Decline In Oxygen Consumption Research Articles

A three-dimensional model to describe complete human corneal oxygenation during contact lens wear.

We perform a novel 3D study to quantify the corneal oxygen consumption and diffusion in each part of the cornea with different contact lens materials. The oxygen profile is calculated as a function of oxygen tension at the cornea-tear interface and the oxygen transmissibility of the lens, with values used in previous studies. We aim to determine the influence of a detailed geometry of the cornea in their modeling compared to previous low dimensional models used in the literature. To this end, a 3-D study based on an axisymmetric volume element analysis model was applied to different contact lenses currently on the market. We have obtained that the model provides a valuable tool for understanding the flux and cornea oxygen profiles through the epithelium, stroma, and endothelium. The most important results are related to the dependence of the oxygen flux through the cornea-lens system on the contact lens thickness and geometry. Both parameters play an important role in the corneal flux and oxygen tension distribution. The decline in oxygen consumption experienced by the cornea takes place just inside the epithelium, where the oxygen tension falls to between 95 and 16 mmHg under open eye conditions, and 30 to 0.3 mmHg under closed eye conditions, depending on the contact lens worn. This helps to understand the physiological response of the corneal tissue under conditions of daily and overnight contact lens wear, and the importance of detailed geometry of the cornea in the modeling of diffusion for oxygen and other species.

Respiratory response of Cirrhinus mrigala (Hamilton, 1822) fingerlings exposed to sub lethal concentration of Fenvalerate

Pesticides are toxic to aquatic fauna, which form significant components of the food chain. In this study to estimate, the lethal concentration LC50 of fenvalerate and sub-lethal concentration of Fenvalerate on the respiratory metabolism of Cirrhinus mrigala fingerlings was recorded in laboratory condition. The median lethal concentration of fenvalerate was estimated, by exposing different concentration such as 0.01, 0.05, 0.1, 0.15 and 0.2 ppm of fenvalerate. The profit analysis, it was estimated that the LC50 value for 96 hrs for the pesticide fenvalerate was calculated as 0.025 ppm. The rate of oxygen consumption increased from 0.44 mg/g/hrs to 0.67 mg/g/hrs. When the partial pressure increase from 80 to 100 (mm/hg) in the exposed to 0.00083 ppm. The rate of oxygen consumption shoots us in 0.00083 and 0.00125 ppm concentration of fenvalarate, when compared with control. In the present investigation, the decline of oxygen consumption was observed in the subsequence exposure of Fenvalerate.

Increased Myocardial Oxygen Consumption Precedes Contractile Dysfunction in Hypertrophic Cardiomyopathy Caused by Pathogenic TNNT2 Gene Variants

BackgroundHypertrophic cardiomyopathy is caused by pathogenic sarcomere gene variants. Individuals with a thin‐filament variant present with milder hypertrophy than carriers of thick‐filament variants, although prognosis is poorer. Herein, we defined if decreased energetic status of the heart is an early pathomechanism in TNNT2 (troponin T gene) variant carriers.Methods and ResultsFourteen individuals with TNNT2 variants (genotype positive), without left ventricular hypertrophy (G+/LVH−; n=6) and with LVH (G+/LVH+; n=8) and 14 healthy controls were included. All participants underwent cardiac magnetic resonance and [11C]‐acetate positron emission tomography imaging to assess LV myocardial oxygen consumption, contractile parameters and myocardial external efficiency. Cardiac efficiency was significantly reduced compared with controls in G+/LVH− and G+/LVH+. Lower myocardial external efficiency in G+/LVH− is explained by higher global and regional oxygen consumption compared with controls without changes in contractile parameters. Reduced myocardial external efficiency in G+/LVH+ is explained by the increase in LV mass and higher oxygen consumption. Septal oxygen consumption was significantly lower in G+/LVH+ compared with G+/LVH−. Although LV ejection fraction was higher in G+/LVH+, both systolic and diastolic strain parameters were lower compared with controls, which was most evident in the hypertrophied septal wall.ConclusionsUsing cardiac magnetic resonance and [11C]‐acetate positron emission tomography imaging, we show that G+/LVH− have an initial increase in oxygen consumption preceding contractile dysfunction and cardiac hypertrophy, followed by a decline in oxygen consumption in G+/LVH+. This suggests that high oxygen consumption and reduced myocardial external efficiency characterize the early gene variant–mediated disease mechanisms that may be used for early diagnosis and development of preventive treatments.

