Glucagon stimulation of mitochondrial respiration.

Acute glucagon treatment of intact rats has been found to cause a stimulation of hepatic mitochondrial respiration as measured by monitoring oxygen uptake polarographically. Rates of State 3 respiration with several NAD-linked substrates and succinate were increased significantly after hormonal treatment and isolation of mitochondria. This stimulation cannot be ascribed to a partial uncoupling effect since State 4 respiration as measured by monitoring oxygen uptake polarographically. Rates of State 3 respiration with either slightly increased or unchanged. Furthermore, rates of uncoupled respiration with these substrates were also stimulated after hormonal treatment. On the other hand, respiratory rates (State 3, 4, and uncoupled) with ascorbate-N,N,N',N'-tetramethyl-p-phenylenediamine as substrate were unaffected by glucagon treatment. The hormonally stimulated rates of respiration produced a corresponding increase in the rate of generation of high energy state as indicated in measurements of Ca2+ uptake by isolated mitochondria. Rates of Ca2+ uptake were monitored by two methods: measurement of initial rates of proton ejection following CaCl2 additions and measurement of disappearance of Ca2+ from the suspension medium using murexide as indicator in a dual wavelength spectrophotometer. A significant stimulation in the initial rate of succinate-dependent Ca2+ uptake was noted after glucagon treatment of animals and isolation of hepatic mitochondria. No effect of the hormonal treatment was seen on the extent of Ca2+ uptake or the stoichiometry of H+ ejected per Ca2+ taken up. That the hormonal effect on Ca2+ transport is at the level of the substrate-induced generation of high energy state is indicated by the observation that no effect of glucagon treatment is seen on ATP-dependent Ca2+ uptake. Glucagon-induced changes in the activities of substrate-metabolizing enzymes are considered unlikely for the following reasons: (a) previously published data showed a lack of a hormonal effect on pyruvate-metabolizing enzymes and (b) data in this study showing no effect of glucagon treatment on the activity of NAD-malate dehydrogenase as measured in mitochondrial lysates. All of these observations are consistent with either an activation of mitochondrial substrate transport and/or a stimulation of mitochondrial electron transport by glucagon treatment. Regardless of the exact mechanism involved, the effect of the hormonal treatment is to produce an increase in ATP synthetic and ion-pumping capability during a period of increased energy demand, i.e. increased gluconeogenesis.     

Biochemistry of nitrate respiration in Pseudomonas stutzeri. I. Aerobic and nitrate respiration routes of carbohydrate catabolism

Spangler, W. J. (Oregon State University, Corvallis), and C. M. Gilmour. Biochemistry of nitrate respiration in Pseudomonas stutzeri. I. Aerobic and nitrate respiration routes of carbohydrate catabolism. J. Bacteriol. 91:245-250. 1966.-The metabolic pathways of glucose catabolism were studied in Pseudomonas stutzeri under aerobic conditions and under conditions of nitrate respiration. Studies on both glucose and gluconate catabolism, by the radiorespirometric method, indicated that these substrates are degraded in the same manner, i.e., the Entner-Doudoroff and pentose phosphate pathways. There appeared to be no major shift in primary metabolic pathways when nitrate was used as the terminal hydrogen acceptor in nitrate respiration as opposed to aerobic respiration with free molecular oxygen. It was shown that glucose is not degraded to any appreciable extent under anaerobic conditions in the absence of nitrate. Tentative evidence suggests that the tricarboxylic acid cycle functions under both conditions of oxygen relationships and that the rate of carbon oxidation via the tricarboxylic acid cycle is slower with nitrate respiration than under aerobic conditions.     

Fractal fluctuations in human respiration.

The present study was designed to characterize respiratory fluctuations in awake, healthy adult humans under resting conditions. For this purpose, we recorded respiratory movements with a strain-gauge pneumograph in 20 subjects. We then used Allan factor, Fano factor, and dispersional analysis to test whether the fluctuations in the number of breaths, respiratory period, and breath amplitude were fractal (i.e., time-scale-invariant) or random in occurrence. Specifically, we measured the slopes of the power laws in the Allan factor, Fano factor, and dispersional analysis curves for original time series and compared these with the slopes of the curves for surrogates (randomized data sets). In addition, the Hurst exponent was calculated from the slope of the power law in the Allan factor curve to determine whether the long-range correlations among the fluctuations in breath number were positively or negatively correlated. The results can be summarized as follows. Fluctuations in all three parameters were fractal in nine subjects. There were four subjects in whom only the fluctuations in number of breaths and breath amplitude were fractal, three subjects in whom only the fluctuations in number of breaths were fractal, and two subjects in whom only fluctuations in breath number and respiratory period were fractal. Time-scale-invariant behavior was absent in the two remaining subjects. The results indicate that, in most cases, apparently random fluctuations in respiratory pattern are, in fact, correlated over more than one time scale. Moreover, the data suggest that fractal fluctuations in breath number, respiratory period, and breath amplitude are controlled by separate processes.     

Nitric oxide and mitochondrial respiration.

