Food Lipids: Chemistry, Nutrition, and Biotechnology

phases of storage [51,187,188]. In these studies, accelerated degradation of tocopherol
corresponded to an increased production of oxidative products. That a shift in
rate of tocopherol degradation and oxidative product generation occurred within similar
time periods suggested that when a critical concentration of tocopherol was
reached, effective competition by tocopherol for peroxyl radicals was no longer possible
and the oxidative propagation of lipids proceeded unchecked. That critical concentration
varied depending on the level of phospholipid PUFAs present in the sample.
Likewise, fatty acid and tocopherol compositions were considered to be the
determinant factors for oxidative stability in an in vitro system [189]. Consequently,
since fatty acid composition does not change in response to varying tocopherol levels
[190–193], dietary supplementation with tocopherol has been found overwhelmingly
to improve oxidative stability of both lipids and proteins in muscle foods as a result
of deposition of the dietary tocopherol within cellular membranes [191–204]. Postmortem
supplementation of tocopherol, in contrast, has not proven as effective as
dietary supplementation when levels in tissue were comparable [205], since exogenous
tocopherol does not reside in the tissue membranes. However, deposition via
dietary supplementation is not uniform throughout the muscles. Levels of �-tocopherol
were found in beef to be highest in oxidative muscles (m. psoas major and m.
gluteus medius) and lowest in glycolytic muscles (m. longissimus thoracis and m.
longissimus lumborum) [206]. In turkey, �-tocopherol levels were higher in leg muscle
than in breast muscle [207], whereas in salmon they were higher in the ventral
area than in the midline [208], and in herring they were lower under the skin than
in other parts of the fillet [34]. The degree to which tocopherol exerts an antioxidant
effect consequently depends on other compositional parameters of the muscle. For
example, oxidative stabilities were improved in breast meat but not in thigh meat
when chickens were supplemented with �-tocopheryl acetate [209]. The variable
deposition of tocopherol homologs into muscle tissue will also factor into the changes
in oxidative stability that are measured in response to dietary supplementation (�tocopherol
is preferentially deposited compared to �-tocopherol [210]). For example,
a decreased improvement in oxidative stability was found when diets included a
natural source of tocopherol (RRR-�, �-, and �-tocopherol) compared with a synthetic
source (all-rac-�-tocopherol) [211].
2. Ascorbic Acid
Exogenous addition of ascorbic acid and its derivatives controls rancidity in a number
of muscle tissues [212–217]. Within these tissues, ascorbic acid may function as an
antioxidant through a variety of mechanisms: it may act as an oxygen scavenger
[218]; it may scavenge free radicals generated in the aqueous phase [219]; it may
maintain heme compounds in a reduced noncatalytic state [220]; and it may regenerate
tocopherol [221]. At the same time, ascorbic acid can act as a prooxidant by
maintaining Fe(II) in its reduced state [220]. In an investigation on ground mullet
tissue, Deng et al. [222] found that ascorbic acid tended to function as a prooxidant
with small quantities and an antioxidant at high concentrations, with dark muscle
requiring lower concentrations of ascorbic acid for the shift to occur than light muscle.
Hence, dietary supplementation with ascorbic acid would only be advantageous
if the levels increase in the tissue beyond these critical concentrations. In fact, several
investigators have found the absence of any enhancement in oxidative stability for
broilers fed ascorbic acid–supplemented diets [202,223]. Enhancement by dietary
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