Chemistry Reference
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The ratio of zeaxanthin to lutein was found to be 1.6 and 1.3 in the retinas of the control and WHAM
chickens, respectively.
Interestingly, a 5.2-fold increase of lutein in the diet of the chickens for 4 weeks led to a substan-
tial 4.4-fold increase in lutein in the plasma of the WHAM chickens, but only a 2.5-fold increase in
control chickens (Connor et al., 2007). Overall, the plasma level of lutein was still 4.8 times greater
in the control chickens than in WHAM chickens fed a lutein-rich diet. Furthermore, both types
of chickens on lutein-rich diet reached similar levels of lutein in their heart and liver. Yet, the dif-
ference in the levels of lutein in the retina of the control and WHAM chickens on lutein-rich diet
became even greater than in chickens on the control diets. The retinas of WHAM chickens accumu-
lated only 6% as much lutein as was accumulated in retinas the control chickens.
Comparisons on WHAM chickens fed a lutein-rich diet with control chickens on control diet
indicate dysfunctional uptake of lutein into the retinas of WHAM chickens (Connor et al., 2007).
Even though the plasma levels of lutein in WHAM chickens on lutein-rich diet was 2.7 times smaller
than its levels in the control chickens on the control diet, the lutein levels in the hearts and livers of
WHAM chickens were 2.1- and 1.4-fold greater than the controls. The concentration of lutein in the
retinas of WHAM chickens on lutein rich diet was 6.1-fold smaller than in the retina of the control
chickens on control diet.
It has been suggested that the smaller accumulation of lutein in the retinas of WHAM chickens
relative to the control chickens was due to a preferential uptake of HDLs into the retina (Connor
et al., 2007): the WHAM chickens exhibiting a relatively lower concentration of HDLs in the plasma
accumulate less lutein in their retinas than the control chickens.
However, lutein is transported in the plasma bound not only to HDL but also to other lipopro-
teins which are taken up by the RPE, such as LDL and VLDL (Calvo et al., 1997, 1998; Duncan
et al., 2002; Elner, 2002; Gordiyenko et al., 2004; Hu et al., 2008; Parker, 1996; Provost et al., 2003;
Ryeom et al., 1996b; Tserentsoodol et al., 2006b; Wang and Anderson, 1993; Wang et al., 2007).
Therefore, it can be suggested that xanthophyll dei ciency in the retina of WHAM chickens is due
not only to dei ciency in the HDL but also due to dysfunctional ABCA1 in the retina. In this hypo-
thetical scenario ABCA1 is responsible for transport of xanthophylls endocytosed by the RPE into
the neural retina. Thus, the dysfunction of a mutated ABCA1 in WHAM chickens may be directly
responsible for the low levels of xanthophylls in their retinas.
In addition to its presence in the RPE, ABCA1 has been found to be localized in the neural
retina, particularly in the ganglion cell layer and rod photoreceptor inner segments (Tserentsoodol
et al., 2006a), suggesting it may be involved in carotenoid transport throughout the retina.
ABCA1 interacts with at least two apo-lipoproteins expressed by the RPE, ApoA1, and ApoE
(Faulkner et al., 2008; Von Eckardstein et al., 2001). The neural retina expresses all apo-lipoproteins,
which are expressed by the RPE, namely, ApoA-I, ApoC-I, ApoC-II, ApoE, and ApoJ (Li et al.,
2006; Tserentsoodol et al., 2006a). ApoA1 was identii ed in the ganglion cell layer, the rod photore-
ceptor inner segment layer, and the rod photoreceptor outer segment layer, presumably localized to
the interphotoreceptor matrix (Tserentsoodol et al., 2006a). In addition, the neural retina expresses
ApoA-II that has not been identii ed in the RPE (Li et al., 2006). It may be speculated that at least
some of these apo-lipoproteins within the neural retina have the potential to act as transporters of
xanthophylls moving from the RPE into the retina.
The neural retina expresses several lipoprotein receptors including SR-BI, SR-BII (Tserentsoodol
et al., 2006a,b), and VLDL receptor (VLDLR) (Hu et al., 2008). Thus, carotenoid l ow through
the RPE and further transport in the neural retina may also be mediated by lipoprotein receptors
(Tserentsoodol et al., 2006a,b). SR-BI and SR-BII have been found to be localized mainly to the
ganglion cell layer and POS in the monkey retina (Tserentsoodol et al., 2006a).
Apart from SR-BI, SR-BII, CD36, and ABCA1, a microarray analysis of gene expression in
human RPE reveals some additional lipid transporters that might potentially be involved in intra-
cellular transport of carotenoids and/or their efl ux from the RPE cells into the neural retina
or out of the retina into the choroidal blood (van Soest et al., 2007). These include other ABC
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