The Ability of Different Ketohexoses to Alter Apo-A-I Structure and Function In Vitro and to Induce Hepatosteatosis, Oxidative Stress, and Impaired Plasma Lipid Profile in Hyperlipidemic Zebrafish

Table 1

Synthesis and characterization of rHDL containing each ketohexose (fructose, tagatose, and psicose).

rHDL	Molar composition	WMF (nm)	Size^a (Å)	Number of apoA-I/particle^b	α-Helicity (%)
Native-A-I	95 : 5 : 1	337 ± 0.1 (344 ± 0.5)^c	109–94		54.4 (32.6)^c
H2O-A-I	95 : 5 : 1	335 ± 0.5 (344 ± 0.5)	109–94	2, 3, 4	82.6 (51.4)
f-A-I	95 : 5 : 1	342 ± 1.6 (344 ± 0.5)	109–94	2, 3, 4, 5	38.4 (38)
t-A-I	95 : 5 : 1	335 ± 1.2 (344 ± 0.5)	93	2, 3, 4, 5	34.7 (15.4)
p-A-I	95 : 5 : 1	335 ± 0.4 (344 ± 0.5)	93	2, 3, 4, 5	35 (25.4)

^aDetermined from 8% to 25% native-gradient gel electrophoresis with densitometric scanning analysis. ^bDetermined from BS₃-crosslinking and 8–25% SDS–PAGGE. ^cThe numbers in the parentheses indicate the proteins in the lipid-free state. H₂O-A-I: H₂O-treated apoA-I; f-A-I: fructose-treated apoA-I; t-A-I: tagatose-treated apoA-I; p-A-I: psicose-treated apoA-I.