Lipid and Protein Oxidation of Chicken Oxidation Levels and Packaging

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Lipid and Protein Oxidation of Chicken
Breast Rolls as Affected by Dietary
Oxidation Levels and Packaging
C: Food Chemistry
Shan Xiao, Wan Gang Zhang, Eun Joo Lee, Chang Wei Ma, and Dong U. Ahn
Abstract: The objective of this study was to determine the effects of dietary treatment and packaging on the oxidative
stability of breast rolls. A total of 120 4-wk-old broiler chickens were randomly assigned to control, oxidized diet (5%
oxidized oil, PV = 100), or antioxidants-added diet (500 IU vitamin E + 200 ppm BHA) and fed for 2 wk. Breast
muscles were separated from the carcasses and breast rolls were prepared. The rolls were cooked in a smoke house
(85 ◦ C) to an internal temperature of 74 ◦ C, cooled, sliced to 2-cm thick pieces, individually packaged in oxygen
permeable bags or vacuum-packaged in oxygen impermeable bags, and stored in a 4 ◦ C cold room for 7 d. Lipid, protein
oxidation and volatiles were determined at 1, 4, and 7 d of storage. Dietary supplementation of antioxidants significantly
reduced lipid oxidation (TBARS) and protein oxidation (carbonyls) in breast rolls, and the effect of dietary antioxidants
on lipid oxidation was more pronounced than protein oxidation. Chicken breast rolls from antioxidants treatment group
produced significantly lower amounts of hexanal and pentanal than those from control and oxidized oil treatments
(P < 0.05). However, dietary oxidized oil did not increase lipid and protein oxidation in breast rolls. Vacuum-packaging
significantly delayed the onset of lipid oxidation and protein oxidation in chicken rolls during 7-day refrigerated storage
(P < 0.05). Therefore, it is suggested that appropriate use of dietary supplementation of antioxidants in combination with
packaging could minimize lipid oxidation in chicken breast rolls.
Keywords: antioxidants, breast roll, lipid oxidation, oxidized diet, protein oxidation
Introduction
Authors Xiao and Zhang are joint lead authors of this paper.
meat during chilled storage (Mason and others 2006; Smet and
others 2008). In addition, dietary supplementation of vitamin E
improves the nutritional value of meat products.
Another approach to control rapid oxidative deterioration of
meat products during storage is the elimination of contact with
oxygen. Vacuum-packaging is shown to reduce lipid oxidation
during the storage of cooked meat (Ahn and others 1992; Nolan
and others 1989). Oxidative stability of processed meat can be
further improved through vacuum-packaging in combination with
dietary addition of vitamin E (Ahn and others 1998).
During the storage of meat and meat products, lipid oxidation
results in quality loss through deterioration of flavor, odor, color,
nutritional value, and safety of foods (Varnam and Sutberland 1995;
Winne and Dirinck 1997; Bou and others 2001; Zouari and others 2010). In addition to lipid oxidation, oxidative reactions of
proteins in raw meat can lead to functional changes in myofibrillar
proteins, and negatively affect the tenderness, water-binding capacity, and juiciness of meat (Huff-Lonergan and Lonergan 2005).
Oxidation of proteins resulted in reduced water-holding capacity
and decreased texture-forming ability in processed meat (Xiong
2000). The oxidative status of fat in diet can have significant impact on the storage stability of raw chicken meats (Racanicci and
others 2008; Zouari and others 2010). However, the effect of
dietary supplementation of vitamin E on protein oxidation of
meat during storage is still inconclusive, especially for processed
meat. The aim of this study was to investigate the effects of dietary supplementation of vitamin E, oxidized oil, and vacuumpackaging alone or in combination on the quality of chicken breast
rolls.
Journal of Food Science r Vol. 76, Nr. 4, 2011
R
C 2011 Institute of Food Technologists
doi: 10.1111/j.1750-3841.2011.02137.x
The consumer demands and popularity of ready-to-eat cooked
meat products are increasing rapidly in recent years. However,
processed meats are more vulnerable to oxidative changes than
raw meat. Also, cooked chicken meat was more susceptible to
oxidation than cooked beef and pork (Rhee and others 1996). It
has been postulated that the amounts of polyunsaturated fatty acids
(PUFA) and antioxidants (Morrissey and others 1994) are critical
determinants of lipid oxidation occurring in processed meat.
