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,2
* Division of Technical Service, Livestock Research Institute, Council of Agriculture, Hsinhua, Tainan 712, Taiwan;
Department of Life Sciences, National Cheng Kung University, Tainan 701, Taiwan; and
** Department of Food Nutrition, Chung Hua College of Medical Technology, Jente, Tainan 717, Taiwan
2To whom correspondence should be addressed. E-mail: sjchang{at}mail.ncku.edu.tw.
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ABSTRACT |
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 TOP ABSTRACT MATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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-tocopherol acetate), respectively. Blood samples were collected and pullets were artificially inseminated at 35 wk of age. Eggs laid beginning on d 2 after insemination were placed in an incubator. At the time of hatching, 12 chicks from each treatment were randomly sampled and killed. Livers and brains of chicks were collected for the subsequent evaluation of antioxidant status. Plasma vitamin E concentrations increased linearly (P < 0.001; r = 0.997) with the increase in supplemental vitamin E, but those in egg yolk reached a plateau at 120 mg/kg supplemental vitamin E. The malondialdehyde (MDA) concentration, an indicator of lipid peroxidation, of chick brain decreased linearly (P < 0.01; r = –0.909) with the increase in supplemental vitamin E. Pullets given 160 mg/kg supplemental vitamin E had lower plasma MDA concentrations than those given 0 mg/kg (P < 0.05). Similar results were found for the reactive oxygen species levels, an indicator of oxidative stress, of chick brain and liver. For antioxidant enzymes, chicks of pullets given 120 mg/kg supplemental vitamin E had higher (P < 0.05) activities of liver catalase than those given 0–80 mg/kg. Chicks of pullets given 160 mg/kg supplemental vitamin E had higher (P < 0.05) activities of brain superoxide dismutase than those given 0–40 mg/kg. These results indicated that maternal supplementation with high levels of vitamin E (120–160 mg/kg) enhances antioxidant capability and depresses oxidative stress in chicks.
KEY WORDS: • vitamin E • maternal supplementation • antioxidant capability • chicks
Animals metabolically produce different reactive oxygen species (ROS),3 i.e., peroxides, singlet oxygen, and free radicals. Effective antioxidant mechanisms include vitamins A, C, and E, glutathione and antioxidant enzymes, making them essential in protecting the organism against damage resulting from ROS (1). Antioxidant enzymes including glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD) (2) are synthesized and regulated endogenously but require dietary supplies of the appropriated nutrients. The components of this defense system work in a cooperative manner; thus, change in the status of one component may affect that of the others.
Several factors such as pulmonary hypertension syndrome (ascites), ventilation, temperature, and diet factors can increase oxidative stress in chickens (3–7). Breeding hens are continuously exposed to oxidative stress over their lifetimes, and the cumulative stress may cause diseases (4,8). Concern has been raised about the antioxidant ability of hatched chicks in which substantial amounts of the tissue lipids are polyunsaturated (9). Hence, an effective antioxidant system for breeding pullets can be of great importance.
Vitamin E supplementation was shown to be beneficial for the reproduction of chickens in our previous studies (10,11). In addition to its role in reproduction, vitamin E is the major fat-soluble antioxidant, which breaks the chain reaction of lipid peroxidation. The nutrients required for chicken embryo development are derived from the nutrients stored in the eggs, and vitamin E can be increased by raising the dietary level of this vitamin (12,13). Thus, the incorporation of vitamin E into the egg may theoretically both increase oxidative stability and provide a source of tocopherols for human nutrition and health.
Data concerning the effects of maternal vitamin E supplementation on the antioxidant status of hatching chicks are scarce. The antioxidant system of the brain is of great importance because of the development of nutritional encephalomalacia, which occurs in young chicks as a result of vitamin E deficiency (14). The principal objective of the study was to evaluate the antioxidant status of brain tissue of newly hatched chicks and to assess the role of vitamin E supplementation in the maternal diet and its possible beneficial effects on the oxidant defense system of pullets and chicks.
