Morpho-functional study of the brain of animals with different types of individual resistance to hypoxia

The experiments on white rats have shown that animals with distinct tolerance to hypoxia were characterized by individual metabolic changes in phylogenetically different brain structures. Adaptation to hypoxia in animals with high tolerance was associated with metabolic changes in the reticular formation and in animals with low tolerance with changes in the cerebral cortex. The experiments have shown that white rats with distinct individual tolerance to hypoxia are characterized by an inherent level of plastic metabolism in different brain structures. A correlation between brain tissue metabolism and individual tolerance of animals to hypoxia is suggested.     

CYCLIC NUCLEOTIDES IN MURINE BRAIN: EFFECT OF HYPOTHERMIA ON ADENOSINE 3'',5'' MONOPHOSPHATE, GLYCOGEN PHOSPHORYLASE, GLYCOGEN SYNTHASE AND METABOLITES FOLLOWING MAXIMAL ELECTROSHOCK OR DECAPITATION

Abstract —The accumulation of adenosine-3',5'-cyclic monophosphate (cyclic AMP) has been investigated in murine brain following electroconvulsive shock and decapitation. Animals were made hypothermic (20°C) to minimize the freezing time of the brain and to delay metabolic events. Cyclic AMP concentrations were decreased in the cerebral cortex of hypothermic rats and mice. Furthermore, the changes in cyclic AMP elicited by electroconvulsive shock and decapitation were delayed. In hypothermic animals, the metabolic rate as determined by high energy phosphate use was decreased to 65% of control values. The interconversions of the active and inactive forms of glycogen phosphorylase and glycogen synthase were sufficiently retarded in hypothermic animals to correlate with changes in cyclic AMP concentrations. The conversion of phosphorylase b to a and synthase a to b occurred when cyclic AMP concentrations had increased from 2 to 5 μmol/kg, following either electroconvulsive shock or decapitation. The results indicate that cyclic AMP plays a role in regulation of glycogen metabolism in cerebral cortex.     

CARBOHYDRATE AND ENERGY METABOLISM IN PERINATAL RAT BRAIN: RELATION TO SURVIVAL IN ANOXIA

The ability of rats of different ages to survive exposure to anoxia was correlated with rates of high energy phosphate consumption (metabolic rates) of the fore-brain. Fetal rats at term, delivered by hysterotomy following maternal decapitation, survived in nitrogen at 37°C twice as long as 1-day-old neo-nates, 5 times longer than 7-day-old rats, and 45 times longer than adults. During ischemia induced by decapitation, the cerebral concentrations of the labile energy reserves (ATP, ADP, P-creatine, glucose and glycogen) and of lactate were determined in fetuses, 1- and 7-day post-natal animals. From the changes, the cerebral energy use rates were calculated to be 1·57 mmol/kg/min in fetuses, 1·33 mmol/kg/min in 1-day-olds and 2·58 mmol/kg/min in 7-day-olds. Maximal rates of lactate accumulation during ischemia, as a measure of glycolytic capacity, were comparable in fetuses and neonates, but were about twice as great in 7-day-old rats. It is concluded that in post-natal animals survival in anoxia and cerebral energy consumption are inversely, and nearly quantitatively, related. However, the reduced cerebral energy requirement cannot entirely account for the greater anoxic resistance of fetuses.     

Dynamics of cerebral metabolism during moderate hypercapnia.

The effects of hypercapnia on the kinetics of cerebral energy metabolism were evaluated in adult rats by the closed system method of LOWRY et al. (1964). Moderate hypercapnia with a Pa_co2 of 61 torr sustained for 20 min resulted in intracellular brain acidosis (7.07-6.97). During hypercapnia the tissue content of glucose increased whereas phosphocreatine, ADP, pyruvate and lactate contents, and the lactate/pyruvate ratio decreased. The ATP/ADP ratio increased from 7.7 to 9.0; the cytoplasmic NADH/NAD + ratio decreased from 2.06 × 10^-3 to 1.49 × 10^-3. There was no change in Energy Charge. Turnover rate of phosphocreatine increased from 3.84 to 4.62 mmol/kg/min, but the turnover rates of ATP, glucose and glycogen were reduced (from 1.98 to 1.86, 6.24 to 4.80, and 3.96 to 2.94 mmol/kg/min, respectively). The utilization rate of total high energy phosphate decreased from 30.6 to 25.4 mmol/kg/min while the post-decapitation EEG during hypercapnia persisted longer than during normocapnia. These results indicate that moderate hypercapnia reduces the overall kinetic activity of cerebral energy metabolism. The steady Energy Charge suggests that the reduction in the rate of high energy phosphate use is proportionally balanced by a lowered production rate of ATP.     

