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O Pastoris

Publications and source records attributed to O Pastoris.

At least 37 records · Page 2Linked to original sources
PubMed1991

Effects of hypoxia and pharmacological treatment on enzyme activities in skeletal muscle of rats of different ages.

The activities of enzymes related to energy metabolism in the gastrocnemius and soleus muscles in young-adult (4 months), mature (12 months), and senescent (24 months) rats were compared after continuous (72 consecutive h) exposure to normobaric hypoxia or normoxia after the vasodilator naftidrofuryl or saline solution had been given intraperitoneally for 30 consecutive days. The maximum rats (Vmax) of the following enzyme activities in the crude extract and/or the crude mitochondrial fraction of each muscle specimen were evaluated for: the anaerobic glycolytic pathway (hexokinase, phosphofructokinase, pyruvate kinase, and lactate dehydrogenase), the tricarboxylic acid cycle (citrate synthase, and malate dehydrogenase), the electron transfer chain (cytochrome oxidase), and the NAD+/NADH redox state (total NADH cytochrome c reductase). The significance of differences between the enzyme activities at different ages or under different experimental conditions in the two tissue preparations of the two muscles were determined by ANOVA. MCA and ETA2 were used to evaluate the net effects of the experimental conditions. First, aging did not seem to affect the soleus and gastrocnemius muscles in the same way. In the gastrocnemius muscle, the major changes were seen in enzymes of the glycolytic pathway, in the crude extracts. In the soleus muscle, the more striking changes in enzyme activities as a function of aging were found in the crude mitochondrial fraction. We also found that hypoxia caused more important changes in 12-month-old rats than in those of other ages (especially the enzyme activities of the gastrocnemius muscle). Naftidrofuryl modified the effects of hypoxia only sometimes and further investigations are necessary before we can draw any conclusions about the pharmacological activity of naftidrofuryl in hypoxia.

Aging↗
PubMed1991

Biochemical changes induced in the myocardial cell during cardioplegic arrest supplemented with creatine phosphate.

The purpose of this work was to evaluate the biochemical changes in the myocardial cell using cardioplegia supplemented with creatine phosphate (CP). Many previous studies have demonstrated the beneficial effect of CP on the ischemic myocardium and its mechanism of action has been assumed to be mainly extracellular. Based on the assumption that CP could also exert some influence on myocardial cellular metabolism, this investigation was carried out. Forty patients undergoing mitral valve replacement were divided into two groups: group 1 was treated with standard cardioplegic solution, and group 2 was treated with cardioplegic solution enriched with CP at a concentration of 10 mmol/L. Samples of papillary muscle, obtained from the removed valve, were studied by means of biochemical methods in order to assess the enzyme activities and the metabolites of the different biochemical pathways related to energy metabolism in the myocardial cell. One papillary muscle sample was used to determine enzyme activities spectrophotometrically; another was used to evaluate metabolite concentrations by spectrophotometric or spectrophotofluorimetric methods. The rate of spontaneous functional recovery after rewarming and weaning from cardiopulmonary bypass (CPB) also was evaluated. In group 2, the Vmax of enzymatic activities was significantly greater (hexokinase, malate dehydrogenase, glutamate dehydrogenase, total NADH cytochrome c reductase) and a better functional state of the heart was observed after CPB. On the basis of the clinical and biochemical data, it is concluded that the myocardium was better preserved when CP was added to the cardioplegic solution. Therefore, the results suggest a possible interaction of exogenous CP with cellular metabolism.

Cardioplegic Solutions↗
PubMed1990

Influence of oxidative stress on the age-linked alterations of the cerebral glutathione system.

The glutathione system (reduced and oxidized glutathione; redox index) was studied in the forebrain of male Wistar rats of 5, 15, and 25 months of age following the administration for 2 months in drinking water of chemicals that induce oxidative stress: paraquat and diethyldithiocarbamate (DDC) to increase superoxide radical formation, aminotriazole and hydrogen peroxide to increase hydroxyl radical generation, as well as diamide and ferrous chloride to decrease the glutathione cycle activity. Chronic oral administration of phosphatidylcholine for 2 months was evaluated in 25-month-old rats. Aging accentuated the changes produced by chemicals that induce oxidative stress; i.e., the changes in the glutathione redox index were most pronounced in the forebrains of the older paraquat-, DDC-, H2O2-, and diamide-treated rats. Markedly different adaptative changes occurred within the various drug groups. The reduced glutathione was increased (by paraquat, DDC and aminotrazole), decreased (by H2O2) or unchanged (by iron and diamide). Furthermore, in older rats, paraquat and DDC increased the glutathione redox index, whereas H2O2 and diamide decreased the glutathione redox index or were ineffective (i.e., aminotriazole, iron). The glutathione redox index altered by chronic drug administration was modified by the concomitant administration of phosphatidylcholine.