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MATERIALS AND METHODS |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Diets. Using the guidelines suggested by the NRC (17) and the Extension Booklet for Taiwan Native Chicken (18), the basal corn-soybean meal diet was designed as a practical diet that would meet the nutrient requirements for Taiwan native chickens for the growing and laying periods, except that vitamin E was omitted from the vitamin premix (Table 1). The premixes were stored in airtight containers at –20°C until the diets were mixed. Complete feeds were mixed biweekly and stored at 5°C to maintain vitamin stability.
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-tocopherol acetate) (Roche, F. Hoffmann-La Roche). At the beginning of the laying period, the photoperiod was increased by an average of 0.5 h/wk using artificial light up to a maximum of 16 h/d and then maintained at 16 h/d thereafter (combination of natural and artificial light). Insemination of pullets and sample collection. At 35 wk of age, all pullets were artificially inseminated with pooled semen (0.02 mL/pullet) that came from the same flock of 15 males. At the same age, blood of 6 pullets from each treatment was randomly collected from the wing vein into heparinized tubes on ice. Plasma was separated and stored at –70°C. All eggs laid from d 3 after a single insemination were collected and marked. Six of the collected eggs in each treatment group were randomly sampled. Yolks were separated using an egg separator and stored at –20°C for subsequent determination of vitamin E content. The remaining eggs were placed in an incubator on the same day, whereupon 12 chicks from each treatment were randomly selected and killed. Liver and brain tissues of the chicks were excised and rinsed twice with ice-cold PBS and then dried by a filter paper to reduce contamination by blood.
Evaluation of antioxidant system of pullets and hatching chicks. ROS measurements. Using the method modified from LeBel et al. (19), an appropriate volume of plasma or brain homogenate was diluted in 100 mmol/L potassium phosphate buffer (pH 7.4) and incubated with a final concentration of 5 µmol/L 2',7'-dichlorofluorescin diacetate in methanol for 15 min at 37°C. The fluorescence measurements were performed with a Hitachi 850 spectrofluorometer at 488 nm for excitation and 525 nm for emission wavelengths. ROS were quantified from the dichlorofluorescin standard curve in methanol (0–100 nmol/L). Results were expressed as mean fluorescence intensity (MFI) for plasma and brain tissue.
ROS generation of liver tissues was monitored by a chemiluminescent technique modified from Barroso et al. (20) using luminal (5-amino-2,3-dihydro-1,4-phalazinedione) as the probe. In brief, 1 mg liver was homogenized in 0.3 mL of 50 mmol/L sodium phosphate (Na-P) buffer and exposed to 50 µL of a 10 µmol/L luminal solution in dimethyl sulfoxide. Chemiluminescence was monitored as counts integrated over a 1-s period in a Lumat LB9507 luminometer (Lumat LB9507, EG&G). Results were expressed as the difference in counts between post- and preluminol (basal) condition [relative light unit (RLU)/mg tissue].
Catalase measurements.
Using the method of Aebi (21), the oxidation of H2O2, which acted as a substrate, was catalyzed by catalase (CAT) to produce H2O and O2. In the presence of CAT, the absorbance of H2O2 was gradually decreased (
240 = 40 cm2/µmol). The change in absorbance was assayed using a spectrophotometer (DU 530, Beckman). One unit of CAT was defined as the amount required to decompose 1 µmol of H2O2 within 1 min.
GPx determination. GPx activity for plasma and brain was assayed by a modification of the methods of Paglia and Valentine (22). GPx in plasma and brain tissue catalyzed the oxidation using cumene hydroperoxide and H2O2 as the substrate, respectively. Oxidized glutathione was then used as a substrate for glutathione reductase, with the subsequent oxidation of added NADPH monitored as a decrease in absorbance at 340 nm. The processing of plasma and brain tissue supernatants followed the method of Chang et al. (23). The solution was assayed immediately to monitor the change of absorbance within 1 min at 340 nm using a spectrophotometer (DU 530, Beckman). One unit of GPx was defined as µmol NADPH oxidized/min.