Nitric oxide (NO) and its derivative peroxynitrite (ONOO-) inhibit mitochondrial respiration by distinct mechanisms. Low (nanomolar) concentrations of NO specifically inhibit cytochrome oxidase in competition with oxygen, and this inhibition is fully reversible when NO is removed. Higher concentrations of NO can inhibit the other respiratory chain complexes, probably by nitrosylating or oxidising protein thiols and removing iron from the iron-sulphur centres. Peroxynitrite causes irreversible inhibition of mitochondrial respiration and damage to a variety of mitochondrial components via oxidising reactions. Thus peroxynitrite inhibits or damages mitochondrial complexes I, II, IV and V, aconitase, creatine kinase, the mitochondrial membrane, mitochondrial DNA, superoxide dismutase, and induces mitochondrial swelling, depolarisation, calcium release and permeability transition. The NO inhibition of cytochrome oxidase may be involved in the physiological regulation of respiration rate, as indicated by the finding that isolated cells producing NO can regulate cellular respiration by this means, and the finding that inhibition of NO synthase in vivo causes a stimulation of tissue and whole body oxygen consumption. The recent finding that mitochondria may contain a NO synthase and can produce significant amounts of NO to regulate their own respiration also suggests this regulation may be important for physiological regulation of energy metabolism. However, definitive evidence that NO regulation of mitochondrial respiration occurs in vivo is still missing, and interpretation is complicated by the fact that NO appears to affect tissue respiration by cGMP-dependent mechanisms. The NO inhibition of cytochrome oxidase may also be involved in the cytotoxicity of NO, and may cause increased oxygen radical production by mitochondria, which may in turn lead to the generation of peroxynitrite. Mitochondrial damage by peroxynitrite may mediate the cytotoxicity of NO, and may be involved in a variety of pathologies.     

Distribution of cytochrome-like respiration in streptococci.

The electron transport systems of 134 strains of streptococci were studied after aerobic growth on glucose in the presence of haematin, by examining the inhibition of electron transport as well as the cellular site of NADH oxidation. Each strain was placed into one of three possible groups: cytochrome-like NADH oxidase; flavin-like NADH oxidase; or no NADH oxidase. Most (88%) of the strains of Streptococcus faecalis and its variants liquefaciens and zymogenes and a few strains of S. lactis and its variant diacetylactis contained cytochrome-like respiratory systems. Other streptococci including S. faecium fell into one of the other groups but did not contain cytochrome-like NADH oxidases.     

Techniques for biochemical respiration measurements.

A small membrane-covered oxygen electrode is described. This electrode is used either as a stationary electrode in stirred solutions or as a vibrating electrode in unstirred solutions. An amplifier system for registration of the electrode current and its time derivative is also described as are two specialized reaction vessels, a miniature vessel of ca. 7-μl volume and a closed vessel for sampling during respiration measurements. The kinetics of oxygen uptake from the atmosphere of respiring solutions is investigated. The uptake follows first-order kinetics and may be calculated from simple equations. The uptake may be prevented by continuously adjusting the air space oxygen tension to the oxygen tension of the solution. This is done with the controlled gas mixer which is described. It makes possible reliable respiration measurements in open reaction vessels (e.g., photometric cuvettes). The techniques described have been developed for work with mitochondria but they have wide applicability.     

氮添加对沙质草地微生物呼吸与根系呼吸的影响

土壤呼吸可以细化为根系呼吸和微生物呼吸,二者对氮添加的响应有所不同.本文以科尔沁沙质草地为研究对象,探讨氮添加对土壤CO₂排放的影响,并细化为微生物呼吸和根系呼吸的响应特征.结果表明: 在观测期(5—10月),土壤呼吸、微生物呼吸月动态均呈先升高后降低的趋势;微生物呼吸是土壤呼吸的主要贡献者,占82.6%;观测期内根系呼吸贡献率随月份而变化,根系呼吸贡献率两个峰值分别出现在5月(占49.4%)和8月(占41.9%),6个月的平均贡献率为17.4%;在10 ℃条件下,根系呼吸较微生物呼吸对氮添加的响应更为敏感,微生物呼吸速率在氮添加后降低了3.9%,而根系呼吸降低了17.7%;氮添加提高了土壤呼吸、微生物呼吸温度敏感性Q₁₀值,也提高了二者对土壤水分变化的敏感程度.     

Cheyne-Stokes respiration in congestive heart failure.

Cheyne-Stokes respiration is an abnormal breathing pattern which commonly occurs in patients with decompensated congestive heart failure and neurologic diseases, in whom periods of tachypnea and hyperpnea alternate with periods of apnea. In the majority of these patients, the ventilatory patterns may not be recognized, and the clinical features are generally dominated by the underlying disease process. Cheyne-Stokes respiration may, however, have profound effects on the cardiopulmonary system, causing oxygen desaturation, cardiac arrhythmias, and changes in mental status. Treatment of Cheyne-Stokes respiration in congestive heart failure with supplemental oxygen or nasal continuous positive airway pressure, in addition to conventional therapy, may improve the overall cardiac function and perhaps the patient's prognosis.     

Neuronal control of respiration in decapod crustacea.

Respiratory exchange in decapod crustacea requires the coordinated activity of the heart and the scaphognathites, appendages which ventilate the gills. There is common central nervous system neuronal modulation of both autogenically active systems as well as direct neuronal communication between both systems. The heart and scaphognathites also respond directly to oxygen tension. The neuronal control of the scaphognathites also respond directly to oxygen tension. The neuronal control of the scaphognathites is analyzed at several levels. Particular attention is directed toward the means by which the innately organized and stereotyped motor pattern for forward beating can be altered to produce reversed beating. The importance of sensory feedback in maintaining normal rates of scaphognathite beating is noted. And the phenomenon of bilateral coordination between the morphologically independent scaphognathites is described. Several different models of parts of the over-all scaphognathite neuronal circuitry are presented for heuristic purposes.