{"title":"Mechanisms of metabolic defense against hypoxia in hibernating frogs","authors":"Robert G Boutilier","doi":"10.1016/S0034-5687(01)00312-7","DOIUrl":"https://doi.org/10.1016/S0034-5687(01)00312-7","url":null,"abstract":"<div><p>The cold submerged frog (<em>Rana temporaria</em>) serves as a useful model for many hibernating ectotherms that take refuge in hypoxic ponds and lakes until more favourable conditions of climate and food availability return. In all such animals, entry into a hypometabolic state effectively extends their survival time by lessening the impact of ATP demands on endogenous substrates. At the cellular level, metabolic depression may be brought about by decreasing energy-consuming processes and/or by increasing the efficiency of energy-producing pathways. Since the mitochondrion is the major contributor to the total energy production during aerobic metabolism and frog survival during winter depends on entry into a hypometabolic state, this review focuses on the respiratory properties of mitochondria that serve to increase the efficiency of energy production in hibernation. Energy conservation during overwintering also occurs through decreases in the ATP demand of the energy-consuming processes. For example, hibernating frogs decrease their ATP demands for Na<sup>+</sup>/K<sup>+</sup>-ATPase activity as part of a coordinated process of energy conservation wherein O<sub>2</sub>-limitation initiates a generalised suppression of ion channel densities and/or channel leak activities. The net result is that cell membrane permeabilities are reduced, thereby lowering the energetic costs of maintaining transmembrane ion gradients.</p></div>","PeriodicalId":20976,"journal":{"name":"Respiration physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0034-5687(01)00312-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91743756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Aging and oxidative stress: studies of some genes involved both in aging and in response to oxidative stress","authors":"Nadine Camougrand, Michel Rigoulet","doi":"10.1016/S0034-5687(01)00314-0","DOIUrl":"https://doi.org/10.1016/S0034-5687(01)00314-0","url":null,"abstract":"<div><p><span>Aging is a complex physiological phenomenon and several theories have been developed about its origin. Among such theories, the ‘mitochondrial theory of aging’ has been supported by numerous studies and reviews. Cell oxidative damage, in particular the accumulation of mtDNA mutations, is determined by the rate of reactive oxygen species production and degradation induced by the antioxidant defense systems. In this review, data from our laboratory and from the recent literature have been examined to provide arguments that reinforce the crucial role of mitochondria in aging. Various genes that affect life span have been described in numerous organisms. Some of them encode </span>signal transduction proteins and participate in the regulation of mitochondrial metabolism.</p></div>","PeriodicalId":20976,"journal":{"name":"Respiration physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0034-5687(01)00314-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91743754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Bioenergetics at low oxygen: dependence of respiration and phosphorylation on oxygen and adenosine diphosphate supply","authors":"Erich Gnaiger","doi":"10.1016/S0034-5687(01)00307-3","DOIUrl":"10.1016/S0034-5687(01)00307-3","url":null,"abstract":"<div><p>Oxygen limitation is generally considered as impairment of mitochondrial respiration under hypoxia and ischemia. Low intracellular oxygen levels under normoxia, however, imply mild oxygen limitation, provide protection from oxidative stress, and result from economical strategies for oxygen transport through the respiratory cascade to cytochrome <em>c</em> oxidase. Both perspectives relate to the critical oxygen pressure, which inhibits mitochondrial respiration. Based on methodological considerations of oxygen kinetics and a presentation of high-resolution respirometry, mitochondrial oxygen affinities (1/P<sub>50</sub>) are reviewed with particular emphasis on the turnover effect under control of adenosine diphosphate ADP concentration, which increases the P<sub>50</sub> in active states. ADP/O<sub>2</sub> flux ratios are high even under severe oxygen limitation, as demonstrated by calorespirometry. Oxygen limitation reduces the uncoupled respiration observed under control by ADP, as shown by relationships derived between ADP/O<sub>2</sub> flux ratios, respiratory control ratios, and ADP kinetics. Bioenergetics at low oxygen versus oxidative stress must be considered in the context of limitation of maximum aerobic activity, ischemia-reperfusion injury, mitochondrial signalling to apoptosis, and mitochondrial theories of ageing.</p></div>","PeriodicalId":20976,"journal":{"name":"Respiration physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0034-5687(01)00307-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78264695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Ageing and the free radical theory.","authors":"A. Wickens","doi":"10.1016/S0034-5687(01)00313-9","DOIUrl":"https://doi.org/10.1016/S0034-5687(01)00313-9","url":null,"abstract":"","PeriodicalId":20976,"journal":{"name":"Respiration physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87408718","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Torsten Porwol, Wilhelm Ehleben, Verena Brand, Helmut Acker
{"title":"Tissue oxygen sensor function of NADPH oxidase isoforms, an unusual cytochrome aa3 and reactive oxygen species","authors":"Torsten Porwol, Wilhelm Ehleben, Verena Brand, Helmut Acker","doi":"10.1016/S0034-5687(01)00310-3","DOIUrl":"https://doi.org/10.1016/S0034-5687(01)00310-3","url":null,"abstract":"<div><p>NADPH oxidase isoforms with different gp91phox subunits as well as an unusual cytochrome aa3 with a heme a/a3 relationship of 9:91 are discussed as putative oxygen sensor proteins influencing gene expression and ion channel conductivity. Reactive oxygen species (ROS) are important second messengers of the oxygen sensing signal cascade determining the stability of transcription factors or the gating of ion channels. The formation of ROS by a perinuclear Fenton reaction is imaged by 1 and 2 photon confocal microscopy revealing mitochondrial and non-mitochondrial generation.