For many years, butylated hydroxytoluene (BHT), butylated hydroxyanisole (BHA), tertiary butyl hydroquinone (TBHQ), and
other synthetic antioxidants have been extensively used to retard
rancidity in meat products. However, consumers are concerned
about using these additives in meat due to their possible carcinogenic effects to humans, and preferred meat products with reduced
additives or use of natural antioxidants (Jan 1991). Vitamin E is a
natural antioxidant that can be enriched to meat through dietary
regimen. Growing number of researches suggested that dietary addition of vitamin E could maintain oxidative stability of processed
MS 20101312 Submitted 11/18/2010, Accepted 1/14/2011. Authors Xiao,
Zhang, Lee, and Ahn are with Dept. of Animal Science, Iowa State Univ., Ames, IA
50011, U.S.A. Authors Ahn, Zhang, and Lee are also with Dept. of Agricultural
Biotechnology, Biomodulation Major, Seoul Natl. Univ., 599 Gwanak-ro, Gwanakgu, Seoul 151-921 Korea. Authors Ma and Xiao are with College of Food Science and
Nutritional Engineering, China Agricultural Univ., Beijing 100083, China. Direct
inquiries to authors Ahn and Ma (E-mails: duahn@iastate.edu, chwma@cau.edu.cn).
C612
Further reproduction without permission is prohibited
Materials and Methods
Animals and diets
One hundred and twenty, 1-day-old commercial broiler chicks
were fed with a standard broiler corn-soybean diet (Table 1) for
28 d. On 29th day, 10 broilers were assigned to each of 12
floor pens. Four floor pens were randomly allotted to one of
the 3 experimental diets including control, oxidized diet, and
antioxidants-fortified diet. Control diet was prepared with fresh
animal-vegetable fat (AV fat) blend (5%, Feed Energy, Co., Des
Moines, Iowa, U.S.A.) with 25 IU vitamin E, oxidized diet was
prepared after oxidizing the same AV fat by exposing to room
temperature for a long time until attaining peroxide value (PV)
value of 100 (AOAC 1965), and the antioxidants-fortified diet
was prepared with the fresh AV fat supplemented with BHA (200
ppm) and vitamin E (500 IU) per kilogram of feed. Each of the
diet was fed to the broilers for 2 wk with free access to water and
diet. The animal work was performed in accordance with ethical
guidelines of Iowa State Univ. and was approved by the Assurance
Committee for the use of Animals in Research.
Sample preparation
At the end of the feeding trial, the birds were slaughtered following USDA guidelines (USDA 1982). Chickens were chilled in ice
water for 2 h, drained and stored in a 4 ◦ C cold room, and deboned
at 24 h after slaughter. The breast muscles from each pen were
pooled and used as a replication. The pooled ground breast meat
was ground through a 3-mm plate, mixed with 1.5% NaCl and
Table 1–Percentage composition of diets fed to broiler.a
Ingredients
Corn
Soybean meal
AV fat
Dicalcium phosphate
Calcium carbonate
Iowa Vit and Min Prx2
Sodium chloride
Methionine, 99%
Biolysine, 50.7%
Threonine, 99%
Choline chloride, 60%
Calculated analysis
Metabolizable energy, kcal/kg
Protein
Total sulfur amino acids
Methionine
Lysine
Arginine
Glycine + Serine
Histidine
Isoleucine
Leucine
Phenylalanine + Tyrosine
Threonine
Valine
Calcium
Available phosphate
Total phosphate
Sodium
Starter
(1 to 2 wk)
Grower
(3 to 4 wk)
Finisher
(5 to 6 wk)b
56.83
35.98
2.47
1.75
1.28
0.63
0.46
0.27
0.24
0.073
0.037
63.95
29.11
2.82
1.26
1.37
0.50
0.46
0.26
0.21
–
0.053
64.13
27.27
5.00
1.28
1.08
0.50
0.46
0.18
0.045
0.041
0.002
3005
22.48
0.98
0.61
1.34
1.45
2.02
0.59
0.92
1.90
1.35
0.91
1.01
1.00
0.45
0.73
0.20
3100
19.71
0.90
0.57
1.14
1.24
1.76
0.52
0.79
1.72
1.17
0.73
0.89
0.95
0.35
0.61
0.20
3226
18.70
0.80
0.48
1.00
1.18
1.68
0.49
0.76
1.65
1.12
0.74
0.85
0.85
0.35
0.60
0.20
a
Control diet, 5% fresh AV fat and Iowa Vitamin and Mineral Premix; Oxidized diet: 5%
oxidized AV fat (100 PV value); Antioxidants diet: 5% fresh Av fat and 500 IU + 200
ppm BHA per kg diet.