Administration, Oral↗
PubMed1990

Influence of aging and drug treatment on the bioenergetics of hypoxic brain.

Synaptosomes isolated from the forebrain of rats of different ages (20, 60 and 100 weeks of age) were incubated in Krebs-Henseleit-Hepes (pH 7.4) buffer, for 10 min at 24 degrees C. The energetic state was defined by the redox state of the intramitochondrial NAD-couple (delta Gox-red) and the phosphorylation state of adenine nucleotide system (delta GATP). The biological energy "lost" by the system during the coupled reactions was estimated by the delta delta G = delta Gox-red - delta GATP. The animals were submitted for 10 min to different degrees of in vivo hypoxia. To elucidate the mechanism of action, the effect of the pretreatment with drugs acting on oxygen availability (almitrine) or on microcirculation and metabolism (delta-yohimbine) was tested. In synaptosomes isolated from the forebrain of animals submitted to moderate degree of hypoxia (oxygen arterial partial pressure ranging between 32 and 29 mmHg) the efficiency of the system was quite similar to that observed in normoxia, with the exception of the older rats. In synaptosomes isolated from the forebrain of rats submitted to severe degree of hypoxia (oxygen arterial partial pressure ranging between 20 and 18 mmHg) the efficiency of the system was markedly altered as a function of both aging and severity of hypoxemia. The pretreatment with the agent increasing the oxygen availability partially modified the efficiency of the system, the alpha-blocking agent being less important. The drug action was markedly related to both the age and the degree of hypoxia.

Adenosine Triphosphate↗
PubMed1990

Factors involved in the age-related alteration in the efficiency of the brain bioenergetics.

The synaptic energy state may be defined by the redox state of the intramitochondrial NAD-couple (delta Gox-red) and the phosphorylation state of adenine nucleotide system (delta GATP). The biological energy 'lost' by the system during the coupled reactions is calculated as delta delta G = delta Gox-red-delta GATP. These evaluations are performed in synaptosomes isolated from the forebrain of rats of different ages (20, 60 and 100 weeks of age) and incubated in Krebs-Henseleit-Hepes (pH 7.4) buffer, for 10 min at 24 degrees C. The animals are submitted for 10 min to different degrees of in vivo hypoxia. To better elucidate the mechanism of action, the effects of the pretreatment with agents inducing vasodilation (papaverine), or acting on cerebral carbohydrate metabolism (hopanthenate), or on neurotransmission and cerebral metabolism (theniloxazine) are tested. In synaptosomes isolated from the forebrain of animals submitted to moderate degree of hypoxia (PaO2 = 32-29 mmHg) the efficiency of the system is quite similar to that observed in normoxia, with the exception of the older rats. In synaptosomes isolated from the forebrain of rats submitted to severe degree of hypoxia (PaO2 = 20-18 mmHg) the efficiency is altered as a function of both aging and severity of hypoxemia. Drug pretreatment may partially interfere with the delta delta G by hypoxemia, the action being related to the rat age and hypoxic degrees. The age-related decrease in the efficiency of the coupled states seems to be related to alteration in the phosphorylation state of adenine nucleotides.

Adenine Nucleotides↗
PubMed1990

Hypoxia and pharmacological treatment in differently aged rats: effect on muscular metabolite concentrations.