</p></div>","PeriodicalId":20976,"journal":{"name":"Respiration physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0034-5687(01)00310-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91743758","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Aging and oxidative stress: studies of some genes involved both in aging and in response to oxidative stress.","authors":"N. Camougrand, M. Rigoulet","doi":"10.1016/S0034-5687(01)00314-0","DOIUrl":"https://doi.org/10.1016/S0034-5687(01)00314-0","url":null,"abstract":"","PeriodicalId":20976,"journal":{"name":"Respiration physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86554225","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Respiratory and circulatory compensation to hypoxia in crustaceans","authors":"Brian R McMahon","doi":"10.1016/S0034-5687(01)00311-5","DOIUrl":"https://doi.org/10.1016/S0034-5687(01)00311-5","url":null,"abstract":"<div><p>Crustaceans are often tolerant of hypoxic exposure and many regulate O<sub>2</sub> consumption at low ambient O<sub>2</sub>. In acute hypoxia, most increase branchial water flow, and many also increase branchial haemolymph flow, both by an increase in cardiac output and by shunting flow away from the viscera. The O<sub>2</sub>-binding affinity of crustacean O<sub>2</sub> carriers increases in hypoxic conditions, as a result of hyperventilation induced alkalosis. In chronic hypoxic exposure some crustaceans do not sustain high ventilatory pumping levels but increased effectiveness of O<sub>2</sub>-uptake across the gills is maintained as a result of the build up of metabolites such as lactate and urate which also function to increase the haemocyanin O<sub>2</sub>-binding affinity. Chronic exposure to hypoxia also may increase O<sub>2</sub>-binding capacity and promote the synthesis of new high O<sub>2</sub>-affinity carrier molecules. Exposure to untenable rates or levels of O<sub>2</sub> depletion causes many decapodan crustaceans to surface and ventilate the gills with air. Burrowing crayfish provide an example of animals, which excel in all these mechanisms. Control mechanisms involved in compensatory responses to hypoxia are discussed.</p></div>","PeriodicalId":20976,"journal":{"name":"Respiration physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0034-5687(01)00311-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91743757","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Mechanisms of metabolic defense against hypoxia in hibernating frogs.","authors":"R. Boutilier","doi":"10.1016/S0034-5687(01)00312-7","DOIUrl":"https://doi.org/10.1016/S0034-5687(01)00312-7","url":null,"abstract":"","PeriodicalId":20976,"journal":{"name":"Respiration physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87018125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Tissue oxygen tension and brain sensitivity to hypoxia","authors":"Maria Erecińska, Ian A. Silver","doi":"10.1016/S0034-5687(01)00306-1","DOIUrl":"10.1016/S0034-5687(01)00306-1","url":null,"abstract":"<div><p>Mammalian brain is a highly oxidative organ and although it constitutes only a small fraction of total body weight it accounts for a disproportionately large percentage of bodily oxygen consumption (in humans about 2 and 20%, respectively). Yet, the partial pressure and concentration of oxygen in the brain are low and non-uniform. There is a large number of enzymes that use O<sub>2</sub> as a substrate, the most important of which is cytochrome <em>c</em> oxidase, the key to mitochondrial ATP production. The affinity of cytochrome <em>c</em> oxidase for oxygen is very high, which under normal conditions ensures undiminished activity of oxidative phosphorylation down to very low P<sub>O<sub>2</sub></sub>. By contrast, many other relevant enzymes have K<sub>m</sub> values for oxygen within, or above, the ambient cerebral gas tension, thus making their operations very dependent on oxygen level in the physiological range. Among its multiple, versatile functions, oxygen partial pressure and concentration control production of reactive oxygen species, expression of genes and functions of ion channels. Limitation of oxygen supply to the brain below a ‘critical’ level reduces, and eventually blocks oxidative phosphorylation, drastically decreases cellular (ATP) and leads to a collapse of ion gradients. Neuronal activity ceases and if oxygen is not re-introduced quickly, cells die. The object of this review is to discuss briefly the central oxygen-dependent processes in mammalian brain and the short-term consequences of O<sub>2</sub> deprivation, but not the mechanisms of long-term adaptation to chronic hypoxia. Particular emphasis is placed on issues which have been the focus of recent attention and/or controversy.</p></div>","PeriodicalId":20976,"journal":{"name":"Respiration physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0034-5687(01)00306-1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88808341","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Haemoglobin function in vertebrates: evolutionary changes in cellular regulation in hypoxia","authors":"Mikko Nikinmaa","doi":"10.1016/S0034-5687(01)00309-7","DOIUrl":"10.1016/S0034-5687(01)00309-7","url":null,"abstract":"<div><p>The evolution of erythrocytic hypoxia responses is reviewed by comparing the cellular control of haemoglobin-oxygen affinity in agnathans, teleost fish and terrestrial vertebrates. The most ancient response to hypoxic conditions appears to be an increase in cell volume, which increases the haemoglobin-oxygen affinity in lampreys. In teleost fish, an increase of cell volume in hypoxic conditions is also evident. The volume increase is coupled to an increase in erythrocyte pH. These changes are caused by an adrenergic activation of sodium/proton exchange across the erythrocyte membrane. The mechanism is important in acute hypoxia and is followed by a decrease in cellular adenosine triphosphate (ATP) and guanosine triphosphate (GTP) concentrations in continued hypoxia. In hypoxic bird embryos, the ATP levels are also reduced. The mechanisms by which hypoxia decreases cellular ATP and GTP concentrations remains unknown, although at least in bird embryos cAMP-dependent mechanisms have been implicated. In mammals, hypoxia responses appear to occur mainly via modulation of cellular organic phosphate concentrations. In moderate hypoxia, 2,3-diphosphoglycerate levels are increased as a result of alkalosis caused by increased ventilation.</p></div>","PeriodicalId":20976,"journal":{"name":"Respiration physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2001-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0034-5687(01)00309-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87593525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}