Transfer and consumption of oxygen during the cultivation of the ectomycorrhizal fungus Rhizopogon nigrescens in an airlift bioreactor.

The study had the objective of examining the aspects involved in the cultivation of ectomycorrhizal fungi for the production of commercially sustainable inoculant to attend the demands of the seedling nursery industry. It focused on certain parameters, such as the oxygen consumption levels, during the cultivation of the ectomycorrhizal fungus Rhizopogon nigrescens CBMAI 1472, which was performed in a 5-L airlift bioreactor. The dynamic method was employed to determine the volumetric coefficient for the oxygen transfer (k L a) and the specific oxygen uptake rate (Q O2 ). The results indicate that specific growth rates (μ X ) and oxygen consumption decline rapidly with time, affected mainly by increases in biomass concentration (X). Increases in X are obtained primarily by increases in the size of pellets that are formed, altering, consequently, the cultivation dynamics. This is the result of natural increases in transferring resistance that are observed in these environments. Therefore, to avoid critical conditions that affect viability and the productivity of the process, particular settings are discussed.

Editorial: Physiology and Cellular Mechanisms of Isothiocyanates and Other Glucosinolate Degradation Products in Plants.

Editorial: Physiology and Cellular Mechanisms of Isothiocyanates and Other Glucosinolate Degradation Products in Plants.

Soothing the sleeping giant: improving skeletal muscle oxygen kinetics and exercise intolerance in HFpEF.

Patients with heart failure with preserved ejection fraction (HFpEF) have similar degrees of exercise intolerance and dyspnea as patients with heart failure with reduced EF (HFrEF). The underlying pathophysiology leading to impaired exertional ability in the HFpEF syndrome is not completely understood, and a growing body of evidence suggests "peripheral," i.e., noncardiac, factors may play an important role. Changes in skeletal muscle function (decreased muscle mass, capillary density, mitochondrial volume, and phosphorylative capacity) are common findings in HFrEF. While cardiac failure and decreased cardiac reserve account for a large proportion of the decline in oxygen consumption in HFrEF, impaired oxygen diffusion and decreased skeletal muscle oxidative capacity can also hinder aerobic performance, functional capacity and oxygen consumption (V̇o2) kinetics. The impact of skeletal muscle dysfunction and abnormal oxidative capacity may be even more pronounced in HFpEF, a disease predominantly affecting the elderly and women, two demographic groups with a high prevalence of sarcopenia. In this review, we 1) describe the basic concepts of skeletal muscle oxygen kinetics and 2) evaluate evidence suggesting limitations in aerobic performance and functional capacity in HFpEF subjects may, in part, be due to alterations in skeletal muscle oxygen delivery and utilization. Improving oxygen kinetics with specific training regimens may improve exercise efficiency and reduce the tremendous burden imposed by skeletal muscle upon the cardiovascular system.

Long‐term variations in the dissolved oxygen budget of an urbanized tidal river: The upper Delaware Estuary

AbstractThe dissolved oxygen budget in the upper Delaware Estuary between 1970 and 2014 was inferred from oxygen concentration measurements using a box model approach. The region was found to be a net biogeochemical sink of oxygen, with net oxygen consumption greater in the tidal fresh portion than in the oligohaline portion. Net oxygen consumption decreased from the 1970s to the 1990s by roughly a factor of 2 before increasing slightly in the 2000s. The dramatic decline in oxygen consumption was presumably due to improvements in wastewater treatment, though a comparison with biological oxygen demand measurements in wastewater was equivocal. Nonalgal oxygen consumption (i.e., oxygen consumption due to heterotrophic respiration and nitrification) was computed as the sum of the estimated net oxygen consumption and historical measurements of primary production. Nonalgal oxygen consumption was found to be highly seasonal and positively correlated with temperature, with Q10 values ranging between 1.4 and 2.3. Annual nonalgal oxygen consumption was found to be several times annual primary production. Exchange with the atmosphere is the main process that balances the net oxygen consumption throughout the study region, with advection also an important process in the tidal fresh portion. Decadal scale variability in oxygen concentration, including the recent decline in the 2000s, appears to be mainly driven by biological, not physical, processes.