Cerebral energy metabolism during experimental status epilepticus.

—The concentration of ATP, ADP, AMP, phosphocreatine and of 5 intermediates of carbohydrate metabolism were determined in rodent brain after single and repeated seizures induced by either electroshock (ES), flurothyl or pentylenetetrazol (PTZ). In paralysed-ventilated rats, one ES produced a 4–5 fold increase in cortical glycolytic flux (estimated from changes in glucose and lactate), and associated increases in pyruvate and in the lactate/pyruvate ratio. Total high energy phosphates declined during the seizure; a decrease was also calculated in cortical tissue pH and in the cytoplasmic [NAD⁺]/[NADH] ratio. Similar changes in brain were observed in ventilated mice after ES, but in paralysed animals, no decrease in high energy phosphates occurred during the first seizure. More vigorous and prolonged chemically-induced seizures in both rats and mice elicited a decrease in the cerebral energy reserves with a rise in lactate and in the lactate/pyruvate ratio. At all times during the seizures the cerebral venous blood had a higher oxygen tension than that of control animals (rats) or was visibly reddened (mice), implying that oxygen availability to brain exceeded metabolic demands. It is proposed that the development of‘non-hypoxic’cerebral lactacidosis during seizures is part of the overall metabolic response of the brain to an abrupt increase in energy consumption. The response constitutes a homeostatic influence which promotes cerebral vasodilatation, thereby increasing blood flow and the delivery of substrates. With repeated seizures, delivered 2 min apart, glycogen declined progressively, but concentrations of the adenine nucleotides appeared to plateau, suggesting that a new energy balance had been established. However, after 20–25 seizures, the attacks became self-generating and there was a further reduction in the tissue high energy phosphate stores, a fall in brain glucose and in the brain/blood glucose ratio. It is concluded that the brain possesses a limited capacity to adjust its metabolism to meet the increased energy requirements of single or repeated seizures, but that this mechanism ultimately fails during status epilepticus unless the abnormal electrical discharges, themselves, are brought under control.     

青年和老年小鼠脑糖原及其代谢的差异

目的:比较青年小鼠和老年小鼠不同脑区糖原及其代谢的差异,为后续相关研究奠定基础。方法:分别取雄性C57BL/6J青年小鼠(8周龄)和老年小鼠(18月龄)皮层、海马、纹状体三个脑区脑组织,通过糖原定量试剂盒检测糖原含量,通过Western Blot检测糖原代谢相关酶(包括糖原合成、糖原分解、葡萄糖转运、乳酸转运相关酶类)的表达水平。结果:与青年小鼠相比,老年小鼠皮层、纹状体糖原含量明显上升,但海马的糖原含量无明显变化。在糖原合成代谢的关键酶中,糖原合成酶在老年小鼠皮层、纹状体的表达水平明显升高,而海马区则无明显差异;糖原分支酶在老年小鼠皮层的表达水平有所下降,在海马和纹状体则无明显变化。在糖原分解代谢的关键酶中,老年小鼠的糖原磷酸化酶在皮层、海马和纹状体均明显升高,而糖原脱支酶在上述脑区则无明显变化。葡萄糖转运体1的表达水平在老年小鼠与青年小鼠各脑区无显著差异。在单羧酸转运体中,老年小鼠单羧酸转运体1在各脑区均明显上升,单羧酸转运体4在皮层明显升高,其余脑区则无明显差异。结论:老年小鼠脑内糖原含量总体上较青年小鼠高,老年小鼠脑糖原代谢通路相关酶的表达与青年小鼠存在明显差异,且不同脑区之间存在异质性。     