Metabolite concentrations in gastrocnemius and soleus muscles were compared in young-adult (4 months), mature (12 months) and senescent (24 months) rats after continuous (72 consecutive hours) exposure to normobaric hypoxia or normoxia with the intraperitoneal administration of the vasodilator naftidrofuryl or saline solution for 30 days consecutively before hypoxia. The following metabolites were assessed in gastrocnemius muscle in relation to: (a) energy mediators: ATP, ADP, AMP; (b) energy store: creatine phosphate; (c) anaerobic glycolysis: glycogen, glucose, glucose 6-phosphate, pyruvate, lactate; (d) Krebs' cycle: citrate, alpha-ketoglutarate, malate; (e) free amino acids related to Krebs' cycle: aspartate, glutamate, alanine; and (f) ammonia. In the soleus muscle only ATP, creatine phosphate, glycogen, glucose, glucose 6-phosphate, pyruvate, lactate, citrate, alpha-ketoglutarate malate, aspartate and glutamate were assessed. Aging does not seem to affect soleus and gastrocnemius muscles in the same way. Some gastrocnemius muscle metabolites show linear changes in their concentrations with aging, while for the soleus muscle the only linear change relates to glucose 6-phosphate. As regards the influence of hypoxia on muscular metabolism, all the most important changes observed in metabolite concentrations in comparison with control values take place at the age of 4 and 24 months. Furthermore, as regards naftidrofuryl action, the most important variations observed concern only 4-month-old animals. Finally our data show that only in certain cases has pharmacological treatment been able to modify the influence of hypoxic conditions on the concentration of muscle metabolites, regardless of the age of the animals.

Adenosine Triphosphate↗
PubMed1989

Age-related effect induced by oxidative stress on the cerebral glutathione system.

In the forebrain from male Wistar rats aged 5, 15 and 25 months, age-related putative alterations in the glutathione system (reduced and oxidized glutathione; redox index) were chronically induced by the administration in drinking water of free radical generators (hydrogen peroxide, ferrous chloride) or of inhibitors of endogenous free radical defenses (diethyl-dithio-carbamate, an inhibitor of superoxide dismutase activity). In hydrogen peroxide administered rats, both reduced glutathione and the cerebral glutathione redox index markedly declined as a function of aging, whereas oxidized glutathione consistently increased. In contrast, chronic iron intake failed to modify the reduced glutathione in forebrain from the rats of the different ages tested, whereas the oxidized glutathione was increased in the older brains. The chronic intake of diethyl-dithio-carbamate enhanced the concentrations of reduced glutathione in the forebrains from the rats of the different ages tested, the oxidized glutathione being unchanged. In 15-month-old rats submitted to chronic oxidative stress, ergot alkaloids (and particularly dihydroergocriptine) interfered with cerebral glutathione system, while papaverine was always ineffective. The comprehensive analysis of the data indicates that: (a) both the type of oxidative stress and the age of the animals modulate the cerebral responsiveness to the putative modifiers in the level of tissue free radicals; (b) aging magnifies the cerebral alterations induced by oxidative stress; the (c) cerebral glutathione system may be modified by metabolic rather than by circulatory interferences; (d) a balance between the various cerebral antioxidant defenses is present, the perturbation of an antioxidant system resulting in the compensatory modified activity of component(s) of another system.

Administration, Oral↗
PubMed1989

Relationship between aging, drug treatment and the cerebral enzymatic antioxidant system.

Four different brain regions (parieto-temporal cortex, caudate-putamen, substantia nigra, and thalamus) were examined in rats aged 5, 10, 15, 20, 25, 30, and 35 months. The following enzyme activities related to the antioxidant system were measured: glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, glutathione peroxidase, glutathione reductase, and superoxide dismutase (as total). Specific enzyme activities vary markedly with age, according to the various regions studied, indicating nonhomogenous vulnerability of different brain regions to aging. In general, both superoxide dismutase and glutathione reductase tended to decline during the last half of life, while glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase tended to increase slightly with age. In rats of 10, 20, or 30 months, chronic treatment for two months with a vasodilator (papaverine) or a calcium-blocker (nicardipine) indicated that the antioxidant enzyme activities are partially influenced according to the exogenous agent used, the brain region tested, and the age of the animals.

Aging↗
PubMed1989

Cerebral enzyme antioxidant system. Influence of aging and phosphatidylcholine.

