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1 Department of Environmental
Health Sciences, Breath ethane, O2
consumption, and CO2 production
were analyzed in 24-mo-old female Fischer 344 rats that had been fed
continuously ad libitum (AL) or restricted 30% of AL level (DR) diets
since 6 wk of age. Rats were placed in a glass chamber that was first flushed with air, then with a gas mixture containing 12%
O2. After equilibration, a sample
of the outflow was collected in gas sampling bags for subsequent
analyses of ethane and CO2. The
O2 and
CO2 levels were also directly
monitored in the outflow of the chamber. O2 consumption and
CO2 production increased for DR
rats. Hypoxia decreased O2
consumption and CO2 production for
the AL-fed and DR rats. These changes reflect changes in metabolic rate
due to diet and PO2. A significant
decrease in ethane generation was found in DR rats compared with AL-fed
rats. Under normoxic conditions, breath ethane decreased from 2.20 to
1.61 pmol ethane/ml CO2. During
hypoxia the levels of ethane generation increased, resulting in a
DR-associated decrease in ethane from 2.60 to 1.90 pmol ethane/ml
CO2. These results support the
hypothesis that DR reduces the level of oxidative stress.
dietary restriction; aging; hypoxia; breath analysis
DIETARY RESTRICTION (DR) without malnutrition is a
well-established approach for altering aging rate in laboratory
rodents, as evidenced by increased life span, reduced incidence of
age-associated pathologies, and improved function into old age (16,
29). Despite the evidence in support of this observation, the specific mechanisms that can explain the wide range of effects on various parameters of aging have not been identified (16).
One plausible theory to explain normal aging is the age-related
increase in oxidative stress (8). Moreover, it has been hypothesized
that DR reduces the production of reactive oxygen species generated
during normal metabolic processes and/or increases the
endogenous antioxidant defenses. These changes will, therefore, reduce
the cellular and molecular damage associated with aging. By measuring
the production of superoxide and hydroxyl radicals in liver microsomes,
Lee and Yu (14) reported that DR rats generated fewer reactive oxygen
species. Evidence supporting increased levels of endogenous
antioxidants is indicated by a reduction in the age-related decline in
glutathione, glutathione reductase, and catalase activities in livers
of DR rats compared with control rats (13).
Lipid peroxidation in various tissues has been examined (31) to measure
the balance between oxidants and antioxidants, i.e., oxidative stress
status (OSS). Most studies have used the thiobarbituric acid-reactive
substances (TBARS) assay as a measure of malondialdehyde (MDA) formed
as a result of lipid peroxidation. These studies suggest that lipid
peroxidation as quantified by MDA is reduced in liver homogenates of
rodents maintained on long-term DR compared with control animals. The
TBARS assay is simple to perform. However, thiobarbituric acid also
reacts with other aldehydes generated during the heating procedure. In
addition, the in vivo lifetime of MDA is short. Therefore, the TBARS
assay is not considered a reliable method to assess in vivo lipid
peroxidation (22).
Volatile hydrocarbons are also products of lipid peroxidation (12).
Ethane, derived from n-3 polyunsaturated fatty acids (i.e.,
linolenic acid), and 1-pentane, derived from n-6 fatty acids
(i.e., linoleic and arachidonic acid), are alternate molecules to probe
lipid peroxidation. These alkanes are produced by Ethane and 1-pentane diffuse across cell membranes and are rapidly
excreted from the lungs. They are also metabolized by cytochrome P-450 monooxygenases, with 1-pentane
being broken down more readily than ethane. Because 1-pentane and
2-methyl-1,3-butadiene (a major hydrocarbon found in exhaled breath)
are difficult to separate by gas chromatography, ethane is considered
the preferred marker of lipid peroxidation.
Recently, using breath ethane as a sensitive, specific, noninvasive
indicator, one of our research group (11, 27) confirmed the link
between cellular injury and free radicals generated in vivo during
reperfusion of ischemic tissues (6) in humans and animal models. Breath
ethane has also been used as a biomarker of vitamin E deficiency and
therapy in children with chronic liver disease (23). This latter
investigation also established that neither fat nor carbohydrate diets
affected the breath ethane measurements. More recently, the oxidative
injury produced during total body irradiation, used therapeutically for
treatment of leukemia and other malignancies of the
hemopoietic system, has also been examined using breath
ethane (1).