Hypoxic Preconditioning and Hypoxic-Ischemic Brain Damage in the Immature Rat: Pathologic and Metabolic Correlates

Abstract: It has been reported that immature rats subjected to cerebral hypoxia-ischemia sustain less brain damage if they are previously exposed to systemic hypoxia compared with animals not exposed to prior hypoxia. Accordingly, neuropathologic and metabolic experiments were conducted to confirm and extend the observation that hypoxic preconditioning protects the perinatal brain from subsequent hypoxic-ischemic brain damage. Six-day postnatal rats were subjected to systemic hypoxia with 8% oxygen at 37°C for 2.5 h. Twenty-four hours later, they were exposed to unilateral cerebral hypoxia-ischemia for 2.5 h, produced by unilateral common carotid artery ligation and systemic hypoxia with 8% oxygen. Neuropathologic analysis, conducted at 30 days of postnatal age, indicated a substantial reduction in the severity of brain damage in the preconditioned rats, such that only 6 of 14 such animals exhibited cystic infarction, but all 13 animals without prior preconditioning exhibited infarction ( p < 0.001). Measurement of cerebral glycolytic and tricarboxylic acid intermediates and high-energy phosphate reserves at the terminus of and at 4 and 24 h following hypoxia-ischemia showed no differences in the extent of alterations in the preconditioned and nonpreconditioned immature rats. A difference was seen in the restitution of high-energy stores during the first 24 h of recovery from hypoxia-ischemia, with a more optimal preservation of these metabolites in the preconditioned animals, reflecting the less severe ultimate brain damage. Accordingly, the neuroprotection afforded to the preconditioned animals was not the result of any differences in the extent of anaerobic glycolysis, tissue acidosis, or depletion in high-energy reserves during hypoxia-ischemia but rather the result of other mechanisms that improved the metabolic status of the immature brain during the early hours of reperfusion following hypoxia-ischemia.     

Cortical metabolism in pyruvate dehydrogenase deficiency revealed by ex vivo multiplet C NMR of the adult mouse brain

The pyruvate dehydrogenase complex (PDC), required for complete glucose oxidation, is essential for brain development. Although PDC deficiency is associated with a severe clinical syndrome, little is known about its effects on either substrate oxidation or synthesis of key metabolites such as glutamate and glutamine. Computational simulations of brain metabolism indicated that a 25% reduction in flux through PDC and a corresponding increase in flux from an alternative source of acetyl-CoA would substantially alter the ¹³C NMR spectrum obtained from brain tissue. Therefore, we evaluated metabolism of [1,6-¹³C₂]glucose (oxidized by both neurons and glia) and [1,2-¹³C₂]acetate (an energy source that bypasses PDC) in the cerebral cortex of adult mice mildly and selectively deficient in brain PDC activity, a viable model that recapitulates the human disorder. Intravenous infusions were performed in conscious mice and extracts of brain tissue were studied by ¹³C NMR. We hypothesized that mice deficient in PDC must increase the proportion of energy derived from acetate metabolism in the brain. Unexpectedly, the distribution of ¹³C in glutamate and glutamine, a measure of the relative flux of acetate and glucose into the citric acid cycle, was not altered. The ¹³C labeling pattern in glutamate differed significantly from glutamine, indicating preferential oxidation of [1,2-¹³C]acetate relative to [1,6-¹³C]glucose by a readily discernible metabolic domain of the brain of both normal and mutant mice, presumably glia. These findings illustrate that metabolic compartmentation is preserved in the PDC-deficient cerebral cortex, probably reflecting intact neuron–glia metabolic interactions, and that a reduction in brain PDC activity sufficient to induce cerebral dysgenesis during development does not appreciably disrupt energy metabolism in the mature brain.     

