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chapter 38
Vitamin Metabolism
o
H
hn/C Y c^ nA c /C ^ c
/CH3
I
J
I
{
Il
I
o^ 'CY n^ S '^ n/C '^ c^ c^ ch
3
I
[
C H 2
H
I
H — C — O H
H — c — O H
I
H — C — O H
[
C H 2O H
Riboflavin
O
H
H N /C- C ^ N- C
- C^
CH3
Isoalloxazine
I
I
li
I
0
^ C''N^C^N''''Cx'C^C'''CH3
I
I
Flavokinase
Z M g ^ Y
ATP
ADP
Ribitol
CH
2
H
H—C —OH
I
H—C —OH
I
H—C —OH
o
I
II
CH
2
— o — P— o
CT
Flavin mononucleotide (FMN)
(also called riboflavin phosphate)
O
H
Il
I
•ch.
\ CH
Flavin nucleotide
pyrophosphorylase
Mg
'*
ATP
PPi
CH
2
H
I
H—C —OH
H—C —OH
I
H—C —OH
Adenine mononucleotide
CH2
I
0
“O— p = o
1
o
“O—P
= 0
nh2
I
c
OH
Flavin adenine dinucleotide (FAD)
FIGURE 38-13
Synthetic pathways connecting riboflavin (vitamin B2) and its two cofactors, FMN and FAD. Riboflavin contains an
isoalloxazine ring system joined to a ribityl group (a sugar alcohol) through a cyclic amine on the middle ring. Because
of the isoalloxazine nucleus, the three compounds are yellow and exhibit a yellow-green fluorescence in aqueous
solutions. FMN is not a true nucleotide because the bond between the flavin (isoalloxazine) ring and the ribityl side
chain is not a glycosidic bond. Two nitrogen atoms and two carbon atoms, identified by the colored area in the
isoalloxazine ring system, participate in the oxidation-reduction reactions of the flavin coenzymes.
Although only synthesized in plants, bacteria, and most
yeasts, riboflavinis ubiquitous in plants and animals. Good
dietary sources include liver, yeast, wheat germ, green
leafy vegetables, whole milk, and eggs. Riboflavin is read-
ily degraded when exposed to light, especially at elevated
temperatures, and considerable decrease in its content in
foods can occur during cooking accompanied by exposure
to light. The greatest amounts of flavin nucleotides are in
the liver, kidney, and heart.
Dietary riboflavin is present mostly as a phosphate,
which is rapidly hydrolyzed before absorption in the
duodenum.In humans, the rapid, saturable absorption of
riboflavin following an oral dose suggests that it is trans-
ported by a carrier-mediated pathway located predom-
inantly in duodenal enterocytes. The process may be
sodium-dependent. Bile salts enhance absorption of ri-
boflavin. Fecal riboflavin is derived from the intestinal
mucosa and the intestinal flora. This is the predominant
excretory route for the vitamin.
Signs of riboflavin deficiency include
cheilosis,
angular
stomatitis,magenta tongue,and localized seborrheic der-
matitis.Some of these conditions may be due to concurrent
deficiency of other B-complex vitamins, since it is diffi-
cult to produce “pure” riboflavin deficiency in humans.
No toxicity following large doses of riboflavin has been
reported.
Pyridoxine (Vitamin B6)
Vitamin B
6
was first recognized as an essential food factor
in 1934; it was called pyridoxine when it was found to be
a substituted pyridine. Three closely related compounds
have vitamin B
6
activity (Figure 38-14).
With the exception of glycogen phosphorylase (Chap-
ter 15), and kynureninase, all of the pyridoxine-requiring
Pyridoxo/
Pyridoxa/
Pyridoxamne
(pyridoxine)
FIGURE 38-14
Structures of the three naturally occurring compounds having vitamin B6
activity.
