Biology Reference
In-Depth Information
urine, bile and blood. Absorption of
3
H-EA occurred mostly within two
hours of oral administration. Levels in blood, bile and tissues were low,
and absorbed compounds were excreted in urine. More than half of the
administered
3
H-EA remained in the gastrointestinal tract after 24 hours.
Approximately 19% of
3
H-EA was excreted in faeces and 22% in urine
at 24 hours.
A rapid absorption and metabolism of EA was reported by Doyle
and Griffiths (1980) in rats. These authors detected two derived
metabolites in faeces and urine: urolithin A and another unidentified
compound, both of microfloral origin, since none of them were found in
germ-free animals. Unchanged EA was not detected in urine or faeces of
normal rats. In contrast, Smart
et al.
(1986) found low to non-detectable
levels of EA in blood, lungs and liver of CD-1 mice after oral
administration and this was interpreted as an indication of poor
absorption and rapid elimination of the compound in these animals.
The results described in mice by Teel and Martin (1988) and by
Smart
et al.
(1986) are in good agreement and suggest that the poor
absorption of EA from the gut may lead to very low concentrations in
tissues, concentrations that may not be sufficient to exert any
in vivo
anticarcinogenic effects. The poor absorption of EA is supported by a
report of the presence of EA calculi in the gastrointestinal tract of
monkeys and goats, whose diet naturally contains EA (Van Tassel,
1976). The low bioavailability may be caused by several factors
including ionization of EA at physiological pH and formation of poorly
soluble complexes with Mg and Ca cations. In addition, extensive
binding of EA to the intestinal epithelium could also diminish absorption
(Whitley
et al.
, 2003).
A more recent work investigated the bioavailability of pomegranate
husk ETs in rats (Cerdá
et al.
, 2003). These ETs are essentially the same
as those found in the commercial juice (Gil
et al.
, 2000). The rats were
given 6% of their diet as pomegranate ETs from the fruit husk, and the
experiment was used to evaluate absorption, tissue distribution and
toxicity. Values around 3-6% of the ingested punicalagin were excreted
as metabolites in faeces and urine. In faeces, punicalagin was
transformed into hydrolysis products and to hydroxy-6
H
-dibenzo-[b,d]-
pyran-6-one derivatives (Fig. 7.2) by the rat colonic microflora. In
