Professional Documents
Culture Documents
discussions, stats, and author profiles for this publication at: https://www.researchgate.net/publication/276108599
CITATION
READS
45
6 AUTHORS, INCLUDING:
Zhigang Song
Huameng Lin
SEE PROFILE
SEE PROFILE
2144
2145
2146
Chunxu et al.
2147
Figure 1. Effect of heat exposure treatment (32 1C for 7 d) on plasma activities of antioxidative enzymes and oxidative damage biomarkers of
broilers. 8-OHdG = 8-hydroxydeoxyguanosine; AIHR = ability to inhibit hydroxyl radicals; CAT = catalase; GSH-Px = glutathione peroxidase; SOD =
superoxide dismutase; TAC = total antioxidant capacity; TBARS = thiobarbituric acid reacting substances.
compared to controls, whereas the activity of GSHPx was not affected (P > 0.05; Fig. 2a). In thigh muscle, however, SOD (P = 0.001) and CAT (P < 0.05)
activities were decreased whereas GSH-Px activity
was increased (P < 0.001) by heat exposure (Fig. 2b).
Compared to control birds, heat-stressed broilers had
higher concentrations of protein carbonyl (P < 0.001)
and TBARS (P < 0.001) in breast and thigh muscles
2148
Chunxu et al.
Figure 2. Effect of heat exposure treatment (32 1C for 7 d) on activities of antioxidant enzymes and contents of oxidative damage biomarkers in
breast and thigh muscles of broilers. 8-OHdG = 8-hydroxydeoxyguanosine; CAT = catalase; GSH-Px = glutathione peroxidase; SOD = superoxide dismutase; TBARS = thiobarbituric acid reacting substances.
DISCUSSION
In the present study, the effect of heat exposure
on the oxidative stress in mitochondria, skeletal muscle, and plasma was investigated. The result indicated
that heat stressinduced oxidative injuries occurred in
mitochondria, skeletal muscles, and the whole body.
Antioxidant enzyme activity responded to heat stress
in a tissue-specific manner. Increased circulating allantoin level demonstrates that urate functions as an
antioxidant during heat stress. The suppressed mitochondrial complex I activity is suggested to be associated with induced oxidative stress by heat exposure.
Heat ExposureInduced Whole Body Oxidative Stress
The antioxidant enzyme system, including SOD,
CAT, and GSH-Px, works in concert with free radical
scavengers to quench ROS and to protect cells from
2149
Figure 3. Effect of heat exposure treatment (32 1C for 7 d) on antioxidant enzymatic activities, the contents of 8-hydroxydeoxyguanosine (8OHdG), and ability to inhibit hydroxyl radicals (AIHR) in mitochondria of breast and thigh muscles of broilers. CAT = catalase; GSH-Px = glutathione
peroxidase; SOD = superoxide dismutase.
in heat-stressed broilers indicated that the nonenzymatic scavenge capacity was lowered by heat exposure. This speculation was supported by the observation that heat-stressed chickens had a lower AIHR,
which was determined to reflect the ability to inhibit
hydroxyl radicals (Liu et al., 2013).
For enzymatic system, the increased SOD, decreased GSH-Px, and unaltered CAT activities imply
that the balance between the production and scavenging of hydroxyl radicals is disrupted, resulting in the
accumulation of hydroxyl radicals. The responses of
antioxidant enzyme activity during heat exposure were
different in previous studies. For example, in laying
ducks, heat exposure decreased plasma activities of
SOD and GSH-Px (Ma et al., 2014). In contrast, plasma SOD activity was increased in heat-stressed laying hens (Lin et al., 2008). Acute heat stress increased
serum activities of SOD, CAT, and GSH-Px (Yang et
al., 2010). In the present study, the decreased GSH-Px
and unaltered CAT activities may be related the high
2150
Chunxu et al.
Figure 4. Effect of heat exposure treatment (32 1C for 7 d) on respiratory chain complex activities in breast and thigh muscle of broilers.
8-OHdG concentrations in breast and thigh muscles indicated that heat stress resulted in oxidative injury in
skeletal muscles of broilers, regardless of muscle type.
The altered antioxidative enzyme activities were
involved in the development of oxidative injury. The elevated SOD and CAT activities and unaffected GSH-Px
activity in breast muscle was in line with previous work
of Ghazi Harsini et al. (2012), who reported that GSHPx activity remained relatively constant whereas SOD
activity levels in breast muscle (pectoralis superficialis) were enhanced on exposure to heat stress. Similarly,
there was a temperature-dependent elevation in Cu/ZnSOD activity whereas GSH-Px activity remained relatively constant during heat stress (Azad et al., 2010).
In contrast, the increased GSH-Px but decreased SOD
and CAT activities in thigh muscle indicated there is a
tissue-specific response in the antioxidative enzymatic
system. As oxidative injuries were detected in breast
and thigh muscle tissues, the result imply that the activation of antioxidative enzymes cannot prevent the oxidative injury induced by heat exposure in breast, and on
the other hand, the suppressed enzyme activities suggests the suppressed radical elimination.
We further evaluated the redox balance in mitochondria of muscle tissues. The higher concentration
of 8-OHdG in breast and thigh muscles of heat stress
chickens compared with control ones indicated that
oxidative stress occurred in mitochondria, in line with
the work of Mujahid et al. (2007c), who reported that
oxidative damage in mitochondrial lipids and proteins
occurred in muscles of heat-stressed chickens (Mujahid
et al., 2007c). Moreover, the decreased AIHR and elevated SOD and decreased GSH-Px and CAT activities
may further imply the arrested reduction capacity for
hydrogen peroxide in mitochondria of skeletal muscles.
During the movement of electrons in the transport
chain, electrons may leak from the respiratory chain before they reach the terminal electron acceptor (Chance
et al., 1979). The overproduction of mitochondrial ROS
in chicken skeletal muscle under heat stress might result
from enhanced substrate oxidation and downregulation
of avUCP (Mujahid et al., 2006, 2007a,b). The oxidative
phosphorylation system consists of 4 multiprotein complexes (I to IV) and ATP synthase (complex V), through
which electrons from reduced substrates pass to oxygen.
Complex I and III are the 2 principal sites of superoxide
generation in mitochondria (St-Pierre et al., 2002; Brand
et al., 2004). The lowered activity of complex I in breast
and thigh muscle tissues of heat-stressed broilers compared to control birds and the differently influenced activity of complex III suggest that complex I is involved
in the enhanced leakage of superoxide during heat stress.
In mammals, complex I inhibition resulted in greater
ROS production and oxidative stress (Pitknen and
2151
2152
Chunxu et al.
2153