presence of aflatoxins in smoked-dried fish sold in abeokuta, ogun ...

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y fungi Aspergillus flavus and A. parasiticus. Aflatoxicosis is poisoning that result from the ingestion of aflatoxin in contaminated foods or seeds (Sorenson et al., 1984). Table 1. Melting-Points and Ultraviolet Absorption of Aflatoxins Aflatoxin Melting-point ( 0 C) Ultraviolet absorption (ethanol) λmax (nm) ε(L mol –1 cm –1 ) B1 268–269 (decomposition) 223 25 600 (crystals from chloroform) 265 13 400 362 21 800 B2 286–289 (decomposition) 265 11 700 (crystals from chloroform-pentane) 363 23 400 G1 244–246 (decomposition) 243 11 500 (crystals from chloroform-methane) 257 9 900 264 10 000 362 16 100 G2 237–240 (decomposition) 265 9 700 (crystals from ethyl acetate) 363 21 000 M1 299 (decomposition) 226 23 100 (crystals from methanol) 265 11 600 357 19 000 Source: O’Neil et al. (2001) 5
1.1.4 Effect on Human Health According to ICRI (2000), Humans are exposed to aflatoxins by consuming foods contaminated with products of fungal growth. Such exposure is difficult to avoid because fungal growth in foods is not easy to prevent. Even though heavily contaminated food supplies are not permitted in the market place in developed countries, concern still remains for the possible adverse effects resulting from long-term exposure to low levels of aflatoxins in the food supply. Evidence of acute aflatoxicosis in humans has been reported from many parts of the world. The syndrome is characterized by vomiting, abdominal pain, pulmonary edema, convulsions, coma, and death with cerebral oedema and fatty involvement of the liver, kidney, and heart. Conditions increasing the likelihood of acute aflatoxicosis in humans include limited availability of food, environmental conditions that favour fungal development in crops and commodities, and lack of regulatory systems for aflatoxin monitoring and control. The expression of aflatoxin related diseases in humans may be influenced by factors such as age, sex, nutritional status, and/or concurrent exposure to other causative agents such as viral hepatitis (HBV) or parasite infestation. Ingestion of aflatoxin, viral diseases, and hereditary factors have been suggested as possible aetiological agents of childhood cirrhosis. There are evidences to indicate that children exposed to aflatoxin breast milk and dietary items such as unrefined groundnut oil, may develop cirrhosis. Malnourished children are also prone to childhood cirrhosis on consumption of contaminated food. Several investigators have suggested aflatoxin as an aetiological agent of Reye’s syndrome in children in Thailand, New Zealand etc. Though there is no conclusive evidence as yet. Epidemiological studies have shown the involvement of aflatoxins in Kwashiorkor mainly in malnourished children. The diagnostic features of Kwashiorkor are edema, damage to liver etc. These outbreaks of aflatoxicosis in man have been attributed to ingestion of contaminated food such as animal products, maize, groundnut etc. Hence it is very important to reduce the dietary intake of aflatoxins by following the procedures for monitoring levels of aflatoxins in foodstuffs. There are differences in species with respect to their susceptibility to aflatoxins, but in general, most animals, including humans, are affected in the same manner. 6
Page 1 and 2: PRESENCE OF AFLATOXINS IN SMOKED-DR
Page 3 and 4: DEDICATION I dedicate this work to
Page 5 and 6: TABLE OF CONTENTS Title Page Certif
Page 7 and 8: CHAPTER THREE 3.0 MATERIALS AND MET
Page 9 and 10: LIST OF PLATES Plate 1: Ethmalosa f
Page 11 and 12: ABSTRACT This study was aimed to es
Page 13 and 14: foods, Nwokolo andOkonkwo (1998) fo
Page 15: Reactivity: The lactone ring is sus
Page 19 and 20: 1.1.7 Cellular Effects Aflatoxins a
Page 21 and 22: order. Adebayo et al. (2006) report
Page 23 and 24: Aspergillus flavus and Aspergillus
Page 25 and 26: Peanuts, maize and cottonseed are a
Page 27 and 28: high proportion of endo-epoxide and
Page 29 and 30: of all mice, but the lesions were j
Page 31 and 32: The mean concentration of aflatoxin
Page 33 and 34: eported and concluded that there wa
Page 35 and 36: Table2: Analytical methods validate
Page 37 and 38: of regulations. Data were not avail
Page 39 and 40: CHAPTER THREE 3.0 MATERIALS AND MET
Page 41 and 42: 3.5 Test Procedure 1. The kit (cont
Page 43 and 44: CHAPTER FOUR 4.0 RESULTS 4.1 Sample
Page 45 and 46: Plate 5: Clarias gariepinus Plate 6
Page 47 and 48: Figure 1: Aflatoxin concentrations
Page 49 and 50: esult also revealed that Aflatoxins
Page 51 and 52: REFERENCES Abulu, E.O., Uriah, N.,
Page 53 and 54: European Commission (2002). Commiss
Page 55 and 56: Hull, J.E., Chen, Z.Y. and Eaton, D
Page 57 and 58: Peterson, S.W., Ito, Y., Horn, B.W.
Page 59 and 60: Wild, C.P., Yin, F., Turner, P.C.,
Page 61: APPENDIX II One -Sample T-test Test

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