Effects of air embolism size and location on porcine hepatic microcirculation in machine perfusion

The handling of donor organs frequently introduces air into the microvasculature, but little is known about the extent of the damage caused as a function of the embolism size and distribution. Here we introduced embolisms of different sizes into the portal vein, the hepatic artery, or both during the flushing stage of porcine liver procurement. The outcomes were evaluated during 3 hours of machine perfusion and were compared to the outcomes of livers with no embolisms. Dynamic contrast-enhanced ultrasound (DCEUS) was used to assess the perfusion quality, and it demonstrated that embolisms tended to flow mostly into the left lobe, occasionally into the right lobe, and rarely into the caudate lobe. Major embolisms could disrupt the flow entirely, whereas minor embolisms resulted in reduced or heterogeneous flow. Embolisms occasionally migrated to different regions of the same lobe and, regardless of their size, caused a general deterioration in the flow over time. Histological damage resulted primarily when both vessels of the liver were compromised, whereas bile production was diminished in livers that had arterial embolisms. Air embolisms produced a dose-dependent increase in vascular resistance and a decline in oxygen consumption. This is the first article to quantify the impact of air embolisms on microcirculation in an experimental model, and it demonstrates that air embolisms have the capacity to degrade the integrity of donor organs. The extent of organ damage is strongly dependent on the size and distribution of air embolisms. The diagnosis of embolism severity can be safely and easily made with DCEUS.

The metabolic phenotype of rodent sepsis: cause for concern?

PurposeRodent models of sepsis are frequently used to investigate pathophysiological mechanisms and to evaluate putative therapeutic strategies. However, preclinical efficacy in these models has failed to translate to the clinical setting. We thus questioned the representativeness of such models and herein report a detailed comparison of the metabolic and cardiovascular phenotypes of long-term faecal peritonitis in fluid-resuscitated rats and mice with similar mortality profiles.MethodsWe conducted prospective laboratory-controlled studies in adult male Wistar rats and C57 black mice. Animals were made septic by intraperitoneal injection of faecal slurry. Rats received continuous intravenous fluid resuscitation, whereas mice received intermittent fluid boluses subcutaneously. Sham-treated animals served as controls. Survival was assessed over 72 h. In separate studies, whole body metabolism (O2 consumption, CO2 production) was measured over 24 h with echocardiography performed at early (6 h) and established (24 h) phases of sepsis. Blood gas analysis was performed at 6 h (rats) and 24 h (rats, mice).ResultsSimilar survival curves were seen in both rodent models with approximately 75% mortality at 72 h. In mice, sepsis caused severity-dependent falls in core temperature and global metabolism. Oxygen consumption in severely septic mice fell by 38% within 2 h, and 80% at 22 h compared with baseline values. This was only partially restored by external warming. By contrast, septic rats maintained core temperature; only severely affected animals showed a pre-mortem decline in oxygen consumption. Significant myocardial dysfunction was seen in mice during early and established sepsis, whereas peak velocity and other hemodynamic variables in rats were similar at 6 h and significantly worse by 24 h in severely septic animals only.ConclusionsMarkedly differing metabolic and cardiovascular profiles were seen in long-term fluid-resuscitated rat and mouse models of bacterial sepsis despite similar mortality. The mouse model, in particular, does not represent the human condition. We urge caution in applying findings in murine models to septic patients, both with regard to our understanding of pathophysiology and the failure to translate preclinical efficacy into successful clinical trials.Electronic supplementary materialThe online version of this article (doi:10.1186/2197-425X-1-6) contains supplementary material, which is available to authorized users.

