Food Lipids: Chemistry, Nutrition, and Biotechnology

anistic studies of LOX inhibitors were reviewed by Veldink and Vliegenthart [133]
in 1991.
LOX is also a self-destructive enzyme; that is, LOX catalyzes its own destruction
during oxygenation of PUFA substrates [134,135]. Soybean L-1 undergoes inactivation
during incubation with PUFA or the exposure to hydroperoxy acids
[135,136]. The inactivation potency is in the following order: 15-hydroperoxy 20:4
> 15 hydroperoxy 20:3 > 9-hydroperoxyoctadecatrienoic acid (HPOT) or 13-HPOT.
The velocity of the LOX-catalyzed reaction decreases as a linear function of substrate
utilization. This inactivation seems to require a homolytic cleavage of peroxide group
and to result from binding of unstable intermediates produced from monohydroperoxy
acids that are bound to the active site. The activity of soybean L-1 may thus
be regulated by this mechanism between the secondary oxygenation and autoinactivation
[137]. LOX self-destruction could also be via modification of protein by
lipid hydroperoxide-derivative free radicals and aldehydes [135].
LOX products, fatty acid hydroperoxides, and their free radical derivatives are
very reactive compounds that result in disruption of membrane integrity [82,138],
inactivation of proteins and amino acids by reacting with sulfhydryl groups [139],
and degradation of DNA by hydroperoxide attack on guanine nucleotides [140].
These properties have led to speculation that lipoxygenase participates in the senescene
process in plants. Mazliak [141] and Watada et al. [85] assume that LOX plays
a key role in the deterioration of plant produce after harvest. In their hypothesis,
processing of vegetables and fruits during harvesting or after harvest results in the
release of PUFAs from glycerides. Free PUFAs are then oxygenated by LOX to form
lipid hydroperoxides. Both lipid peroxidation and lipid hydroperoxides promote loss
of membrane integrity, protein, and chlorophyll, causing accelerated deterioration of
plant tissues. Changed activity of LOX has been reported as one of the early events
in plant senescence. During fruit ripening and storage, LOX activity was shown to
rise [142–144]. Pauls and Thompson [145] found that with advancing age of the
cotyledons of Phaseolus vulgaris, LOX activity increased with enhanced lipid hydroperoxides
in microsomal membranes, suggesting that these increases ultimately
lead to membrane disruption in senescing tissues. In senescing bean cotyledons and
carnation (Dianthus caryophyllus L.) flowers, Thompson et al. [146] found that increased
LOX activities were associated with fluorescent products of lipid peroxidation.
With pea leaf senescence, LOX activity increased by more than sixfold. Addition
of LOX inhibitors retarded the senescence with reduced activation of LOX
activity by about 50% [147,148]. Senescing carnation petals showed phospholipid
degradation and a rise in membranous LOX activity [149,150]. Phenidone, a known
LOX inhibitor, delayed senescence in carnations [151].
The literature provides contradictory data regarding changes in LOX activities
during deterioration. Declines in LOX activity occurred during senescence of wheat
and rye leaves [152] and soybean cotyledons [153]. Twenty-month-old potato tubers
had a lower activity of LOX than 8-month-old tubers [154]. During broccoli (Brassica
oleracea L.) floret deterioration, increases in lipid peroxidation are closely associated
with reduced LOX activities [155–157]. In addition, accumulated studies
show that higher LOX activity is more commonly associated with young and fast
growing rather than senescing plant tissues and organs [158]. For example, LOX
activity decreased by 70% during soybean leaf maturation on plants [95]. As the
soybean cotyledons turned yellow and senesced, LOX activity decreased. Removal
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