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

Analyses of breast milk in Ghana, Nigeria, Sierra Leone and Sudan showed primarily aflatoxin
M1, aflatoxin M2 and aflatoxicol. Aflatoxin exposure pre- or post-natally at levels ≥ 100 µg/l
was very often associated with illness in the child (Maxwell, 2008). Exposure of infants to
aflatoxin M1 from mothers’ breast milk in the United Arab Emirates has been measured by Saad
et al. (1995). Among 445 donors of breast milk, 99.5% of samples contained aflatoxin M1 at
concentrations ranging from 2–3 µg/l. The mothers were of a wide range of nationalities, ages
and health status; no correlation was observed between these factors and aflatoxin M1 content of
the milk.
2.6 Absorption, Metabolism and Excretion in Humans
Rigorous quantitative comparisons of dietary intakes and aflatoxin metabolites in body fluids
following absorption and distribution are lacking, aflatoxin M1 concentrations in urine and
human milk have been correlated with dietary aflatoxin intake. However, studies of human
exposure have yielded quantitatively very different correlations between aflatoxin concentrations
in foods and either aflatoxin–protein or aflatoxin–DNA adducts in urine and sera (Hall et al.,,
1994). Hudson et al. (1992) very carefully measured aflatoxin intake based on plate foods in a
village in The Gambia. They found intakes less than those estimated from aflatoxin–serum and
urinary adduct levels in the same individuals. In humans, as with other species, the DNA binding
and carcinogenicity of aflatoxin B1 result from its conversion to the 8,9-epoxide by cytochrome
P450 (CYP) enzymes (Essigman et al., 2002). There is individual variability in the rate of
activation of aflatoxin, including between children and adults, which may be material to the
pharmacokinetics (Wild et al., 2001). The pharmacokinetics of aflatoxins in humans are still not
clearly known.
Factors that explain variation in response to aflatoxin between individual humans, animal species
and strains include the proportion of aflatoxin metabolized to the 8,9- epoxide (mainly by CYP
enzymes) relative to the other much less toxic metabolites and the prevalence of pathways
forming non-toxic conjugates with reduced mutagenicity and cytotoxicity. The metabolism of
aflatoxins in humans has been extensively studied and the major CYP enzymes involved have
been identified as CYP1A2 and CYP3A4 (Gallagher et al., 1998). CYP3A4 mediates formation
of the exo-epoxide and aflatoxin Q1 while CYP1A2 can generate some exo-epoxide but also a
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