SOD measurement. SOD was assayed by a modification of the method of Marklund and Marklund (24). The processing of brain tissue supernatants followed the method of Chang et al. (23). The final solution was assayed to monitor the change of absorbance measured within 1 min at 325 nm using a spectrophotometer (DU 530, Beckman). One unit of SOD activity was defined as the amount of the enzyme inhibiting the autoxidation of pyrogallol by 50%.
TBARS. Lipid peroxidation of plasma and brain homogenates were measured as TBARS expressed in malondialdehyde (MDA) equivalents (25). The fluorescence intensity was measured at excitation and emission wavelengths of 515 and 553 nm, respectively. Lipid peroxidation was expressed as nmol MDA.
Protein assay. Protein was measured using the bicinchoninic acid protein assay kit (Pierce). All enzyme activities were expressed as units/mg protein.
Vitamin E determination.
Vitamin E (total tocopherol) was determined using HPLC. In brief, samples were saponified with ethanolic potassium hydroxide in the presence of pyrogallol, and the tocopherols were extracted from the mixture with hexane. The extract was dried under nitrogen, redissolved in methanol, and injected into the HPLC system (Hitachi L-7480) fitted with a reverse-phase HPLC column (30 cm x 4 mm). Chromatography was performed using a mobile phase of methanol:water (98:2, v:v) at a flow rate of 1.5 mL/min. Fluorescence detection of tocopherol involved excitation and emission wavelengths of 290 and 330 nm. Standard solutions of -tocopherol in methanol were used for instrument calibration and tocol was used as an internal standard.
Statistical analysis. Statistical analysis of the data was performed using the General Linear Model (GLM) procedure of SAS (26). Means of the 5 treatments were compared by Duncan’s Multiple Range Test. Data with unequal variance were reanalyzed after square root transformation. Correlations among the traits were analyzed by Pearson’s correlation adjusted for treatments. A regression equation was used to determine the relation between levels of supplemental vitamin E and yolk and plasma vitamin E. Differences were considered significant at P < 0.05.
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RESULTS |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Plasma antioxidant status was affected only by high level (160 mg/kg) supplemental vitamin E (Table 3). Plasma MDA and ROS concentrations did not differ among pullets fed 0–120 mg vitamin E/kg. Pullets given 160 mg/kg supplemental vitamin E had lower plasma MDA concentrations and greater plasma ROS concentrations than those given 0–80 mg/kg. Pullets given 120 mg/kg supplemental vitamin E had lower (P < 0.05) plasma GPx activity than pullets given 0 and 40 mg/kg.
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DISCUSSION |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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The formation of ROS was prevented by an antioxidant system that included nonenzymatic antioxidants (ascorbic acid, glutathione, tocopherols), enzymes regenerating the reduced forms of antioxidants, and ROS-scavenging enzymes such as SOD, GPx, and CAT (30). Plasma GPx and ROS were not correlated in this study. Simon et al. (31) showed that antioxidant vitamin supplements did not reduce ROS activity in the short term. Chen et al. (32) reported that vitamin E had antioxidant activity at a low concentration and prooxidant activity at a high concentration (120 mg vitamin E/kg diet) in laying hens. It is not clear whether the rise of plasma ROS levels in pullets was due to the prooxidant effect of vitamin E when the pullets were fed 160 mg supplemental vitamin E/kg. Further studies are warranted to elucidate the mechanisms of the possible prooxidant effect.
Vitamin E functions biologically as a membrane-specific scavenger of free radicals, and GPx functions as a destroyer of peroxides (33). Yang et al. (34) reported that both excess and deficient amounts of vitamin E significantly depressed the activity of GPx in liver and plasma of rats. The activities of GPx and vitamin E have complementary roles against oxidative agents. In this study, plasma GPx activities of pullets were depressed (P < 0.05) by higher levels of supplemental vitamin E (120 mg/kg) suggesting a compensation of the oxidant defense system. The results were in agreement with a report of Eder (35), but not with those of Meydani et al. (36) and Chow et al. (37). We speculate that high plasma vitamin E concentrations might have reduced the susceptibility to lipid peroxidation and thus lowered GPx activity.