Increased cerebral uptake and oxidation of exogenous betaHB improves ATP following traumatic brain injury in adult rats

There is growing evidence of the brain's ability to increase its reliance on alternative metabolic substrates under conditions of energy stress such as starvation, hypoxia and ischemia. We hypothesized that following traumatic brain injury (TBI), which results in immediate changes in energy metabolism, the adult brain increases uptake and oxidation of the alternative substrate beta-hydroxybutyrate (betaHB). Arterio-venous differences were used to determine global cerebral uptake of betaHB and production of 14CO2 from [14C]3-betaHB 3 h after controlled cortical impact (CCI) injury. Quantitative bioluminescence was used to assess regional changes in ATP concentration. As expected, adult sham and CCI animals with only endogenously available betaHB showed no significant increase in cerebral uptake of betaHB or 14CO2 production. Increasing arterial betaHB concentrations 2.9-fold with 3 h of betaHB infusion failed to increase cerebral uptake of betaHB or 14CO2 production in adult sham animals. Only CCI animals that received a 3-h betaHB infusion showed an 8.5-fold increase in cerebral uptake of betaHB and greater than 10.7-fold increase in 14CO2 production relative to sham betaHB-infused animals. The TBI-induced 20% decrease in ipsilateral cortical ATP concentration was alleviated by 3 h of betaHB infusion beginning immediately after CCI injury.     

Neonatal tolerance to hypoxia: a comparative-physiological approach.

Newborn mammals exhibit a number of physiological reactions which differ from normal adult physiology and are often regarded as signs of immaturity. However, when looked upon from a comparative point of view, it becomes obvious that some of these 'physiological peculiarities' bear striking similarity to adaptation mechanisms known from hypoxia-tolerant animals and may thus contribute to the well-established, yet poorly understood, phenomenon of neonatal hypoxia tolerance. As the mammalian fetus lives at oxygen partial pressures corresponding to 8000 m altitude, the first line of perinatal hypoxia defense consists of long-term adaptations to limited intrauterine oxygen supply: (1) improved O2 transport by fetal acclimatization to high altitude, (2) reduced metabolic rate by hibernation-like deviation from metabolic size allometry, (3) diminished cerebral vulnerability by functional analogies to diving turtle brain, and (4) enhanced metabolic flexibility by optional repartitioning of energy supply from growth to maintenance metabolism. In the case of birth asphyxia, these background mechanisms are complemented by short-term responses to acute oxygen lack: (1) reduction of body temperature as in natural torpor, (2) reduction of heart rate and redistribution of circulation as in diving mammals, (3) reduction of respiration rate typical of 'hypoxic hypometabolism', and (4) reduction of blood pH according to the concept of 'acidotic torpidity'. Although anaerobic metabolism is improved in neonatal mammals by increased glycogen stores, reduced metabolic demands, and sustained wash-out of acid metabolites, neonatal hypoxia tolerance seems to be primarily based on the ability to maintain tissue aerobiosis as long as possible. This is even reflected by isoenzyme patterns which do not consistently favour anaerobic glycolysis and, thus, are reminiscent of the 'lactate paradox' found in high altitude adaptation. Altogether, from a biological point of view, the perinatal period appears as a source of adaptive mechanisms that can be refound, in varying combinations, in many survival strategies. From a clinical point of view, the interplay of long- and short-term mechanisms offers a novel approach to estimation of the newborn's ability to withstand temporary oxygen lack. However, most of these mechanisms are not unambiguous and, above all, not unlimited in their protective effect so that they do not release obstetricians or neonatologists from their obligation to counteract fetal or neonatal hypoxia without delay.     

Lactate, 3-hydroxybutyrate,and glucose as substrates for the early postnatal rat brain

The dependence of cerebral energy metabolism upon glucose, 3-hydroxybutyrate, and lactate as fuel sources during the postnatal period was investigated. The brain of 6 day old suckling pups used very little glucose, but by the 15th postnatal day glucose was the major catabolite. Hydroxybutyrate was not a major brain fuel at either 6 or 15 days of age. Its utilization accounted for only 19% of the brain's total energy needs at 15 days of age, even though blood ketone concentrations are near maximal at this time. Seventy percent of the cerebral metabolic requirements were met by lactate in animals aged 6 days. The major role played by lactate as a substrate for brain metabolism in young pups was not a result of abnormally elevated blood lactate concentrations. The slow catabolism of glucose in young brain can not be explained by low rates of influx or inadequate enzymatic capacity.     