To obtain a comprehensive profile of the age-related changes of the antioxidant enzyme system in discrete brain regions (cortex, caudate-putamen, substantia nigra, thalamus), the present study involved practically the total life span of male Wistar rats (from 5 to 35 months of age). The activities of both glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase increase from 5 to 25 months of life and remain relatively constant or decrease scantily thereafter. In thalamus, the activity of total superoxide dismutase (SOD) increases from 5 to 20 months of rat life and decreases thereafter. Conversely, in both substantia nigra and caudate-putamen, enzyme activity declines steadily with age, while in parietotemporal cortex enzyme activity deteriorates from the 25th month onward. In both caudate-putamen and parietotemporal cortex, the activity of glutathione peroxidase increases from 5 to 20 months of life and remains relatively constant thereafter, while in substantia nigra the enzyme activity is practically unmodified during the life span. Furthermore, the activity of glutathione reductase in parietotemporal cortex declines from the 20th month onward, while in caudate-putamen and thalamus, enzyme activity deteriorates after an increase from 5 to 20 months of life. The interference of phosphatidylcholine and/or its metabolite(s) with the cerebral enzyme antioxidant system shows a characteristic specificity as regards both the time of onset and the enzyme activities involved, namely, SOD and glutathione reductase. The interference with SOD is related to the cytosolic form of the enzyme and affects the cortex only of 5-month-old animals and also extends to the thalamus of 15-month-old rats and all regions in 25-month-old ones.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1989

Congenital muscle fibre type disproportion: clinical, morphological and biochemical findings in children.

Muscle biopsies from quadriceps femoris muscle of normal subjects and subjects with symptoms of congenital myopathy, aged 1-3 years, were examined for morphological and biochemical differences. Four patients showed clinical signs of Congenital Fibre Type Disproportion (CFTD) as described originally by Brooke (1973), while the other cases showed only signs of hypotonia and diffuse weakness as described by Clancy et al. (1980). No morphological differences between patients with different clinical signs were found in any biopsy sample from the quadriceps femoris muscle, as regards fibre size; type I fibres were always smaller than type II fibres. The difference in fibre size was more than 15% in all cases, and the variability coefficient of the larger type II fibres was less than 250. Nevertheless, as regards fibre occurrence, two patients showed more type I fibres than type II fibres, four patients showed more type II fibres than type I fibres and one patient had a marked type II fibre predominance. Enzyme activities assayed in the crude mitochondrial fraction showed no abnormalities between normal subjects and patients. An increase in the activity of lactate dehydrogenase in the crude extract was found in all cases.

Child, Preschool↗
PubMed1988

Changes induced by aging and drug treatment on cerebral enzymatic antioxidant system.

The age-related modifications of the participants to the cerebral enzymatic antioxidant system (superoxide dismutase, glutathione peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase) were evaluated in four brain regions from male Wistar rats aged 5, 10, 15, 20, 25, 30, and 35 months. Both the specific enzyme activity and the profile of any enzyme tested markedly differ with age according to the region examined: parieto-temporal cortex, caudate-putamen, substantia nigra and thalamus. This inhomogeneous age-related profile of enzyme activities could explain both the controversial data of literature and the different regional vulnerability of the brain tissue to damage with aging. In rats aged 10, 20, or 30 months, the chronic i.p. treatment for two months with papaverine or ergot alkaloids (dihydroergocristine, dihydroergocornine, dehydroergocriptine) suggests that the antioxidant enzyme activities may be influenced according to the agent utilized, the brain region tested, and the age of the animal. In any case, small differences in the drug structure support marked differences in the type and extent of the intervention on the antioxidant enzymatic system.

Aging↗
PubMed1987

[Effects of aging and various pharmacologic agents on the brain energy metabolism in the course of post-hypoglycemic recuperation in the rat].

Severe acute hypoglycaemia with isoelectric electroencephalogram induces a major deterioration of the energy state and amino acid contents of the brain. During post-hypoglycaemia recovery of adult animals, brain glucose concentrations return to normal values, whereas glycogen turnover remains low as aspartate and pyruvate concentrations increase. ATP levels rise, but the adenine-nucleotide pool remains small despite return to normal of ADP and AMP. Brain phosphocreatine levels return to normal values, with reciprocal changes in creatine content. In adult rats one also notes during recovery an increase in brain glutamine and glutamate, whereas the gamma-aminobutyrate returns to normal. Finally, ammonium and aspartate remain below, and alanine remains above normal values. Aging has no effect on cerebral metabolic disturbances induced by hypoglycaemia, but it influences the cerebral metabolic restoration processes that develop during post-hypoglycaemia recovery. The restitution of cerebral metabolites is weaker in mature and senescent rats than in adult rats. In the oldest rats, in particular, the concentrations of most of the amino acids and of adenyl nucleotides remain largely abnormal. The effects of dihydroergocristine, erbunamonine, raubasine, almitrine and of the almitrine-raubasine combination on post-hypoglycaemia recovery were evaluated in adult, mature and senescent rats. During recovery these pharmacological agents exert different effects on glycolytic metabolites, amino acids and energy-rich phosphates.