These studies establish the validity of breath ethane as a reliable
noninvasive measure of the oxidant-antioxidant balance. We report on
our experiments designed to evaluate the utility of breath ethane as a
biomarker of oxidative stress during DR. We have investigated the
levels of ethane in exhaled breath for 24-mo-old female Fischer 344 DR
and ad libitum (AL)-fed rats. Additionally, these same rats were
studied under hypoxic stress, since reduced levels of
O2 have been shown to increase
lipid peroxidation (3, 24, 25, 30). The goal of these studies was to
evaluate the measure of breath ethane as a biomarker for the role of
oxidative stress and its potential manipulation by DR.
Animal Protocol
ABSTRACT
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Abstract
Introduction
Methods
Results
Discussion
References
INTRODUCTION
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Abstract
Introduction
Methods
Results
Discussion
References
-scission of the
lipoalkoxyl radical to produce the alkyl radical followed by hydrogen
abstraction to produce ethane or 1-pentane. Although only a small
fraction of the lipid peroxides actually produces ethane or 1-pentane,
the production of these alkanes reflects the extent of lipid
peroxidation (12) and, thereby, the in vivo OSS of the organism.
METHODS
Top
Abstract
Introduction
Methods
Results
Discussion
References
The rats were housed singly in plastic cages suspended from a metal rack, with water provided AL via an automated watering system. The vivarium was maintained at 21°C with a 12:12-h light-dark photocycle (lights on 6:00 AM Eastern Standard Time). The experiments were conducted 2 mo after entry to the Gerontology Research Center. At that time the mean body weight for the DR rats was 168.4 g, 42% less than that of the AL-fed rats. One DR animal died before the start of the experiment.
Methods for Breath Collection
Hydrocarbon-free gases. Air and 12% O2 with hydrocarbon levels of <1.0 ppb (Scott Specialty Gases, Plumstedville, PA) were used for this study.
Exposure protocol.
The rats were brought to the laboratory 
1 h before the experiment was
initiated and placed in a specially designed 2-liter flow-through Pyrex
glass chamber, so they would adjust to the new environment. This
conditioning reduced the stress of the rats during breath collection
(9). The chamber was cleaned between rats and kept sealed when not in
use to minimize wall adsorption of hydrocarbons from the laboratory
air. A fan was installed in one end of the chamber to provide adequate
mixing of the gas in the chamber. Teflon tubing was used for all
connections between the gas cylinders, the rat chamber, and the
sampling bags.
Breath collection.
Samples of chamber air and background hydrocarbon-free air were
collected in inert gas sampling bags (3 liters, Calibrated Instruments,
Hawthorne, NY). Samples were analyzed within 6-8 h after
collection. Previous research (11) has shown that breath and air
samples are stable in these bags for 48 h.
Analysis of CO2 in Exhaled Breath
Aliquots (20 ml) of collected gas (under normoxic and hypoxic conditions) were used for the determination of the concentrations of CO2 (LB-3 CO2 monitor, Beckman) in the gas sampling bags. This instrument was calibrated daily using certified gas standards of CO2.For determination of the CO2 production during the period of low flow, an in-house-constructed infrared CO2 monitor was connected directly to the outlet of the chamber. Corresponding readings were obtained under identical flow conditions by using the empty chamber. The differences between the measured CO2 for the chamber containing the rat and the blank without the rat were used to calculate CO2 production for each rat.
Analysis of O2 in Exhaled Breath
PO2 was determined (model 2717 Orbisphere O2-measuring system) during the period of low flow at the outflow of the chamber for air and the 12% O2 gas mixture. O2 readings were corrected for humidity and temperature. Corresponding readings were obtained under identical flow conditions by using the empty chamber. The differences between the measured PO2 for the chamber containing the rat and the blank without the rat were used to calculate O2 consumption for each rat.Analysis of Ethane in Exhaled Breath
Concentrating gas samples.
A stainless steel wide-bore capillary tube (15 cm, 1.65 mm OD, 1.19 mm
ID) packed with
2,6-diphenyl-p-phenylene oxide (60-80 mesh, Tenax, Alltech Associates, Deerfield, IL) connected to a six-port
stainless steel gas sampling valve (1.59-mm inlets, Valco Instruments,
Houston, TX) was used in place of the standard gas sampling loop. The
length of the Tenax packing was 10 cm, and the packing was retained on
either side with silanized glass wool. This collection tube was
submerged in an ethanol-liquid nitrogen slush bath (
117°C).