Impact of different acclimation temperatures and duration on the chill coma temperature and oxygen consumption in the tenebrionid beetleAlphitobius diaperinus

When the ambient temperature is lowered to an insect's lower thermal limit, the insect enters into chill coma. Chill coma temperature and chill coma recovery can vary within species as a result of thermal acclimation, although the physiological basis of the onset of chill coma remains poorly understood. The present study investigates how the temperature of acclimation (0, 5, 10, 15 and 20 °C for 2 or 7 days) affects chill coma temperature and oxygen consumption in adultAlphitobius diaperinusPanzer (Coleoptera: Tenebrionidae). It is hypothesized that the threshold decline in metabolic rate corresponds to the entry into chill coma. Oxygen consumption (as a proxy of metabolism) is measured across the chill coma temperature threshold, and a strong decline in oxygen consumption is expected at entry into chill coma. The acclimation decreases the chill coma temperature significantly from 6.6 ± 1.1 °C in control insects to 3.1 ± 0.7 °C in those acclimated to 10 °C. The change in metabolic rate (Q10) after acclimation to temperatures ranging from 10 to 20 °C is 3.7. Despite acclimation, the metabolic rate ofA. diaperinusconforms to Arrhenius kinetics, suggesting that the response of this beetle does not show metabolic compensation. The data suggest the existence of a threshold decline in metabolic rate during cooling that coincides with the temperature at which an insect goes into chill coma.

Decline in oxygen consumption correlates with lifespan in long-lived and short-lived mutants of Caenorhabditis elegans

In humans, the basal energy metabolism is thought to decline linearly with age. On the other hand, in the nematode Caenorhabditis elegans, two research groups reported independently that it declined exponentially. In this study, furthermore, we used various lifespan-mutant strains to determine whether the previous conclusion is more likely to be true. We can indirectly estimate the metabolic energy by conveniently measuring the oxygen consumption rates of C. elegans using an optical apparatus. From the profile of respiratory rates as a function of age, we can quantitatively isolate the physiological decline rate, λ, that exponentially represents the decay rate of respiratory activity with age. In addition, quantitative analysis indicates that the respiratory activity of worms has a finite value in advanced age. We also show that the maximum and mean lifespans strongly correlate with the reciprocal of the λ. These findings offer crucial biochemical evidence for a molecular mechanism at work in biological aging. Consequently, we here propose a mechanism based on a chemical reaction and offer a definition of the physiological decline rate and the finiteness of respiratory activity in advanced age.

Metabolic modulation in Labeo rohita fingerlings during starvation: Hsp70 expression and oxygen consumption

An experiment was conducted to study the metabolic modulation of Labeo rohita fingerlings (mean wt. 3.75 g) during starvation in terms of heat shock protein (Hsp70) expression in liver and muscle tissues and oxygen consumption rate. Hsp70 expression and oxygen consumption were measured following starvation of 0, 1, 2 or 3 weeks for the respective groups. The quantity of Hsp70 in liver increased linearly ( y = 1.837 x − 2.43; R 2 = 0.91) with the duration of starvation; but it was undetectable in the control group (no starvation). Though Hsp70 was expressed in muscle, only 3-week-starved fish exhibited a significantly higher ( p < 0.05) quantity of Hsp70 than the other groups. A decline in oxygen consumption was also observed in the feed deprived fingerlings suggesting that the fish are capable of adjusting their metabolic rate by reducing oxygen intake during starvation. An inverse relationship was observed between the magnitude of Hsp70 elevation and the oxygen consumption ( y = − 11.237 x + 161.08; R 2 = 0.89), suggesting that both Hsp70 and reduced oxygen consumption act to protect the fingerlings against the starvation stress. This prima facie report on carp suggests that enhanced Hsp70 expression and reduced metabolic activity are two important strategies adapted by L. rohita fingerlings to overcome the stress due to starvation.