Adenosine Triphosphate↗
PubMed1987

Energetic state of aged brain during hypoxia.

Synaptosomes isolated from the forebrain of rats of different ages (20, 60, 100 and 140 weeks of age) and incubated in Krebs-Henseleit-Hepes pH 7.4 buffer (for 10 min at 24 degrees C) were utilized to define the redox state of the intramitochondrial NAD couple (delta Gox-red) and the phosphorylation state of adenine nucleotide system (delta GATP). The free-energy change (delta delta G) for the coupled reactions was calculated. The animals were subjected for 10 min to different degrees of in vivo hypoxia (52 greater than or equal to PaO2 greater than or equal to 11 mm Hg). In synaptosomes isolated from the forebrain of animals submitted to moderate degrees of hypoxia, the trend of delta delta G was quite similar to that observed in normoxia. In synaptosomes isolated from the forebrain of rats submitted to severe degrees of hypoxia, the delta delta G was markedly altered as function of both aging and severity of hypoxemia. The extensive delta delta G changes were largely supported by alteration of the phosphorylation state of adenine nucleotides. However, in synaptosomes from severely hypoxic rats, aging affected the redox state, too.

Aging↗
PubMed1986

Hopantenate interference on the adaptation of muscular energy metabolism to intermittent hypoxia.

In rat gastrocnemius muscle, the concentrations of glycolytic fuels, intermediates and end-products; Krebs cycle intermediates and related free amino acids; ammonia; energy store and mediators; and the energy charge potential were evaluated in normoxia or after repeated, alternate hypoxic and normoxic exposures (12 hr of hypoxia daily; for 5 days) with or without treatment with hopantenate (HOPA). Furthermore, in the crude extract and/or mitochondrial fraction the maximum rate (Vmax) of some muscular enzymes related to the anaerobic glycolytic pathway; the tricarboxylic acid cycle; and the electron transfer chain were evaluated. Hopantenate was administered daily at the dose of 250 mg.kg-1 i.p., for 5 days, 30 min before the beginning of the experimental normobaric hypoxia. The biochemical adaptation to intermittent normobaric hypoxic-normoxic exposures was characterized by the decrease of the muscular concentrations of citrate, alpha-ketoglutarate and glutamate, in absence of changes in the Vmax of the muscle enzymes related to energy transduction. In gastrocnemius muscle from hypoxic rats, by HOPA treatment, both citrate and alpha-ketoglutarate maintained normal values, aspartate decreased, while glutamate remained reduced to subnormal values. In the muscle from hypoxic animals, by hopantenate treatment the Vmax of the mitochondrial enzymes tested (citrate synthase, malate dehydrogenase, total NADH cytochrome c reductase, cytochrome oxidase) decreased in comparison with both hypoxic and normoxic untreated animals. This behaviour could be tentatively related to a mitochondrial sparing action concomitant with an intervention of the glutamate group of amino acids, even if the results do not allow a clear interpretation of the mechanism of HOPA action.

Animals↗
PubMed1985

Influence of aging and exogenous substances on cerebral energy metabolism in posthypoglycemic recovery.

In rats of different ages, acute severe hypoglycemia with isoelectric EEG induced extensive deterioration of the energy state and gross alteration of amino acid contents. During recovery of adult animals, tissue glucose concentration returned to normal, while the rate of glycogen synthesis was slow, both lactate and pyruvate concentrations increasing above normal. In the recovery period of "adult" rats, the ATP concentration increased but the adenine nucleotide pool remained reduced, even if the ADP and AMP concentrations were close to normal. Phosphocreatine was restored to normal concentrations with reciprocal changes in creatine content. In adult rats, during the recovery there was a rise in glutamate and glutamine concentrations, gamma-aminobutyrate concentration returning to normal value. Ammonia and aspartate decreased below normal, while alanine increased above normal. Aging does not affect the cerebral metabolic derangement occurring in severe hypoglycemia, but rather the metabolic changes that the brain tends to reverse during the posthypoglycemic restitution. In fact, there was lower restitution of the concentrations of cerebral cortical metabolites of "mature" and "senescent" rats in comparison with "adult" ones. Particularly, in older brains the concentrations of many amino acids and adenylate nucleotides remained largely abnormal. The effect of some agents on the posthypoglycemic recovery was tested: (a) dihydroergocristine; (b) eburnamonine; (c) raubasine; (d) almitrine; (e) piracetam. During the posthypoglycemic recovery, these different agents exhibited different interferences on glycolytic metabolites, amino acids and energy-rich phosphates. However, a more limited effect of the tested agents, which decrease with aging, was observed.

