Health aspects of oxidized dietary fats - Oxidation in Foods and Beverages and Antioxidant Applications - page 159

Kok et al., 1988). Moreover, Huang et al. (1988) noted that administration of
oxidized fat to rats was accompanied by an increased hemolysis of red blood
cells which also implies that the vitamin E status was compromised by the
oxidized fat. These findings provided strong evidence to suggest that ingestion
of oxidized fat induces oxidative stress and causes a depletion of antioxidants.
Subsequent studies aimed to investigate whether the oxidative stress induced
by oxidized fat could be alleviated by supplementation with antioxidants. For
instance, the study from Liu and Huang (1995) demonstrated that reduced
concentrations of -tocopherol and increased concentrations of TBARS in
various tissues of rats fed oxidized fat could be alleviated by supplementation
with a high concentration of dietary vitamin E. These authors, however,
postulated that the reduction of -tocopherol concentrations in plasma and
tissues of rats fed oxidized fat is not only due to an increased consumption of -
tocopherol by lipid hydroperoxides ingested from the oxidized fat or formed in
vivo but also due to a reduced absorption of vitamin E from the diet. Never-
theless, a subsequent study from the same group (Liu and Huang, 1996) clearly
established that ingestion of oxidized fat is accompanied by an increased -
tocopherol catabolism and/or turnover due to the following reasons:
· The -tocopherol concentrations in tissues were lower in rats receiving a
vitamin E-devoid diet containing oxidized fat compared to rats receiving a
vitamin E-devoid diet containing fresh fat during a 9-week depletion period.
· The response of the oxidized fat group to -tocopherol repletion by intra-
peritoneal injection of all-rac--tocopherol was less than that of the control
group as evidenced by reduced -tocopherol concentrations in tissues of rats
fed the oxidized fat diet during the repletion period compared to those fed the
fresh fat diet.
Another study in Sprague-Dawley rats demonstrated that the susceptibility of
LDL to lipid peroxidation is increased by feeding oxidized fats (Eder et al.,
2003a). The susceptibility of LDL to lipid peroxidation depends mainly on their
PUFA contents and their concentrations of antioxidants (Esterbauer et al., 1989).
Since the percentages of PUFA in LDL total lipids were not different between
rats fed the oxidized fat and those fed the fresh fat (Eder et al., 2003a), it has
been suggested that the increased susceptibility of LDL to lipid peroxidation of
rats fed oxidized fat was due to their lower vitamin E concentrations. As
expected, supplementing the oxidized fat diets with a high vitamin E
concentration prolonged the lag time before onset of lipid peroxidation during
incubation of LDL with copper ions (Eder et al., 2003a), which is indicative of a
decreased susceptibility of LDL to lipid peroxidation.
Similar to vitamin E, the vitamin C status is also impaired by feeding
oxidized fat as demonstrated in guinea pigs (Liu and Lee, 1998), which, like
humans, lack an ascorbate synthetic pathway. Guinea pigs fed oxidized fat had
lower vitamin C and vitamin E concentrations in plasma and all tissues
investigated than those fed oxidized fat (Liu and Lee, 1998). However, the
vitamin C and vitamin E status of the guinea pigs significantly improved with