Effects of Combination of Nitrate with β1-4 Galacto-oligosaccharides and Yeast (Candida kefyr) on Methane Emission from Sheep

The objective of the present study was to determine whether β1-4 galacto-oligosaccharides (GOS) and Candida kefyr combined with nitrate as manipulators could suppress rumen methanogenesis without nitrate poisoning in sheep. Four rumen fistulated wethers were allocated to a 4x4 Latin square design. Nitrate (1.3 g NaNO 3 kg - 0 . 7 5 body weight) with and without GOS and Candida kefyr were administered into the rumen through fistula as a single dose 30 min after the morning meal. GOS and Candida kefyr were supplemented by sprinkling onto the feed and through rumen fistula, respectively. The four treatments consisted of saline, nitrate, nitrate plus GOS and nitrate plus GOS plus Candida kefyr. Physiological saline was used as the control treatment. Compared to saline treatment, the administration of nitrate alone resulted in a very marked decrease in rumen methanogenesis and an increase in rumen and plasma nitrite production and blood methaemoglobin formation consequently causing a decline in oxygen consumption, carbon dioxide production and metabolic rate. When compared to nitrate alone, the simultaneous administration of nitrate with GOS decreased nitrite accumulation in rumen and plasma and nitrate-induced methaemoglobin, while retaining low methane production. However, GOS could not fully restore metabolic parameters reduced by nitrate. When compared to the simultaneous administration of nitrate with GOS, the simultaneous administration of nitrate with GOS plus Candida kefyr lowered rumen methanogenesis to a negligible level, but did not decrease rumen and plasma nitrite accumulation as well as blood methaemoglobin formation. Thus, these results suggest that combination of nitrate with GOS may be a potent manipulator to suppress rumen methanogenesis with abating the hazards of nitrate-nitrite toxicity in ruminants.

Effect of toxins of the 'red-tide' dinoflagellate Alexandrium spp. on the oxygen consumption of marine copepods

Toxic algal species produce a variety of responses in copepod consumers ranging from avoidance to retching behavior to high mortality. Toxic algae have also been observed to induce rapid heartbeat in copepods, but little is known of other specific physiological effects. The following experiment tested the effect of exposure to a toxic diet on the oxygen consumption rates and citrate synthase activities of five copepod species that co-occur with the toxic dinoflagellate Alexandrium tamarense in the Gulf of Maine. Experimental animals were presented with diets of toxic and non-toxic Alexandrium isolates, as well as ambient food, for 24 h before measuring oxygen consumption rates. In addition, citrate synthase activities were determined on two copepod species exposed to toxic and non-toxic isolates of A. tamarense over a 3 to 4 day period. Calanus finmarchicus, Pseudocalanus spp. and Acartia hudsonica consumed Alexandrium and showed no response of oxygen consumption rates to the experimental treatments. Citrate synthase activities of A. hudsonica and Temora longicornis were also unaffected by Alexandrium toxin content. Finally, Metridia lucens had lower rates after exposure to both Alexandrium isolates. However, Metridia fed little on either Alexandrium isolate, and in a subsequent experiment short-term starvation produced a similar decline in oxygen consumption, which is likely to account for the declines observed in the prior experiment. Thus, it appears that the toxin content of Alexandrium has little if any short-term effect on the respiration rates of these copepods.

Rate and mechanism of maximal oxygen consumption decline with aging: implications for exercise training.