b
Iowa vitamin and mineral premix supplies per kg diet: retinyl acetate = 8065 IU; cholecalciferol = 1580 IU; 25-hydroxy-cholecalciterol = 31.5 μg; dL-α-tocopheryl acetate =
25 IU; vitamin B12 = 16 μg; menadcre = 4 mg; riboflavin = 7.8 mg; pantothenic acid
= 12.8 mg; niacin = 75 mg; Choline chloride = 509 mg; folic acid = 1.62 mg; biotin
= 0.27 mg; Mn = 80 mg; Zn = 90 mg; Fe = 60 mg; Cu = 12 mg; Se = 0.147 mg;
sodium chloride = 2.247 g.
0.25% phosphate (Brifisol), 1.5% transglutaminase, 0.5% sodium
caseinate, 0.5% dextrose, and 6.25% water for 5 min, stuffed into
150-mm collagen casings, and cooked in a 85 ◦ C smoke house
with relative humility of 92% until the center temperature reached
74 ◦ C. After cooling to room temperature by a cold-water shower,
the rolls were cut into 2-cm thick slices and individually packaged
in vacuum bags (nylon/polyethylene, 9.3 mL O2 /m2 per 24 h at
0 ◦ C, Koch, Kansas City, Mo., U.S.A.) or oxygen-permeable bags
(polyethylene, 2,300 mL/m2 per 24 h, 4 × 6, 2 MIL, Associated
Bag Company, Milwaukee, Wis., U.S.A.). Samples were stored in
a 4 ◦ C cold room for 7 d. Lipid, protein oxidation and volatiles
were determined after 1, 4 and 7 d of storage.
Lipid and protein oxidation
Lipid oxidation was determined by a 2-thiobarbituric acid reactive substances (TBARS) method (Ahn and others 1998). Protein oxidation was determined by the method of Levine and
others (1994) with minor modifications. One gram of muscle
was homogenized using a Brinkman Polytron (Type PT 10/35;
Brinkman Instrument, Inc., Westbury, N.Y., U.S.A.) in 10 mL
of pyrophosphate buffer (2.0 mM Na4 P2 O7 , 10 mM Trizmamaleate, 100 mM KCl, 2.0 mM MgCl2 , and 2.0 mM EGTA,
pH = 7.4). Two equal volume of meat homogenate (2 mL) were
precipitated with 2 mL of 20% trichloroacetic acid (TCA) and
centrifuged at 12000 × g for 5 min at room temperature. After centrifugation, the pellet from one sample was treated with
2 mL of 10 mM 2,4-Dinitrophenylhydrazine (DNPH) dissolved
in 2 M HCl and the other was incubated with 2 M HCl as a blank.
During 30-min incubation in dark, samples were vortex-mixed for
10 s every 3 min. The proteins were further precipitated with 2
mL 20% TCA and centrifuged 12000 × g for 5 min. DNPH was
removed by washing 3 times with 4 mL of 10 mM HCl in 1:1
(V/V) ethanol-ethyl acetate followed by centrifuge at 12000 ×
g for 5 min after each washing. The pellets were finally solubilized in 2 mL of 6.0 M guanidine hydrochloride dissolved in 20
mM potassium dihydrogen phosphate (pH = 2.3). The samples
were kept at 5 ◦ C overnight. The next day, the samples were
centrifuged to remove insoluble material. The absorbance of supernatant was read at 370 nm. The absorbance values for blank
samples were subtracted from their corresponding samples values. Protein concentration was determined using a Protein Assay
kit from Bio-Rad laboratories. Briefly, protein determination was
measured using a spectrophotometer at 595 nm. Protein concentration was expressed as milligram per milliliter. The carbonyl
content was calculated as nmol/mg protein using an absorption
coefficient of 22000 M−1 cm−1 as described by Levine and others
(1994).