Birds exposed to an oxidative stress such as the hatching period were expected to react with a compensatory induction of endogenous antioxidants. In hatching chicks, the brain is highly susceptible to oxidative stress because of the accumulation of PUFAs (38). Hence, the antioxidant system of the brain was of great importance because the chicks’ nutritional encephalomalacia could be induced by diets rich in oxidized oil and deficient in vitamin E (14).
Lipid peroxidation was initiated when the generation of ROS such as H2O2, the hydroxyl radical, and superoxide, hydroperoxides, or other free radicals exceeded the antioxidant capabilities of cells or tissues (39). Levels of ROS were assayed as an indicator of oxidative stress. ROS play an important role in the etiology of many diseases associated with a micronutrient deficiency. Theoretically, antioxidant enzymes and antioxidant vitamins provide a defense against damage to cells by ROS in living systems. However, excessive ROS generation might have overwhelmed the protective mechanism. This study showed that maternal supplementation of vitamin E significantly decreased ROS levels in brain and liver of the progeny.
SOD plays an important role in protecting cells from damage caused by ROS. SOD converts superoxide to H2O2 and oxygen In turn, H2O2 is reduced by CAT and GPx to H2O and oxygen. Normally GPx is considered qualitatively more important in maintaining low cellular H2O2 levels because it has a much lower Km than CAT (40). Studies of the effects of dietary vitamin E on antioxidant enzyme activities remain controversial (29,41,42). In the present study, liver CAT activities of hatching chicks were significantly increased when pullets were fed 120 mg/kg supplemental vitamin E compared with those in the 0–80 mg/kg groups. Elevation of CAT and SOD could be an indication of increased antioxidant protection of the tissues.
Vitamin E, GPx, SOD, CAT, and other antioxidant defense mechanisms are present in different tissues with a variety of concentrations and activities. These cooperative antioxidant defense mechanisms minimize oxidative damage. Dietary vitamin E could accumulate in various tissues of chicks (43). In addition, maternal dietary vitamin E was found to accumulate in liver and brain of chicks and the concentration in the liver was much higher than that in the brain (38). The liver was reported to be the most responsive to vitamin E manipulation (44).
In the present study, pullets given a high level (160 mg/kg) of supplemental vitamin E had progeny with greater brain SOD but not CAT and GPx activities compared with those given 0 and 40 mg/kg vitamin E. Another report showed that CAT and GPx activities were low in the brain compared with other major tissues, and SOD was the main enzyme of antioxidant defense in the brain (45).
The increase in the activities of brain SOD and CAT led to an increased defense of cell membranes against oxygen and lipid free radicals. We speculate that natural antioxidants accumulated in the egg yolk as a result of their transfer from the maternal diet, and antioxidant enzymes in hatching chicks might play an important role in tissue protection against lipid peroxidation. Although Combs (46) reported that GPx, CAT, or SOD activities in liver or brain were not affected in chicks fed supplemental vitamin E (100 mg/kg), the results of this study showed that not only the liver but also the brain was a vulnerable organ whose antioxidant system could be altered through maternal supplementation of vitamin E.
We conclude that enhancement of the antioxidant status of hatching chicks can occur through supplementation of vitamin E to the maternal diets and that maternal dietary vitamin E would be beneficial in protecting the tissues of the progeny from oxidative injury.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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3 Abbreviations used: CAT, catalase; GPx, peroxidase; MDA, malondialdehyde; MFI, mean fluorescence intensity; RLU, relative light unit; ROS, reactive oxygen species; SOD, superoxide dismutase.
Manuscript received 25 February 2005. Initial review completed 26 April 2005. Revision accepted 11 July 2005.
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