CB1 receptor blockade counters age‐induced insulin resistance and metabolic dysfunction

The endocannabinoid system can modulate energy homeostasis by regulating feeding behaviour as well as peripheral energy storage and utilization. Importantly, many of its metabolic actions are mediated through the cannabinoid type 1 receptor (CB1R), whose hyperactivation is associated with obesity and impaired metabolic function. Herein, we explored the effects of administering rimonabant, a selective CB1R inverse agonist, upon key metabolic parameters in young (4 month old) and aged (17 month old) adult male C57BL/6 mice. Daily treatment with rimonabant for 14 days transiently reduced food intake in young and aged mice; however, the anorectic response was more profound in aged animals, coinciding with a substantive loss in body fat mass. Notably, reduced insulin sensitivity in aged skeletal muscle and liver concurred with increased CB1R mRNA abundance. Strikingly, rimonabant was shown to improve glucose tolerance and enhance skeletal muscle and liver insulin sensitivity in aged, but not young, adult mice. Moreover, rimonabant‐mediated insulin sensitization in aged adipose tissue coincided with amelioration of low‐grade inflammation and repressed lipogenic gene expression. Collectively, our findings indicate a key role for CB1R in aging‐related insulin resistance and metabolic dysfunction and highlight CB1R blockade as a potential strategy for combating metabolic disorders associated with aging.     

Permeability of the blood-brain barrier to fructose and the anaerobic use of fructose in the brains of young mice

—Fructose levels were determined in plasma and brain of 8- to 12-day-old mice at intervals after the injection of 30 mmol/kg intraperitoneally; controls received NaCl, 15 mmol/kg. In normal animals brain fructose increased very slowly despite a rapid rise in plasma levels (120 times the control value in 5 min). At 40 min the cerebral level was 1.54 ± 0.23 mmol/kg; the corresponding plasma level was 47.1 ± 4.8 mM. The data suggest that fructose can serve as a source of energy to the brain in times of critical need: during insulin hypoglycemia brain fructose increased to only 0.88 ± 0.05 mmol/kg during the same interval (40 min) despite plasma fructose values equal to those in control animals; also 30 s after cerebral ischemia (decapitation) brain fructose fell from a zero time value of 1.19 ± 0.09 mmol/kg (20 min after fructose injection) to 0.76 ± 0.06 mmol/kg (P= 0.005). Under both circumstances (hypoglycemia and ischemie anoxia) an apparent threshold concentration of fructose for utilization was observed—0.6–0.7 mmol/kg. The most likely explanation for this finding appears to be that this level of fructose was in the extracellular space of the brain. Hexokinase activity in brain homogenates of 8- to 12-day-old mice with fructose and ATP at concentrations found in vivo and during ischemie anoxia did not appear to be rate-limiting. We concluded that the major handicap to the use of fructose by the brain was the limited penetration of fructose from the blood to the brain.     

Cerebral carbohydrate metabolism during acute hypoxia and recovery

Abstract— The levels of ATP, ADP, AMP and phosphocreatine, of four amino acids, and of 11 intermediates of carbohydrate metabolism in mouse brain were determined after: (1) various degrees of hypoxia; (2) hypoxia combined with anaesthesia; and (3) recovery from severe hypoxia. Glycogen decreased and lactate rose markedly in hypoxia, but levels of ATP and phosphocreatine were normal or near normal even when convulsions and respiratory collapse appeared imminent. During 30 s of complete ischaemia (decapitation) the decline in cerebral ATP and phosphocreatine and the increase in AMP was less in mice previously rendered hypoxic than in control mice. From the changes we calculated that the metabolic rate had decreased by 15 per cent or more during 30 min of hypoxia. Hypoxia was also associated with decreases of cerebral 6-phosphogluconate and aspartate, and increases in alanine, γ-aminobutyrate, α-ketoglutarate, malate, pyruvate, and the lactate :pyruvate ratio. Following recovery in air (10 min), increases were observed in glucose (200 per cent), glucose-6-phosphate, phosphocreatine and citrate, and there was a fall in fructose-1, 6-diphosphale. Similar measurements were made in samples from cerebral cortex, cerebellum, midbrain and medulla. Severe hypoxia produced significant increases in lactate and decreases in glycogen in all areas; γ-aminobutyrate levels increased in cerebral cortex and brain stem, but not in cerebellum. No significant changes occurred in ATP and only in cerebral cortex was there a significant fall in phosphocreatine. Phosphocreatine, ATP and glycogen were determined by quantitative histochemical methods in four areas of medulla oblongata, including the physiological respiratory centre of the ventromedial portion. After hypoxia, ATP was unchanged throughout and the changes (decreases) in phosphocreatine and glycogen were principally confined to dorsal medulla, notably the lateral zone. Thus there is no evidence that respiratory failure is caused by a ‘power’ failure in the respiratory centre. It is suggested that in extremis a protective mechanism may cause neurons to cease firing before high-energy phosphate stores have been exhausted.     