Analysis of volatile compounds
To determine the volatiles responsible for off-odor of the
samples, a dynamic headspace analysis was performed using a
Solatek 72 Multimatrix vial autosampler and a Purge & Trap Concentrator 3000 (Tekmar-Dohrmann, Cincinnati, Ohio, U.S.A.)
connected to a gas chromatography-mass spectrometry (GC/MS,
Agilent Technologies, Wilmington, Del., U.S.A.) according to the
method of Nam and others (2007). Identification of volatiles was
achieved by comparing mass spectral data of samples with those
of the Wiley library (Agilent Technologies). Standards were used
to confirm the identification by the mass selective detector. The
area of each peak was integrated using ChemStationTM software
(Agilent Technologies), and the total peak area was reported as an
indicator of volatiles generated from the meat samples.
Vol. 76, Nr. 4, 2011 r Journal of Food Science C613
C: Food Chemistry
Dietary oxidation on meat oxidation . . .
Dietary oxidation on meat oxidation . . .
Statistical analysis
The experiment was a factorial design with 3 diet, 2 packaging,
and 4 replications. Data were analyzed by the procedure of generalized linear model using SAS 9.1 software (SAS Inst. 1995). Mean
values and standard error of the means (SEM) were reported.
C: Food Chemistry
Results and Discussion
Lipid oxidation
No significant difference on TBARS was found between the
rolls produced from the chickens fed oxidized and control diets
during whole storage period (Table 2). Addition of oils (animal
or vegetable) is a common practice in formulating broiler diet
because it could not only give high energy but also provide unsaturated fatty acids, which are very important for the fast growth
and the nutritional demands of broilers (Bou and others 2001;
Baião and Lara 2005). Nevertheless, the supplemental oils could
increase the possibility of dietary lipid oxidation. Therefore, many
studies were conducted on the effects of dietary consumption of
oxidized oil on performance, carcass characteristics, and oxidative
stability of meats from various animal species. Many previous studies showed that dietary addition of oxidized oil adversely affected
the oxidative stability of raw chicken meat (Engberg and others
1996; Bölükbaşi and others 2006; Zouari and others 2010). Some
researchers reported that consumption of oxidized oil decreased
deposition of endogenous α-tocopherol in muscle and lowered
oxidative stability and shelf-life of fresh meat (Sheehy and others
1994; Ursini and Sevanian 2002). Our results, however, showed
that adding 5% oxidized oil (PV = 100) to chicken diet before
slaughter had no negative effect on lipid oxidation of chicken
breast rolls during storage (Table 2), probably because the level of
oxidized oil supplemented in diet was relatively low and the duration of feeding was relative short. Another reason could be due
to the heat-induced changes of meat during cooking. Cooking
process damages the structural integrity of muscle tissues and dramatically increases the oxidative stability of meat (Ahn and others
1992). All these reasons could, in some degree, have contributed
to our observation in which no adverse effect was found in the
chicken rolls from chickens fed oxidized diet.
Feeding broilers with a diet containing 500 IU vitamin E/kg
diet for 2 wk before slaughter significantly improved the storage
stability of chicken breast rolls evidenced by lower TBARS level
during the whole storage period (Table 2). TBARS values of
chicken rolls from the antioxidants group were 0.30, 0.40, and
0.48 mg MDA/kg meat at day 1, 4, and 7, which were 78%,
85%, and 87%, respectively, lower than those of the control group.