Because of the influence of cardiorespiratory fitness on functional independence, quality of life, and cardiovascular disease and all-cause mortality, tremendous interest has been directed towards describing the age-related change in maximal oxygen consumption (VO(2max)). Current evidence supports a 10% per decade decline in VO(2max) in men and women regardless of activity level. High-intensity exercise may reduce this loss by up to 50% in young and middle-aged men, but not older men, if maintained long term. Middle-aged and older women do not appear to be able to reduce loss rates in VO(2max) to less than 10% per decade, which may be related to estrogen status. However, maintaining high-intensity training seems limited to approximately one decade at best and to a select few individuals. While the factors limiting the ability to maintain high-intensity training are not completely known, aging most likely plays a role as studies have demonstrated that training maintenance becomes more difficult with advancing age. Age-related loss of VO(2max) seems to occur in a non-linear fashion in association with declines in physical activity. In sedentary individuals, this non-linear decline generally occurs during the twenties and thirties whereas athletic individuals demonstrate a non-linear decline upon decreasing or ceasing training. Non-linear loss rates are also demonstrated in individuals over the age of 70 years. The decline in VO(2max) seems to be due to both central and peripheral adaptations, primarily reductions in maximal heart rate (HR(max)) and lean body mass (LBM). Exercise training does not influence declines in HR(max), while LBM can be maintained to some degree by exercise. Recommendations for exercise training should include aerobic activities utilising guidelines established by the American College of Sports Medicine for improving CV fitness and health, as well as strength training activities for enhancing LBM.

Developmental changes in the hypoxic ventilatory response in C57BL/6 mice

C57BL/6 mice are the strain into which most null mutations for neurotransmitters or their receptors are backcrossed. A number of these transgenic mice have recently been shown to have an abnormal respiratory phenotype; however, the postnatal development of the ventilatory response to hypoxia has not been characterized in C57BL/6 mice. The effect of 8% oxygen for 5 min was examined in mice at five periods from P1 to P30 using a body plyethysmograph. Neonatal and juvenile animals from P7 to P30 showed a biphasic pattern in hypoxia in which the increase in minute ventilation achieved in the first min declined towards baseline by the fifth minute and was decreased below baseline in the first minute of return to air breathing. In contrast P1–P3 C57BL/6 mice had a sustained increase in both respiratory frequency and tidal volume and their minute volume remained above baseline on return to air. The decline in oxygen consumption, measured in the fifth minute of hypoxia, was not different in P1–P3 mice compared to P8–P10. These results suggest that the earliest response to hypoxia of the respiratory system in this strain is not characterized by a time dependent depression as seen in older animals and in species whose motor systems are relatively more developed at birth.

Acetyl-L-carnitine treatment stimulates oxygen consumption and biosynthetic function in perfused liver of young and old rats.

The effect of treatment with acetyl-L-carnitine on hepatic mitochondrial respiration and biosynthetic function in perfused liver from young (90 days) and old (22-24 months) rats was studied. Rats were given a 1.5% (w/v) solution of acetyl-L-carnitine in their drinking water for 1 month and oxygen consumption together with the rate of gluconeogenesis, urea synthesis, and ketogenesis with and without added substrates were measured in perfused liver. Mitochondrial oxygen consumption was also assessed in liver homogenate and isolated mitochondria to determine the maximal capacity for oxidative phosphorylation. Acetyl-L-carnitine treatment almost completely restored the age-dependent decline in oxygen consumption, gluconeogenesis, urea synthesis, and ketogenesis found in perfused liver of old rats to the levels found in young rats. In addition, acetyl-L-carnitine treatment increased oxygen consumption and biosynthetic function in perfused liver from young rats. After acetyl-L-carnitine treatment, we found detectable 3-oxoacyl-CoA-transferase activity associated with a consumption of ketone bodies in young and old rats. Finally, oxygen consumption measured in homogenate and isolated mitochondria did not change with age and acetyl-L-carnitine treatment. Our results show that in perfused liver, acetyl-L-carnitine treatment slows the age-associated decline in mitochondrial respiration and biosynthetic function. In addition, treatment of young rats with acetyl-L-carnitine has a stimulating effect on liver metabolism, probably through an increase in ATP production.

