Chemistry Reference
In-Depth Information
0.1
2400
2000
0.08
1600
1200
800
0.06
400
(a)
0
0.04
0
20
40
60
80
100
120
140
160
(b)
(Ascorbic acid) (μM)
0.02
(c)
(d)
0
0
0.005
0.01
0.015
0.02
Time (s)
FIGURE 14.12
Decay of β-CAR
•+
in unilamellar DPPC liposomes (a) without ascorbic acid, (b) with 10 μM
ascorbic acid, (c) with 50 μM ascorbic acid, (d) with 150 μM ascorbic acid. Inset: Quenching plot.
acid can penetrate far into the hydrophobic regions of the model membranes. It is known that nonpo-
lar carotenoids, in particular the carotenes, can decrease the penetration barrier for small molecules
to the membrane headgroup region of phospholipid vesicles (Chaturvedi and Kurup 1986, Strzalka
and Gruszecki 1994). This is most probably due to additional space in the headgroup region result-
ing from the pigment-lipid interaction in the hydrophobic region of the phospholipid bilayer. This
greater permeability in the head group region may in fact aid ascorbic acid diffusion throughout the
entire lipid leal et, by acting as a portal of entry for ascorbic acid. In addition, the fact that ZEA has
a rigidifying effect as it spans the membranes may slow the diffusion of small molecules, such as
vitamin C, into the membrane.
The second-order rate constant for the repair of LUT
•+
is approximately half the value observed
for ZEA
•+
(5.2 × 10
6
M
−1
s
−1
). This lower second-order rate constant for LUT may rel ect LUT's
orientation within the bilayer, as discussed in Section 14.2 for the quenching of singlet oxygen
by LUT.
The aforementioned results refer to unilamellar membrane models but essentially similar results
are obtained in multilamellar vesicles, though the kinetics are more complex in such systems. The
numerical values observed in these model membranes simply show that one or more of the afore-
mentioned factors arise; however, in the
in vivo
situation, the preeminent effect is unknown but may
well be the proximity of the hydroxyl group to the water interface.
14.4.3.2 Amino Acids
The studies of tyrosine and cysteine show that at pH 7, both of these amino acids react with CAR
•+
(see Table 14.11), thus oxidizing these amino acids to their corresponding radicals:
•+
•
+
CAR
+
TyrOH
→+
CAR
TyrO
+
H
(14.12)
•
+
•
+
(14.13)
CAR
+
CysH
→+
CAR
Cys
+
H
This suggests the possible deleterious effects of carotenoids, for example, on membrane proteins, if,
following a radical scavenging reaction, the radical cations so formed are not efi ciently repaired.
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