红景天苷对运动后自由基和能量代谢改变的影响

目的:探讨红景天苷在运动过程中对自由基和能量代谢相关指标的作用,从抗氧化系统、能量代谢系统等方面研究红景天苷抗运动性疲劳的机制。方法:本研究采用小鼠运动模型,40只雄性小鼠随机取分为4组(n=10):红景天苷运动组,红景天苷安静组,运动对照组,安静对照组。红景天苷运动组和安静组两组以150 mg/(kg.d)的红景天苷灌胃给药,运动和安静对照组两组以同样体积蒸馏水灌胃,连续给药2周;末次灌胃30 min后,运动组进行无负重游泳120 min,然后测定与运动性疲劳相关的生化指标。结果:研究结果表明,红景天苷能够提高运动小鼠肝脏内超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)等抗氧化酶活性,降低丙二醛(MDA)含量;红景天苷具有稳定运动小鼠血糖,增加肝、肌糖原储备,防止长时间运动后血糖和肝、肌糖原水平降低的作用;红景天苷可提高运动小鼠血浆总胆固醇(TC)、甘油三酯(TG)及游离脂肪酸(FFA)的水平,有影响不同状态下的脂肪代谢,促进脂肪利用的作用。结论:红景天苷对运动过程中自由基和能量代谢改变的影响是其抗运动性疲劳的机制之一。     

Relationships between energy reserves and function in rat superior cervical ganglion

—Major components of the energy reserves of the isolated superior cervical ganglion (ATP, phosphocreatine, glucose, glycogen and lactate) were measured under aerobic and anaerobic conditions. Complete anaerobiosis was maintained by incubation in mineral oil through which N₂ had been bubbled. From the initial rate of change in the energy reserves, a metabolic rate was calculated which would be equivalent to the consumption of 93 m-moles of O₂ per kg per hour. Under aerobic conditions (oxygenated moist chamber) a similar metabolic rate was calculated. In contrast to the anaerobic state, initial energy expenditure was almost exclusively at the expense of glucose. Continuous supramaximal stimulation in O₂ increased energy expenditure by a factor of three; both glucose and glycogen were utilized from the outset, and lactate accumulated in the initial periods. Ganglionic transmission failed in both resting and stimulated states in spite of the continued presence of very substantial levels of ATP and phosphocreatine. Failure seemed to be associated not with ATP depletion but rather with the complete disappearance of glucose and glycogen.     

Influence of age on brain edema formation, secondary brain damage and inflammatory response after brain trauma in mice