PENGARUH SUHU DAN OKSIGEN TERLARUT TERHADAP TINGKAT METABOLISME DAN KELANGSUNGAN HIDUP LARVA IKAN BAUNG Mystus nemurus Cuv &amp; Val

The rearing technology of green catfish larvae has not yet established. Hight mortality occurred in the early larval stages. This experiment was conducted to study the effect of temperature and dissolved oxygen on metabolic rate and survival rate of green catfish larvae. 3600 green catfish larvae with initial individual mean weights of 1.24 0.19 mg and lengths 5.85 0.71 mm (one day after hatching) were reared in the aquarium of 30 cm x 30 cm x 40 cm dimension. Treatments were done at 3 levels of temperature 27C, 30C, and 33C; and 3 levels of dissolved oxygen 6.47 ml/L, 1.05 ml/L, and 0.78 ml/L and 3 replications. The result showed that temperature and dissolved oxygen was significant to the oxygen consumption. Oxygen consumption of 0.67 0.25 mg O2/h/g and 0.86 0.005 mg O2/h/g was highest in larval reared at 33C and dissolved oxygen 6.47 ml/L for 3 weeks. The higher water temperature the greater the oxygen consumption. The oxygen consumption decline with decreasing dissolved oxygen in the water, indicating an axyconformer type. The temperature was not significant to the survival rate and growth of the larvae. However the effect of dissolved oxygen was significant to the growth rate (Pless than 0.05). Growth rate of 25.69 0.55 percent was highest in larval reared at 6.47 mg/L for 3 weeks.

Effect of food deprivation on oxygen consumption and body composition of growth-enhanced transgenic Atlantic salmon ( Salmosalar)

The influence of food deprivation on the rate of oxygen consumption and the rate of mobilization/utilization of energy reserves in F 2 generation growth-enhanced transgenic Atlantic salmon were compared relative to their non-transgenic counterparts, over a pre-smolt weight interval of 8 to 55 g. Throughout most of the 8 weeks of food deprivation, transgenic fish exhibited a greater rate of oxygen consumption compared to control salmon, but also exhibited a more rapid decline in oxygen consumption as starvation progressed. Consequently, depending on initial weight and length of food deprivation, the rate of oxygen consumption of transgenic fish declined to where it equaled or was less than the oxygen consumption of control fish. Transgenic fish depleted body protein, dry matter, lipid and energy at a faster rate than did the controls. Additionally, in both groups, lipid was catabolized faster than was protein. Although transgenic fish demonstrated the ability to reduce their metabolic rate during starvation, as also observed in the non-genetically modified control salmon, their persistence in maintaining a higher metabolic rate, combined with their lower initial endogenous energy reserves, suggests that the likelihood of growth-enhanced transgenic salmon achieving maximum growth or even surviving outside intensive culture conditions may be lower than that of non-transgenic salmon.

Oxidative phosphorylation-dependent and -independent oxygen consumption by individual preimplantation mouse embryos.

The self-referencing electrode technique was employed to noninvasively measure gradients of dissolved oxygen in the medium immediately surrounding developing mouse embryos and, thereby, characterized changes in oxygen consumption and utilization during development. A gradient of depleted oxygen surrounded each embryo and could be detected >50 microm from the embryo. Blastocysts depleted the surrounding medium of 0.6+/-0.1 microM of oxygen, whereas early cleavage stage embryos depleted the medium of only 0.3+/-0.1 microM of oxygen, suggesting a twofold increase in oxygen consumption at the blastocyst stage. Mitochondrial oxidative phosphorylation (OXPHOS) accounted for 60-70% of the oxygen consumed by blastocysts, while it accounted for only 30% of the total oxygen consumed by cleavage-stage embryos. The amount of oxygen consumed by non-OXPHOS mechanisms remained relatively constant throughout preimplantation development. By contrast, the amount of oxygen consumed by OXPHOS in blastocysts is greater than that consumed by OXPHOS in cleavage-stage embryos. The amount of oxygen consumed by one-cell embryos was modulated by the absence of pyruvate from the culture medium. Treatment of one-cell embryos and blastocysts with diamide, an agent known to induce cell death in embryos, resulted in a decline in oxygen consumption, such that the medium surrounding dying embryos was not as depleted of oxygen as that surrounding untreated control embryos. Together these results validate the self-referencing electrode technique for analyzing oxygen consumption and utilization by preimplantation embryos and demonstrate that changes in oxygen consumption accompany important physiological events, such as development, response to medium metabolites, or cell death.