TBARS value of 0.5 to 1.0 mg malonaldehyde (MDA)/kg tissue
is considered as a threshold for detection of oxidized flavor in
meat (Boles and Parrish 1990). The TBARS value of chicken
breast rolls produced from antioxidants diet increased from 0.30
to 0.48 mg MDA/kg meat while that from control diet increased
from 1.36 to 3.56 mg MDA/kg after 7 d of storage indicating
that dietary addition of vitamin E improved the oxidative stability
of breast rolls. The results agreed with the reports of Wen and
others (1996) who showed that cooked turkey burgers produced
from turkeys fed a diet containing 300 or 600 mg a-tocopheryl
acetate/kg feed were significantly more stable to lipid oxidation
than those from control turkeys. Hams and bacons produced from
pigs fed a-tocopherol supplemented diet had significantly lower
TBARS levels than those produced from the control diet (Winne
and Dirinck 1997; Walsh and others 1998; Cava and others 1999).
Vitamin E, a natural and chain-breaking, lipid-soluble antioxidant, can react with peroxyl radical 200 times faster than synthetic antioxidant BHT (Burton and Traber 1990). Therefore, a
small amount of vitamin E can protect large amount of PUFA
from oxidation. In general, the higher the vitamin E and the
longer the duration, the stronger antioxidant effect could be obtained (Morrissey and others 1994). A number of reports demonstrated that vitamin E significantly retarded lipid oxidation in raw
chicken (Bölükbaşi and others 2006; Zouari and others 2010),
pork (Nam and others 2007), turkey (Ahn and others 1998), and
beef (Arnold and others 1993). Compared to raw meat, however,
Table 2–Effects of diets and packaging on lipid oxidation during refrigerated storage of chicken rolls.1
Storage time (d)
TBARS (mg MDA/kg meat)
Treatment
diet
Control
Oxidized
Antioxidants
SEM
P
1.36a
2.60a
3.56a
1.48a
2.56a
3.84a
0.30b
0.40b
0.48b
0.038
0.19
0.16
<0.05
<0.001
<0.001s
O2 -permeable
1.16a
2.48a
3.92a
Vacuum
0.96b
1.20b
1.32b
0.022
0.16
0.13
<0.001
<0.001
<0.001
1
4
7
Package
1
4
7
1
On the same row, means with different letters differ significantly.
Table 3–Effects of diets and packaging on protein oxidation during refrigerated storage of chicken breast rolls.1
Storage time (d)
Carbonyl content (nmol/mg protein)
Treatment
diet
Control
a
1
4
7
Packaging
Oxidized
a
4.12
4.81a
5.63a,b
O2 -permeable
4.50
5.26a
6.31a
Vacuum
4.22
5.06a
6.42a
4.00
4.53b
4.92b
1
4
7
1
On
2
the same row, means with different letters differ significantly.
NS = not significant.
C614 Journal of Food Science r Vol. 76, Nr. 4, 2011
Antioxidants
b
3.71
4.32b
5.06b
SEM
P
0.14
0.22
0.26
<0.05
<0.05
<0.05
0.11
0.10
0.023
NS2
<0.001
<0.001
processed meat is more susceptible to oxidative damage because
meat products undergo physical manipulations during manufacturing process, which results in the disruption of muscle structure and
exposure of muscle lipids to oxidative environment. Also, antioxidant enzymes in muscle are denatured and iron can be released
from iron-protein during cooking process, which accelerates lipid
oxidation. Furthermore, some ingredients added in processed meat
can have positive or negative effects to the oxidative susceptibility
of processed meat products: NaCl could promote lipid oxidation
possibly through the displacement of iron from heme proteins
(Kanner and others 1990; Ahn and others 1993) while phosphate
has an antioxidant effect (Cheng and Ockerman 2003).
Unlike the vitamin E added to meat during processing, dietary
vitamin E can be directly deposited into subcellular structures.
Deposited vitamin E becomes an integral part of muscle and fat
tissues and is more effective against lipid oxidation (Winne and
Dirinck 1997). Heating could result in around 25% of vitamin E
loss based on the studies by analyzing the content of vitamin E
after cooking and during storage of the cooked products (Wen and
others 1996; Jensen and others 1998). Therefore, dietary supplementation of vitamin E can be of great significance to processed
meat.