Aging↗
PubMed1985

Adaptation of skeletal muscle energy metabolism to repeated hypoxic-normoxic exposures and drug treatment.

Muscular glycolytic fuels, intermediates and end-products (glycogen, glucose, glucose-6-phosphate, pyruvate, lactate), Krebs cycle intermediates (citrate, alpha-ketoglutarate, succinate, malate), related free amino acids (glutamate, alanine), ammonia, energy store (creatine phosphate), energy mediators (ATP, ADP, AMP) and energy charge potential were evaluated. Furthermore the maximum rate (Vmax) of the following muscular enzyme activities was evaluated in the crude extract and/or mitochondrial fraction: for the anaerobic glycolytic pathway: hexokinase, phosphofructokinase, pyruvate kinase, lactate dehydrogenase; for the tricarboxylic acid cycle: citrate synthase, malate dehydrogenase; for the electron transfer chain: total NADH cytochrome c reductase, cytochrome oxidase. The rat gastrocnemius muscles were analyzed in normoxia and after repeated, alternate hypoxic and normoxic exposures (12 hours of hypoxia daily; for 5 days). Naftidrofuryl was administered daily at three different doses: 10, 15 and 22.5 mg/kg i.m., 30 min before the beginning of the experimental hypoxia. The biochemical adaptation to intermittent normobaric hypoxic-normoxic exposures was characterized by the decrease of the muscular contents of creatine phosphate, citrate, alpha-ketoglutarate and glutamate. This adaptation occurred in absence of significant changes in the Vmax of the muscle enzymes tested. By naftidrofuryl treatment, in gastrocnemius muscle from hypoxic rats both alpha-ketoglutarate and creatine phosphate contents maintained normal values, while glutamate concentration remained reduced to subnormal values. With the exception of hexokinase, naftidrofuryl treatment did not modify the Vmax of marker enzymes related to energy transduction.

Animals↗
PubMed1985

Modification of the skeletal muscle energy metabolism induced by intermittent normobaric hypoxia and treatment with biological pyrimidines.

Muscular glycolytic fuels, intermediates and end-products (glycogen, glucose, glucose-6-phosphate, pyruvate, lactate), Krebs cycle intermediates (citrate, alpha-ketoglutarate, succinate, malate), related free amino acids (glutamate, alanine), ammonia, energy store (creatine phosphate), energy mediators (ATP, ADP, AMP) and energy charge potential were evaluated. Furthermore the maximum rate (Vmax) of the following enzyme activities was evaluated in the crude extract and/or mitochondrial fraction: for the anaerobic glycolytic pathway: hexokinase, phosphofructokinase, pyruvate kinase, lactate dehydrogenase; for the tricarboxylic acid cycle: citrate synthase, malate dehydrogenase; for the electron transfer chain: total NADH cytochrome c reductase, cytochrome oxidase. The rat gastrocnemius muscles were analysed in normoxia and after normobaric intermittent hypoxia (12 hours continuously daily; for 5 days). Cytidine and/or uridine were administered daily at the dose of 120 mg/kg, i.p., 30 min before the beginning of the experimental hypoxia. The intermittent normobaric hypoxia induced a biochemical adaptation characterized by the decrease of the muscular contents of creatine phosphate, citrate, alpha-ketoglutarate and glutamate. This adaptation occurred in the absence of significant changes in the Vmax of the tested muscle enzymes. In gastrocnemius muscle from hypoxic rats, the two biological pyrimidines tested induced various discrete, but often related, modifications of the contents of some Krebs cycle intermediates (i.e., alpha-ketoglutarate, malate) and related free amino acids (i.e., glutamate, alanine). In any case, the treatment with cytidine and/or uridine did not modify the Vmax of marker enzymes related to energy transduction.

Adaptation, Physiological↗