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

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The pr<strong>in</strong>cipal target organ for <strong>aflatox<strong>in</strong>s</strong> is the liver. After the <strong>in</strong>vasion <strong>of</strong> <strong>aflatox<strong>in</strong>s</strong> <strong>in</strong>to the<br />

liver, lipids <strong>in</strong>filtrate hepatocytes and leads to necrosis or liver cell death. The ma<strong>in</strong> reason for<br />

this is that aflatox<strong>in</strong> metabolites react negatively with different cell prote<strong>in</strong>s, which leads to<br />

<strong>in</strong>hibition <strong>of</strong> carbohydrate and lipid metabolism and prote<strong>in</strong> synthesis. In correlation with the<br />

decrease <strong>in</strong> liver function, there is a derangement <strong>of</strong> the blood clott<strong>in</strong>g mechanism, icterus<br />

(jaundice), and a decrease <strong>in</strong> essential serum prote<strong>in</strong>s synthesized by the liver. Other general<br />

signs <strong>of</strong> aflatoxicosis are edema <strong>of</strong> the lower extremities, abdom<strong>in</strong>al pa<strong>in</strong>, and vomit<strong>in</strong>g.<br />

1.1.5 Acute toxicity<br />

ICRI (2000) also acute toxicity is less likely than chronic toxicity. The pr<strong>in</strong>cipal target organ for<br />

<strong>aflatox<strong>in</strong>s</strong> is the liver. After the <strong>in</strong>vasion <strong>of</strong> <strong>aflatox<strong>in</strong>s</strong> <strong>in</strong>to the liver, lipids <strong>in</strong>filtrate hepatocytes<br />

and leads to necrosis or liver cell death. The ma<strong>in</strong> reason for this is that aflatox<strong>in</strong> metabolites<br />

react negatively with different cell prote<strong>in</strong>s, which leads to <strong>in</strong>hibition <strong>of</strong> carbohydrate and lipid<br />

metabolism and prote<strong>in</strong> synthesis. In correlation with the decrease <strong>in</strong> liver function, there is a<br />

derangement <strong>of</strong> the blood clott<strong>in</strong>g mechanism, icterus (jaundice), and a decrease <strong>in</strong> essential<br />

serum prote<strong>in</strong>s synthesized by the liver. Other general signs <strong>of</strong> aflatoxicosis are edema <strong>of</strong> the<br />

lower extremities, abdom<strong>in</strong>al pa<strong>in</strong>, and vomit<strong>in</strong>g.<br />

1.1.6 Chronic Toxicity<br />

Animals which consume sub-lethal quantities <strong>of</strong> aflatox<strong>in</strong> for several days or weeks develop a<br />

sub acute toxicity syndrome which commonly <strong>in</strong>cludes moderate to severe liver damage. Even<br />

with low levels <strong>of</strong> <strong>aflatox<strong>in</strong>s</strong> <strong>in</strong> the diet, there will be a decrease <strong>in</strong> growth rate, lowered milk or<br />

egg production, and immunosuppression. There is some observed carc<strong>in</strong>ogenicity, ma<strong>in</strong>ly related<br />

to aflatox<strong>in</strong> B1. Liver damage is apparent due to the yellow color that is characteristic <strong>of</strong><br />

jaundice, and the gall bladder will become swollen. Immunosuppression is due to the reactivity<br />

<strong>of</strong> <strong>aflatox<strong>in</strong>s</strong> with T-cells, decrease <strong>in</strong> Vitam<strong>in</strong> K activities, and a decrease <strong>in</strong> phagocytic activity<br />

<strong>in</strong> macrophages (ICRI, 2000).<br />

7

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