Vacuum-packaging significantly delayed the onset of lipid oxidation in chicken breast rolls during the 7-d refrigerated storage
(P < 0.001) (Table 2). The TBARS value of chicken rolls treated
with vacuum-packaging (from 0.96 to 1.32 mg MDA/kg meat)
were lower than those with oxygen-permeable packaging (1.16 to
3.92 mg MDA/kg meat). Packaging can reduce lipid oxidation in
meat and meat products by controlling oxygen interactions at the
meat surface. For meat, especially processed meat, elimination of
oxygen from packing bags after cooking is very important to minimize lipid oxidation (Ahn and others 1992; Brewer and others
Table 4– The interactive effects of diet and packaging on lipid 1992). Significant interactive effects between diet and packaging
on lipid oxidation were found (P < 0.01) (Table 4). Lipid oxand protein oxidation of chicken rolls.
idation
in chicken breast rolls increased as the oxidation of oils
Storage
Probability
Probability
in
diet
increased.
However, vacuum-packaging of cooked breast
Source
time (d)
DF
(TBARS)
(Carbonyl)
rolls reduced the oxidative changes during storage. Therefore, it
Diet × Packaging
1
2
0.0032
0.34
is suggested that appropriate use of dietary supplementation of
4
2
0.0037
0.23
antioxidants in combination with packaging could minimize lipid
7
2
<0.001
0.14
oxidation in chicken rolls.
Table 5–Volatile profile during refrigerated storage of chicken rolls.1
Diet
Volatiles
2
Con
Oxi
Anti
SEM
O2 -per
Packaging
Vac
SEM
Total ion counts × 10
Hydrocarbons
Octane
Pentane
Hexane
Heptane
1
Storage period (d)
4
7
SEM
4
3006a
14257a
959a
1595a
3785a
14663a
1029a
1895a
2266b
7853b
420b
363b
207
2024
89
173
3577a
14804a
985a
1683a
2461b
9711b
620b
885b
170
1634
74
144
1135c
5028b
304c
354c
3477b
16677a
867b
1431b
4443a
15067a
1236a
2066a
205
2024
89
173
252a
3249a
54643
458a
454
225a
2790b
53464
434a
441
97b
3802a
50581
0b
0
10
252
2557
70
164
263a
5036a
55519
595a
560a
121b
1525b
50272
0b
0b
8
204
2064
58
134
76
1077c
37338b
0b
0b
200
2937b
59685a
0b
0b
298
5827a
61663a
892a
899a
10
252
2585
69
162
2466a
1559b
597
870
148937a
31563a
8403a
150a
730b
2214a
1356b
653
942
130359b
29169a
8259a
202a
1247a
222b
1905a
676
554
26413c
3477b
553b
27b
0c
199
172
33
116
4974
1903
624
25
148
3015a
2570a
764a
1070
173417a
38548a
10742
252a
1318a
253b
643b
520b
642
30390b
4257b
736
0b
0b
165
138
27
143
4090
1582
512
20
122
166c
339c
292c
330
19101c
2566c
198c
0b
0b
1383b
1493b
718b
862
113483b
20907b
5066b
153a
0b
3352a
2987a
915a
1340
173124a
40734a
11952a
224a
1796a
198
172
33
122
4919
1903
616
24
147
1597
455
1950
654
1602
635
189
79
1665
836a
1728
327b
120
66
1734
604a
1685
804a
1729
335b
188
78
1246a
268a
69
1415a
289a
53
151b
0b
61
190
20
6.43
1721a
372a
122a
154b
0b
0b
44
16
23
0b
0b
0b
0b
0b
87a
2812a
557a
96a
187
19
6.36
140
424b
104
616a
90
629a
21
71
119
848a
104
265b
17
58
0c
1156a
134b
0c
200a
513b
20
72
Ketones
2-Pentanone
2-Butanone
2-Propanone
2-Heptanone
2,3-Octanedione
Aldehydes
Butanal
2-Methylpropanal
3-Methylbutanal
2-Methylbutanal
Hexanal
Pentanal
Heptanal
Nonanal
Octanal
Sulfur components
Dimethyldisulfide
Carbondisulfide
Alkenes
1,3-Octadiene
2,4-Octadiene
Limonene
Aromatics
Tetrahydrofuran
Thiobismethane
the same row, means with different letters differ significantly (P < 0.05).