The collection tube was maintained in the low-temperature slush bath
for 6 min to allow the adsorbent to equilibrate to 117°C,
and then a gastight syringe was used to draw 100 ml of collected gas
through the adsorbent. A disposable trap containing Ascarite was placed
between the sample bag and the collection tube to remove
CO2 from the gas sample. After the gas had been sampled, the liquid nitrogen slush bath was replaced with
a specially designed heating block maintained at 160°C, and the
concentrated gas sample was injected immediately onto the gas
chromatographic column by rotation of the gas sampling valve. We have
determined that the collection tube and adsorbent reach 160°C
within 30 s. The valve was rotated back to its fill position after 45 s, and the collection tube was flushed with nitrogen to clean it before
collection of the next sample.
117°C all the molecules studied can be collected with ~100% efficiency by
using volumes of breath of up to 200 ml. Similarly, we have established
that the thermal desorption temperature (160°C) quantitatively desorbed the molecules of interest without significant tailing of the
solute peaks (1).
Capillary gas chromatographic analysis. A modification of the technique reported previously (1) was used to analyze the concentrated gas samples. Analysis of the components of breath was performed using capillary gas chromatography with flame ionization detection. Separation was achieved on a fused silica capillary column, the walls of which were coated with a thick film of dimethyl silicone (60 m, 0.53 mm ID, 7 µm). The capillary column was connected directly to the gas sampling valve to improve efficiency of the resulting chromatographic separation.
The temperature protocol for the separation was as follows: isothermal at 25°C for 10 min, 25-200°C at 5°C/min, and isothermal at 200°C for 5 min. Linear gas velocities of 25 cm/s at 25°C were used. The analytic method was calibrated daily by injection of a standard mixture of hydrocarbons. The limit of quantification with use of 100 ml of exhaled breath is 0.05 ppb for ethane. A typical coefficient of variation (5) for replicate samples was 3% (n = 10).Pathology and Blood Testing
To be certain that pathology common to older rats (4) did not confound the results, on completion of the experiment, whole trunk blood was collected and sent to a commercial laboratory for evaluation (Maryland Medical, Baltimore, MD). Gross necropsy was then performed visually to identify lesions in each rat. This examination involved an assay of peripheral organs (lung, spleen, gastrointestinal tract, and reproductive organs) and a visual inspection of the pituitary, in which tumors are common in this rat strain (4).Statistical Analysis
Statistical analysis of the effect of diet on O2 consumption, CO2 production, and ethane generation was performed using t-tests of the average of the normoxic and hypoxic results for each animal. This procedure provided a method to determine the effects of diet on the basis of the combined normoxic and hypoxic results. Because hypoxic and normoxic measurements were made on the same animals, the statistical analysis of the effect of hypoxia on O2 consumption, CO2 production, and ethane generation was performed using paired t-tests.| |
RESULTS |
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Methods
Results
Discussion
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Respiration
PO2 and PCO2 were measured continuously when each rat was in the chamber. Table 1 shows a summary of the O2 consumption and CO2 production (corrected for flow and body weight) as well as the respiratory quotient obtained from these data. The values of the respiratory quotient between 0.73 and 0.80 indicate no major changes in the relative metabolism of fats and carbohydrates. The significant increase in O2 consumption and CO2 production under normoxic and hypoxic conditions for the DR rats is consistent with the published (19) increase in metabolic rate from 112.8 kcal · kg body wt
1 · day1
for AL-fed rats to 124.3 kcal · kg body
wt1 · day1
for DR rats when metabolic results are normalized relative to the
weights of the animals. Table 1 also shows that hypoxia produced a
significant decrease in O2
consumption and CO2 production for the AL-fed and DR rats. These decreases are probably associated with a
drop in metabolic rate. Because DR influences
O2 consumption and
CO2 production, a more meaningful
determination of the effect of hypoxia can be obtained by combining the
DR and AL-fed rats and performing a paired
t-test. This analysis provides very
highly significant (P < 0.00001)
effects of hypoxia, with t values of 11.0 for O2 consumption and 6.7 for CO2 production. Considering the normoxic and hypoxic results as two determinations on each rat, we
have also averaged both results and then performed
t-tests (for
O2,
t = 4.7, P < 0.001; for
CO2,
t = 4.9, P < 0.0001) to establish the
significance of the effects of diet on
O2 consumption and
CO2 production.
