Biochemical and Histopathological Effects of Aflatoxin on ...

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Enzyme pr<strong>of</strong>ile <strong>of</strong> hepatic neoplasm induced by AFB 1 in rainbow trout was studied. Though activities <strong>of</strong> ethoxy resomfin-O-diethylase (EROD), microsomal <strong>and</strong> cytosolic epoxide hydroxylase (mEH <strong>and</strong> cEH), aldehyde dehydrogenase (ALDH), DT diaphorase, gamma-glutamyl transferase (gamma GT), glutathione transferase (GST), uridine diphospho-glucuronyl bansferase(UDGPT), <strong>and</strong> p450 IAI were measured, only aldehyde dehydrogenase <strong>and</strong> gamma-glutamyl transferase showed increase. Induction <strong>of</strong> aldehyde dehydrogenase, uridine diphosphoglucuronyl transferase <strong>and</strong> depression <strong>of</strong> cytochrome p450 IAI were also noticed. Hepatic accumulation <strong>of</strong> aflatoxin BI deferred in rainbow trout <strong>and</strong> tilapia (Ngethe et al, 1993). The major target organ involved following chronic exposure <strong>of</strong> AFB1 is the liver, but tumours <strong>of</strong> other organs appear, although these are less prevalent. As is the case with acute toxicity, there exist significant species differences with respect to susceptibility. The Mt. Shasta strain <strong>of</strong> rainbow trout is by far the most sensitive species <strong>of</strong> animal or fish to the hepatocarcinogenic effects <strong>of</strong> AFB I (Sinnhuber et al, 1977). Less than 1 ppb (parts per billion) in the diet will cause liver tumours in 20 months. The LDso (dose causing death in 50% <strong>of</strong> the subjects) for aflatoxin in 50-gram rainbow trout is 500 to 1000 ppb. Signs <strong>of</strong> severe aflatoxicosis in rainbow trout are liver damage, pale gills <strong>and</strong> reduced red blood cell concentration. The use <strong>of</strong> rainbow trout in AFB1 carcinogenesis studies grew out <strong>of</strong> observations <strong>of</strong> increased liver cancers in domesticated rainbow trout in many hatcheries in the V.S from 1957 to 1960. Since then, the rainbow trout has proven to be an attractive animal model for chemical carcinogenesis studies. A diet containing O.4ppb AFB 1 fed to trout over a 14 month period resulted in a 14% incidence <strong>of</strong> hepatocellular carcinomas (Lee et al, 1968). 10
When the dose was increased ten fold, a 60% incidence during the same time period was seen. In contrast, wild steelhead trout had an incidence <strong>of</strong> only 6% after 12 months on 8ppb AFB1 (Sinnhuber et al, 1977). Research carried out in Auburn University in 1991 revealed that all fishes are not sensitive to mycotoxins. Rainbow trouts are extremely sensitive but brook trouts, coho salmon are less sensitive to aflatoxin ingestion (Halver <strong>and</strong> Mitchell, 1967). In coho salmon, aflatoxin did not produce hepatoma but liver lesions were present. This included necrosis <strong>of</strong> hepatocytes <strong>and</strong> fatty change (Bruenger <strong>and</strong> Greuel, 1982). In tilapia culture aflatoxicosis was a major cause <strong>of</strong> losses (Roberts <strong>and</strong> Sommerville,1982). In carps, aflatoxin did neither produce any liver lesions nor any alteration in haematological values. There was no accumulation <strong>of</strong> aflatoxins in fish muscles. (Svobodova <strong>and</strong> Piskac,1982). Warm water fish are less sensitive to aflatoxin. The LDso for channel catfish was found to be approximately 30 times that for rainbow trout. Pathological signs in channel catfish fed lethal dose <strong>of</strong> aflatoxin were death, liver damage <strong>and</strong> injury to the lining <strong>of</strong> the stomach, intestines, spleen, heart <strong>and</strong> kidney. Some authors also stated that channel catfish fingerlings showed a relatively low response when fed aflatoxin in doses upto 100mg/kg body weight (Ashley,1967). 2.8. Chronic aflatoxicosis The response <strong>of</strong> trout to aflatoxicosis varies with size <strong>and</strong> duration <strong>of</strong> dose. A chronic response may arise from low prolonged dosages <strong>and</strong> usually results in a significant incidence <strong>of</strong> hepatoma, while acute response usually involves force feeding <strong>of</strong> single or repeated massive dosages <strong>of</strong> 15 or more mg/kg body weight in 25-50 g fish. These fish generally die within 8-10 days after exposure. Crude aflatoxin fed to rainbow trout at only 20 ppb resulted 11
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 23 and 24: neoplastic cells and</stron
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
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(Madhusudhanan et al, 2000). But in
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5.0. Introduction Structural <stron
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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
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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) <
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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
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New M B (1987). Feed and</s
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Saber N A (1995). Depression <stron
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Soni KB, Rajan A and</stron
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Verma R J, Kolhe A Sand</st
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