Con = control; Oxi = oxidized; Anti = antioxidants; O2 -per = oxygen-permeable; Vac = vacuum.
1
On
2
Vol. 76, Nr. 4, 2011 r Journal of Food Science C615
C: Food Chemistry
Dietary oxidation on meat oxidation . . .
Dietary oxidation on meat oxidation . . .
C: Food Chemistry
Protein oxidation
Similar to lipid oxidation, protein oxidation is considered as a
chain reaction, which involves initiation, propagation, and termination steps. Protein damages in meat and meat products result
in generation of carbonyls, formation of protein polymers, and
scission of peptide bonds, which can lead to changes in protein
structure and hydration (Xiong 2000). These changes in protein
result in diverse functional consequences including lower waterholding capacity, and emulsification, and gelation properties (Hufflonergan and Lonergan 2005), which can partly contribute to the
quality deterioration of meat and meat product. Recently, more
attentions have been paid to the protein modification in meat and
meat products. However, the influence of dietary addition of antioxidants on protein oxidation of meat is not studied extensively.
No significant difference in carbonyls levels between rolls produced from the chickens fed oxidized diet and control diet
during 7-d storage period was detected (Table 3). Protein
oxidation of chicken rolls produced from the birds treated with
different diets, monitored by carbonyls content, was ranged from
3.71 to 6.31 nmol/mg protein (Table 3), which much higher
than those in raw meats (0.30 to 0.76 nmol/mg protein, unpublished data). This phenomenon could be explained by the
fact that processed meat is more susceptible to protein oxidation
than raw meat because of high concentration of oxidizable lipids,
heme pigments, transition metal ions, and oxidative enzymes in
processed meat products. In addition, as discussed above, many
extrinsic factors such as temperature, restructuring, nonmeat ingredients, and heating have been changed during meat processing
(Rhee 1999). ROS (reactive oxygen species) can also be generated
during processing, which can strongly induce protein oxidation
(Xiong 2000).
The rolls manufactured from the chickens fed a diet containing 500 IU vitamin E/kg feed for 2 wk before slaughter had a
significantly lower level of protein oxidation than those from the
control diet at 1-, 4-, and 7-d storage point (P < 0.05) (Table 3).
The initial level of protein oxidation in vitamin E supplemented
group was approximately 3.71 nmol/mg of protein. The content
of carbonyls increased to 5.06 nmol/mg protein level during the
7-d storage period. At 1-, 4-, and 7-d storage point, vitamin E
supplemented group had 7.52%, 10.19%, and 10.12% lower carbonyl values than the control group at the respective storage day,
which were much weaker than the inhibitory effect of vitamin
E on lipid oxidation (78%, 85%, and 87% at each storage point).
Salminen and others (2006) demonstrated that the inhibitory effect of dietary supplements on protein oxidation was marginal
compared to that of lipid oxidation. They postulated that the inhibition of lipid oxidation was the primary target for antioxidants,
but protein oxidation was the secondary target. Vitamin E is fat
soluble, which may be why there was a more protective effect on
lipid oxidation than protein oxidation. Thus, dietary addition of
vitamin E showed a weaker effect in preventing protein oxidation
than lipid oxidation in chicken breast rolls.
Xiong (2000) demonstrated that oxidation of lipids and proteins occurred at the oil-water interface or at the fragmented lipid
membrane. Due to the fact that a-tocopherol can compete for
peroxyl radicals much faster than PUFA, a-tocopherol can protect
a large amount of PUFA by breaking the chain of lipid oxidation
(Morrissey and others 1994). Since lipid and protein oxidation
are probably coupled with each other in meat and meat products
(Reyftmann and others 1990), dietary addition of vitamin E may
protect meat products from both lipid and protein modifications.
C616 Journal of Food Science r Vol. 76, Nr. 4, 2011
Based on current study, it is suggested that dietary treatment of
vitamin E is an excellent method to protect proteins from chemical and functional damages during processing and storage of meat
products.