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Breath Ethane
Table 2 compares the ethane results for 11 DR rats and 10 age-matched AL-fed controls. The results for ethane are presented in two ways. First, the concentrations of ethane were corrected for flow rate and body weight (pmol · 100 g1 · min1).
This method of calculating the data has been used in most of the
previous studies on ethane generation in rats, including those dealing
with DR (7, 17). No significant effects were obtained by this method.
Second, the concentrations of ethane were normalized by the
CO2 production (pmol ethane/ml
CO2). Because the ethane and
CO2 are determined from the same
gas collection bag, the flow rate and weight of the animal cancel out
of this calculation. A t-test
performed on the average of the ethane levels during hypoxia and
normoxia indicates that the effect of diet was significant (t = 2.9, P < 0.01). Included in Table 2 are
the data obtained under hypoxic conditions produced by replacing the
air with a gas mixture containing 12%
O2. The increased ethane
generation with hypoxia, when analyzed by a paired
t-test combining AL-fed and DR rats,
indicated P < 0.07, which was almost
significant.
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No significant correlations emerged between any of the measures of pathology and ethane levels measured. Therefore, pathology per se did not significantly contribute to the results obtained in the current study. Support for increased pathologies in the AL-fed rats is, however, suggested by the significantly larger mean cell volume in the AL-fed than in the DR rats (P < 0.015 by a 2-tailed t-test). The larger mean cell volume in the AL-fed rats, which was also significantly correlated with the number of white blood cells, is frequently associated with stressed erythropoiesis and other pathologies (28).
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DISCUSSION |
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Diet and Ethane Generation
When the ethane results were calculated in units (pmol · 100 g1 · min1)
used by other investigators who have studied ethane generation in DR
rats (7, 17), no effect of DR on ethane was found. This finding agrees
with the earlier results in which this form of analysis was used on
male Fischer 344 rats. Matsuo et al. (17) measured exhaled 1-pentane
and ethane in long-term DR and control male Fischer 344 rats as a
function of age. They reported increased concentrations of alkanes in
exhaled breath in older animals, consistent with increased oxidative
stress during aging. However, DR did not significantly affect the
concentration of breath alkanes before 28 mo of age. For these old
rats, decreases in the concentrations of ethane and 1-pentane were
observed, although the difference was statistically significant only
for 1-pentane.
In our study we are looking for a measure of ethane release that reflects the OSS of the animal. We are comparing animals on different dietary regimens and under different PO2 that are seen to have altered metabolic rates (Table 1). Because metabolic rate will influence ethane generation, a reliable measure of OSS necessitates a correction for metabolic rate rather than the simple body weight. We have, therefore, used exhaled CO2 (CO2 generation) in the same gas collection bag as a measure of metabolic rate. Because no CO2 is present without respiration, this normalization is more reliable than normalization by O2 consumption, which involves differences between two large numbers. As shown in Table 2, this method of analysis results in a significantly lower value for ethane generation in DR than in AL-fed rats, suggesting reduced oxidative stress in the DR rats.
This method is analogous to the preferred method for ethane generation used in human studies. In those studies it has been shown (21) that a more reliable method to express the concentration of molecules in exhaled breath is to normalize the concentrations of the analyte molecules to the alveolar concentration of CO2 (40 Torr). That method for expressing the concentration of molecules in exhaled breath corrects for respiration rate as well as respiratory dead space air and for incomplete breath collection.
In evaluating our ethane results, considering the source of the ethane generated during respiration is helpful. If the entire animal is equilibrated with the gas flowing through the chamber, then the ethane generated should depend on the total cellular concentrations of the linolenic acid derivatives of the polyunsaturated fatty acids. Although the DR rats have decreased total mass, this does not affect all tissues in the same way. A dramatic difference in the relative mass of the hindlimb muscle, which depends on diet, has been documented by Luhtala et al. (15). This muscle shows a drop in mass during aging for AL-fed rats that does not occur in DR rats. Additionally, different tissues may have different levels of antioxidants and will be peroxidized to a different extent. Because the main sources of excreted hydrocarbons in the body are liver, erythrocytes, and lung, ethane generation rates corrected to body mass will tend to underestimate ethane generation rates in AL-fed rats. Therefore, a metabolic body weight has been used in our studies.