After traumatic brain injury (TBI) elderly patients suffer from higher mortality rate and worse functional outcome compared to young patients. However, experimental TBI research is primarily performed in young animals. Aim of the present study was to clarify whether age affects functional outcome, neuroinflammation and secondary brain damage after brain trauma in mice. Young (2 months) and old (21 months) male C57Bl6N mice were anesthetized and subjected to a controlled cortical impact injury (CCI) on the right parietal cortex. Animals of both ages were randomly assigned to 15 min, 24 h, and 72 h survival. At the end of the observation periods, contusion volume, brain water content, neurologic function, cerebral and systemic inflammation (CD3+ T cell migration, inflammatory cytokine expression in brain and lung, blood differential cell count) were determined. Old animals showed worse neurological function 72 h after CCI and a high mortality rate (19.2%) compared to young (0%). This did not correlate with histopathological damage, as contusion volumes were equal in both age groups. Although a more pronounced brain edema formation was detected in old mice 24 hours after TBI, lack of correlation between brain water content and neurological deficit indicated that brain edema formation is not solely responsible for age-dependent differences in neurological outcome. Brains of old naïve mice were about 8% smaller compared to young naïve brains, suggesting age-related brain atrophy with possible decline in plasticity. Onset of cerebral inflammation started earlier and primarily ipsilateral to damage in old mice, whereas in young mice inflammation was delayed and present in both hemispheres with a characteristic T cell migration pattern. Pulmonary interleukin 1β expression was up-regulated after cerebral injury only in young, not aged mice. The results therefore indicate that old animals are prone to functional deficits and strong ipsilateral cerebral inflammation without major differences in morphological brain damage compared to young.     

Acute toxicity of boric acid on energy metabolism of the breast muscle in broiler chickens

Short-and long-term oral exposures to boric acid (BA) in laboratory animals and birds caused toxic effects. However, the toxicity data on adult poultry skeletal muscles of BA was not documented with metabolic studies. Livability, weight gain, and feed conversion might be adversely affected in broilers as a result of changes in energy metabolism. Therefore, this study was conducted to investigate the influences of acute BA doses on energy metabolism of chick pectoral muscle (PM). Chicks were fed by giving the aqueous solutions supplemented with BA (0, 0.27, 0.54, 1.08, 1.35, 2.25, 3.375 and 4.5 mmol B/kg b.wt.). Breast muscle samples were taken at 24, 48 and 72 h and analyzed histochemically, ultrastructurally and biochemically. Data collected in these analyses indicated that consumption of diets containing up to 2.25 mmol B/kg at 24, 48 and 72h was not detrimental to broiler PM. However, 3.375 mmol B/kg b.wt. (at 24 h) and 4.5 mmol B/kg b.wt. (at 24 and 48 h) caused decreased metabolite concentrations (glucose, glycogen, lactate and ATP) in muscle fibers (Type IIB). Subsarcolemmal (SS) mitochondria and intermyofibrillar (IM) mitochondrial damage (cristae dissolution) were also observed by toxic effect of BA (4.5 mmol B/kg b.wt.). These observations proved that BA at the high doses (3.375 and 4.5 mmol B/kg b.wt.) causes to altered energy metabolism in Type IIB as dependent on time. Based on these results we think that energy protection in muscle against BA toxicity will be the most important study subject. Thus, high BA doses will not have detrimental effects on broiler performance.     

Metabolic responses in two species of crayfish (Parastacus defossus and Parastacus brasiliensis) to post-hypoxia recovery

The period of post-hypoxia recovery is essential for the rapid replenishment of energy reserves and for the removal of metabolic end products formed during hypoxia. Periods of post-hypoxia recovery were analyzed in two crayfish species, where Parastacus defossus is a fossorial species, and Parastacus brasiliensis lives in lotic environments with higher oxygen levels. After 4 h of hypoxia (2 mg O(2)/L), groups of animals were placed in tanks with oxygenated water and were then removed at intervals of 1, 3, 6, and 9 h. Hemolymph and tissues (hepatopancreas, muscle, and anterior and posterior gills) were extracted for the determination of glucose, lactate, free glucose, glycogen, total proteins, total lipids, arginine phosphate, and arginine. As expected, lactate levels were restored more rapidly in P. defossus than in P. brasiliensis. P. defossus restored its glycogen reserves of the hepatopancreas and muscle tissue. Free glucose was quickly restored in all tissues of both species. In relation to arginine phosphate reserves, P. defossus showed a greater ability to restore this metabolite in the hepatopancreas. Both species recovered their arginine phosphate reserves, but they also used this metabolite in longer periods of recovery. Mainly in P. brasiliensis the reserves of total lipids seem to be an important source of energy during the recovery period. The animals developed various metabolic strategies to post-hypoxia recovery, mainly P. defossus which restored its reserves more completely and more rapidly than did P. brasiliensis.