times more toxic than the crude aflatoxin previously used (Halver, 1969). <strong>Histopathological</strong>ly, gills from acutely toxic fish had generalized edema <strong>and</strong> <strong>of</strong>ten the branchial vessels were greatly engorged with blood. Livers had varying degrees <strong>of</strong> pathological change, depending on total amount <strong>of</strong> aflatoxin ingested. Some had only slight hepatitis with scattered groups <strong>of</strong> hepatocytes whose nuclei were pycnotic, karyolytic or had chromatin margination. More severe toxic responses included varying degrees <strong>and</strong> amounts <strong>of</strong> hepatic necrosis with or without hyperemia <strong>and</strong> patches <strong>of</strong> haemorrhage. Electron microscopy <strong>of</strong> classical trabecular hepatoma in rainbow trout was reported by Scarpelli et at (1963) <strong>and</strong> by scarpelli (1967). These authors observed highly developed endoplasmic reticulum <strong>and</strong> absence <strong>of</strong> glycogen within the neoplastic cell. The golgi complex was well developed in 12
neoplastic cells <strong>and</strong> was characterized by lamellae <strong>and</strong> vesicles associated with increased numbers <strong>of</strong> dense granules in some preparations. Peripherally, the cell was poorly organized <strong>and</strong> free ribosomes were increased. Plasma membranes were reticular <strong>and</strong> <strong>of</strong>ten dense material appeared to be passing into extracellular spaces. Microsomal incorporation <strong>of</strong> 14C-lysine from trout hepatomas was greater than that from normal livers. A well-organized endoplasmic reticulum generously supplied with ribosomes occurred in most hepatomas. The evidence pointed out toward extensive protein synthesis <strong>and</strong> reduced level <strong>of</strong> lipid <strong>and</strong> glycogen material in tumour cells. Nucleic acids were formed in abundance <strong>and</strong> upon staining showed intense basophilia typical <strong>of</strong> neoplastic cells in trout hepatoma. Electrophoretic patterns <strong>of</strong> serum from normal <strong>and</strong> tumour bearing trout showed an increase in plasma protein components in hepatomatous fish (Snieszko et al, 1966). The susceptibility <strong>of</strong> individual animals to aflatoxins vanes considerably depending on species, age, sex, <strong>and</strong> nutrition. Once absorbed into the blood, AFB] binds avidly to plasma proteins <strong>and</strong> loosely to red blood cells (Kumagai et al, 1983; Luthy et al, 1980). Besides liver damage, aflatoxins cause decreased milk <strong>and</strong> egg production, recurrent infection as a result <strong>of</strong> immunity suppression (eg. Salmonellosis), in addition to embryo toxicity in animals consuming low dietary concentrations. While the young <strong>of</strong> a species are most susceptible, all ages are susceptible but in different degrees for different species. Clinical signs <strong>of</strong> aflatoxicosis in animals include gastrointestinal dysfunction, reduced reproductivity, reduced feed utilization <strong>and</strong> efficiency, anaemia, <strong>and</strong> jaundice. Nursing animals may be affected as a result <strong>of</strong> the conversion <strong>of</strong> aflatoxin BI to the metabolite aflatoxin M I excreted in the milk <strong>of</strong> dairy cattle. The induction <strong>of</strong> cancer has been extensively studied. <strong>Aflatoxin</strong>B I, aflatoxinlvl, <strong>and</strong> aflatoxirrGj have been shown to cause various types <strong>of</strong> cancer in different animal species.
Page 1: BIOCHEMICAL AND HISTOPATHOLOGICAL E
Page 6 and 7: CHAPTER 1 Introduction CHAPTER2 Rev
Page 8 and 9: Estimation ofAST E
Page 10 and 11: 1.0 Introduction Aquaculture today
Page 12 and 13: distribution of ma
Page 14 and 15: C H A P T E R Review of</st
Page 16 and 17: 2.3 Structures of
Page 18: animals. As is the case with other
Page 21: When the dose was increased ten fol
Page 25 and 26: 2.10 b. Carbohydrate and</s
Page 27 and 28: Any discussion in multistage carcin
Page 29 and 30: 3.0 Introduction Fungi grow on pell
Page 31 and 32: imperative to use a method which is
Page 33: MgS04.7H20 FeS0 4.7H20 Distilled wa
Page 36 and 37: 3.3.6 Preparation of</stron
Page 38 and 39: Aflatoxin biosynth
Page 40 and 41: The solubility of
Page 42 and 43: 4.0 Introduction Chemical compounds
Page 44 and 45: Generalized Scheme for Oxidative In
Page 46 and 47: Initiation and pro
Page 49 and 50: (d) Glutathione peroxidase (E.C.l.l
Page 51 and 52: 4.9.l.b Estimation of</stro
Page 53 and 54: Preparation of Tis
Page 55: Procedure Tissues homogenates were
Page 60: was 0.559. Concentration 0.375 ppm
Page 72 and 73:
(Madhusudhanan et al, 2000). But in
Page 74:
5.0. Introduction Structural <stron
Page 79 and 80:
PLATE 8.5 Section of</stron
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The GlIb section of</strong
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All experimental fish appeared norm
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lesion, serving as precursors <stro
Page 89 and 90:
C H A P T E R 6 Aflatoxin</
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Biochemically, afl
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}.2 Materials and
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incubation, 0.2ml of</stron
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times. Waited for 10 minutes till a
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2. Buffer: Sodium carbonate- bicarb
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added to O.Sml of
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Procedure 2g of fl
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diluent solution. Using a commercia
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Parameter Treatment Urea ( J1 moles
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4 3 .... Cl 2 1 o Control 0.375ppm
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300 250 200 "Cm150 E 100 50 o Contr
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Treatment Parameter P value Cholest
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I Source of Variat
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113 type seem to take an active rol
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C H A P T E R 7 Electrophoretic Ana
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116 Among the many biornarkers the
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118 refrigerator for some time to e
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7.1.2b Reagents for electrophoresis
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7.1.2c Preparation of</stro
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3) 10% SDS 4) 6 M Sodium chloride 5
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) Serum Protein (Non SDS Page) 129
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fragments of simil
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C H A P T E R 8 Effect of</
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may result from destabilization <st
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2) Buffer: Citrate buffer (O.05M) <
Page 163 and 164:
Source of Variatio
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Groups Pvalue Control vs 0.375ppm N
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8.1 Studies on the Erythrocyte Memb
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4) To O.lml of the
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8.ID Discussion The results obtaine
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a) Preparation of
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Source of Variatio
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8.3 Studies On Muscle Retention 8.3
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Detection: Waters 440 Absorbance at
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8.3C Results The results are presen
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9.0 Summary The present study was u
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• Aflatoxin resi
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BIBLIOGRAPHY Abedi A Hand</
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Bruenger, A and Gr
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Egmond H P V and W
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Hendricks J D, Wales J H, Sinnhuber
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Lowry 0 H, Rosenbrough N J, Farr A
Page 202 and 203:
New M B (1987). Feed and</s
Page 204 and 205:
Saber N A (1995). Depression <stron
Page 206 and 207:
Soni KB, Rajan A and</stron
Page 208 and 209:
Verma R J, Kolhe A Sand</st
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