Habib et al. (7) also reported a decrease in ethane generation for young male Fischer 344 rats (6 wk of age) undergoing short-term DR for 2 wk and found decreased ethane generation consistent with our data. It has been reported (18) that male Fischer 344 rats undergo a transient decrease in the metabolic rate when DR is initiated. However, after 24 wk of DR, no change in the 24-h metabolic rate or the basal metabolic rate is found. These initial changes in metabolic rates appear to coincide with a significant decrease in ethane production that can be detected even without correcting for CO2.
Our studies have been performed on female Fischer 344 rats. Unfortunately, all other studies on ethane generation rates have been done with male Fischer 344 rats. Male and female rats have significant physiological differences, including their ability to respond to oxidative stress. The activities of superoxide dismutase and catalase in the livers of Fischer 344 rats generally fall with age in males but increase with age in females (2). Future studies are planned to investigate the effects of gender, DR, and OSS.
Hypoxia
The relationship between DR, stress, and OSS was investigated using hypoxia. As indicated in Table 2, hypoxia produces a similar nonsignificant increase in ethane for DR and AL-fed rats when ethane is normalized to CO2 production. This increase is, in fact, almost significant when a paired t-test was used to analyze all the animals studied. Although 12% O2 was used in the hypoxic experiments, PO2 at the outlet of the flow-through chamber varied from 9.8 to 7.8% O2. The observation of an increase in ethane with hypoxia supports a recent hypothesis that implicates hypoxia in the release of oxyradicals from erythrocytes (26). This process involves the autoxidation of Hb bound to the inner surface of the erythrocyte membrane (25). Autoxidation would be expected to induce lipid peroxidation of the erythrocyte membrane, lipoproteins, and adjacent endothelial cells (10).Several in vitro studies have shown that higher levels of ethane are produced at reduced PO2 (3, 24), even though lipid peroxidation as determined by other methods increases with increasing PO2. These observations have been attributed to a preferential reaction of O2 with the alkyl radicals, producing O2-containing products instead of alkanes. The possible contribution of such in vitro mechanisms to the enhanced ethane release detected under hypoxic conditions needs to be considered.
However, a number of in vivo studies have demonstrated enhanced lipid peroxidation by various methods under hypoxic conditions and during ischemic insults (25). During chronic hypoxia, with rats maintained at 15% O2 for 2 wk, Yoshikawa et al. (30) found increased lipid peroxidation as measured by MDA formation in abdominal aortic wall tissue, brain tissue, and serum. An increase in lipid hydroperoxide was also found in rat hearts on adaptation to high-altitude hypoxia (10). MDA production increased in brain and blood of stroke-prone spontaneously hypertensive rats for which evidence of regional ischemia was present. The loss of unsaturated fatty acids was found in cat brain with middle cerebral artery occlusion. Increases in MDA were found in experimentally induced canine heart infarcts and in ischemic rat heart (20). Ischemia of the hindlimbs of dogs was found to produce an increase in hydroperoxide and diene conjugation of sarcoplasmic reticulum membranes. These results suggest that hypoxic conditions do actually increase oxidative stress. The studies reported here are consistent with this hypothesis. Increasing the number of animals in each group may enable statistical differences on the effect of hypoxia to be observed.
Conclusion
The decrease in breath ethane from 2.20 to 1.61 pmol ethane/ml CO2 for DR rats at normoxic PO2 and from 2.60 to 1.90 pmol ethane/ml CO2 at a hypoxic PO2 indicates a significant dependence on diet. These results support the hypothesis that DR reduces oxygen free radical damage. The establishment of breath ethane as a reliable biomarker for such damage was shown to require normalization by CO2 production. In this way it was possible to correct for differences in metabolic activity, providing a more reliable measure of the OSS of the animal.| |
ACKNOWLEDGEMENTS |
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The editorial assistance of S. Sehnert is gratefully acknowledged.
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FOOTNOTES |
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This study was supported in part by National Institute of Environmental Health Sciences Grant ES-03156 and US Air Force Grant F-49620-95-0270.
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Address for reprint requests: J. M. Rifkind, Gerontology Research Center, National Institute on Aging, 5600 Nathan Shock Dr., Baltimore, MD 21224.
Received 8 July 1998; accepted in final form 20 October 1998.
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References
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