The carbonyls contents of vacuum-packaged chicken rolls were
4.53 and 4.92 nmol/mg protein after 4 and 7 d storage, respectively (Table 3), which were 10.4% and 23.39% lower than those
packaged in oxygen-permeable bags because oxygen catalyzes protein oxidation. It appeared that limiting oxygen contact to meat
through vacuum-packaging was an effective method to minimize
protein modifications.
Volatiles
Flavor precursors including lipid, carbohydrates, and other
water-soluble nonprotein compounds such as amino acids, peptides, reducing sugars, vitamins, and nucleotides are originally
present in raw meat. Hundreds of volatile compounds can be produced from the precursors upon heating, but only a few of those
play significant roles in the development of characteristic flavor
and aroma of meat.
In current study, 25 volatile compounds were identified during
the storage of chicken rolls (Table 5). They were classified into 6
groups, which include aldehydes, hydrocarbons, ketones, alkenes,
aromatics, and sulfur components. Among them, aldehydes were
the most abundant component, and were dominated with hexanal and pentanal. These results were in agreement with those
of Winne and Dirinik (1997) who claimed that aldehydes were
the most important contributor for the rancidity development in
meat products. The work of Shahidi and Pegg (1993) as well as our
results showed that aldehydes (hexanal and pentanal) were mainly
responsible for rancidity development in chicken rolls. Varnam
and Sutberland (1995) demonstrated that the unsaturated C18
fatty acid of meat, defined as Olenic acid (C18:1n-9), Linoleic
acid (C18:2n-6), and Linolenic acid (18:3n-3), were responsible
for producing low molecular weight (C3-C12) aldehydes, such
as hexanal and pentanal. Thus, the methods that protect these
fatty acids from modification could retard the onset production of
aldehydes.
Hexanal levels of the rolls prepared from chickens fed control
and oxidized diet were 5.65-fold and 6.45-fold higher than that
from antioxidants diet. A significant difference (P < 0.01) was also
found between the rolls prepared from the chicken fed control diet
and oxidized oil diet. These results indicated that adding vitamin E
and oxidized oil to chicken diet significantly retarded or increased
the production of hexanal during storage of chicken breast rolls.
A significant difference in pentanal content was found between
the rolls from chickens fed with oxidized oil and control diet
(P < 0.01). These results coincided with the results of lipid oxidation measured by TBARS. Vacuum-packaged chicken breast rolls
produced 82% and 89% lower amounts of hexanal and pentanal,
respectively, than that of the oxygen-permeable packaged ones.
This suggests that vacuum-packaging is very effective in preventing the production of hexanal and pentanal during the storage of
chicken rolls.
In order to detect the extent of lipid oxidation in meat and
meat products, TBARS and rancidity development (especially
production of hexanal) were widely used as indicators of lipid
oxidation. Some studies reported strong correlations between 2
methods (TBARS and hexanal values) (Ahn and others 1998).
It has been recognized that the contribution of a single volatile
compound to the overall odor depended upon its odor quality
and threshold (Varnam and Sutberland 1995). It should address
that aldehydes played a critical role for the development of rancidity in meat products because they have low odor threshold values.
However, single aldehyde may be not used as a sole index for lipid
oxidation. From our study, hexanal and pentanal together could be
used as an indicator of rancidity development during refrigerated
storage of chicken breast rolls.
Conclusions
Dietary addition of vitamin E significantly decreased lipid and
protein oxidation and the inhibitory effect of dietary antioxidants
on lipid oxidation was more pronounced than that on protein oxidation. Vacuum-packaging significantly reduced lipid and protein
oxidation, and dietary antioxidants in combination with vacuumpackaging could be an effective method to control lipid oxidation
in chicken rolls. Hexanal and pentanal could be utilized as an indicator for the development of rancidity in chicken rolls during
refrigerated storage.
Acknowledgment
This study was supported jointly by the Chinese Scholarship
Council, Iowa State Univ., and WCU (World Class Univ.) program (R31-10056) through the Natl. Research Foundation of
Korea funded by the Ministry of Education, Science and Technology.
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