-
Biochimica Et Biophysica Acta Jun 2015While oxygen limitation can be extremely damaging for many animals, some vertebrates have perfected anaerobic survival. Freshwater turtles belonging to the Trachemys and... (Review)
Review
BACKGROUND
While oxygen limitation can be extremely damaging for many animals, some vertebrates have perfected anaerobic survival. Freshwater turtles belonging to the Trachemys and Chrysemys genera, for example, can survive many weeks without oxygen, and as such are commonly used as model animals for vertebrate anoxia tolerance.
SCOPE OF REVIEW
In the present review we discuss the recent advances made in understanding the biochemical and molecular nature of natural anoxia tolerance of freshwater turtles.
MAJOR CONCLUSIONS
Research in recent years has shown that activation of several important pathways occurs in response to anoxia in turtles, including those that function in the stress response, cell cycle arrest, inhibition of gene expression and metabolism. These likely contribute to anoxia tolerance in turtle tissues by minimizing cell damage in response to anoxia, as well as facilitating metabolic rate depression.
GENERAL SIGNIFICANCE
The research discussed in the present review contributes to the understanding of how freshwater turtles can survive without oxygen for prolonged periods of time. This could also improve understanding of the molecular nature of hypoxic/ischemic injuries in mammalian tissues and suggest potential ways to avoid these.
Topics: Adaptation, Physiological; Animals; Antioxidants; Energy Metabolism; Gene Expression Regulation; Hypoxia; Oxidative Stress; Oxygen; Signal Transduction; Transcription Factors; Turtles
PubMed: 25662819
DOI: 10.1016/j.bbagen.2015.02.001 -
Comparative Biochemistry and... Jun 2007Freshwater turtles of the Trachemys and Chrysemys genera are champion facultative anaerobes able to survive for several months without oxygen during winter hibernation... (Review)
Review
Freshwater turtles of the Trachemys and Chrysemys genera are champion facultative anaerobes able to survive for several months without oxygen during winter hibernation in cold water. They have been widely used as models to identify and understand the molecular mechanisms of natural anoxia tolerance and the molecular basis of the hypoxic/ischemic injuries that occur in oxygen-sensitive systems and underlie medical problems such as heart attack and stroke. Peter L. Lutz spent much of his career investigating turtle anaerobiosis with a particular focus on the mechanisms of brain ion homeostasis and neurotransmitter responses to anoxia exposure and the mechanisms that suppress brain ion channel function and neuronal excitability during anaerobiosis. Our interests intersected over the mechanisms of metabolic rate depression which is key to long term anoxia survival. Studies in my lab have shown that a key mechanism of metabolic arrest is reversible protein phosphorylation which provides coordinated suppression of the rates of multiple ATP-producing, ATP-utilizing and related cellular processes to allow organisms to enter a stable hypometabolic state. Anoxia tolerance is also supported by selective gene expression as revealed by recent studies using cDNA library and DNA array screening. New studies with both adult T. scripta elegans and hatchling C. picta marginata have identified prominent groups of genes that are up-regulated under anoxia in turtle organs, in several cases suggesting aspects of cell function and metabolic regulation that have not previously been associated with anaerobiosis. These groups of anoxia-responsive genes include mitochondrially-encoded subunits of electron transport chain proteins, iron storage proteins, antioxidant enzymes, serine protease inhibitors, transmembrane solute carriers, neurotransmitter receptors and transporters, and shock proteins.
Topics: Adaptation, Physiological; Animals; Calcium; Gene Expression Regulation; Hypoxia; Organ Specificity; Turtles
PubMed: 17035057
DOI: 10.1016/j.cbpa.2006.03.019 -
The American Journal of the Medical... Jul 1964
Review
Topics: Cerebral Hemorrhage; Humans; Hypertension; Hypoxia; Hypoxia, Brain; Intracranial Hemorrhage, Hypertensive
PubMed: 14177932
DOI: 10.1097/00000441-196407000-00013 -
American Journal of Physiology. Lung... Nov 2002
Review
Topics: Animals; Biosensing Techniques; Humans; Hypoxia; Oxygen
PubMed: 12376344
DOI: 10.1152/ajplung.00205.2002 -
Lancet (London, England) Apr 1963
Topics: Female; Fetal Diseases; Fetal Hypoxia; Humans; Hypoxia; Labor, Obstetric; Maternal-Fetal Exchange; Pregnancy
PubMed: 14023570
DOI: 10.1016/s0140-6736(63)91619-2 -
Lancet (London, England) Sep 1957
Topics: Brain; Brain Diseases; Brain Injuries; Humans; Hypoxia; Hypoxia, Brain
PubMed: 13464111
DOI: No ID Found -
Bulletin Medical
Topics: Hypoxia
PubMed: 13094278
DOI: No ID Found -
Respiratory Physiology & Neurobiology Nov 2006Oxygen depleted environments are relatively common on earth and represent both a challenge and an opportunity to organisms that survive there. A commonly observed... (Review)
Review
Oxygen depleted environments are relatively common on earth and represent both a challenge and an opportunity to organisms that survive there. A commonly observed survival strategy to this kind of stress is a lowering of metabolic rate or metabolic depression. Whether metabolic rate is at a normal or a depressed level the supply of ATP (glycolysis and oxidative phosphorylation) must match the cellular demand for ATP (protein synthesis and ion pumping), a condition that must of course be met for long-term survival in hypoxic and anoxic environments. Underlying a decrease in metabolic rate is a corresponding decrease in both ATP supply and ATP demand pathways setting a new lower level for ATP turnover. Both sides of this equation can be actively regulated by second messenger pathways but it is less clear if they are regulated differentially or even sequentially with the onset of anoxia. The vertebrate brain is extremely sensitive to low oxygen levels yet some species can survive in oxygen depleted environments for extended periods and offer a working model of brain survival without oxygen. Hypoxia tolerant vertebrate brain will be the primary focus of this review; however, we will draw upon research involving hypoxia/ischemia tolerance mechanisms in liver and heart to offer clues to how brain can tolerate anoxia. The issue of regulating ATP supply or demand pathways will also be addressed with a focus on ion channel arrest being a significant mechanism to reduce ATP demand and therefore metabolic rate. Furthermore, mitochondria are ideally situated to serve as cellular oxygen sensors and mediator of protective mechanisms such as ion channel arrest. Therefore, we will also describe a mitochondria based mechanism of ion channel arrest involving ATP-sensitive mitochondrial K(+) channels, cytosolic calcium and reaction oxygen species concentrations.
Topics: Acclimatization; Adenosine Triphosphate; Animals; Humans; Hypoxia; Models, Biological; Neurons; Potassium; Potassium Channels; Vertebrates
PubMed: 16621734
DOI: 10.1016/j.resp.2006.03.004 -
Journal of Comparative Physiology. B,... Apr 2019Pacific hagfish, Eptatretus stoutii, can recover from 36 h of anoxia and their systemic hearts continue to work throughout the exposure. Recent work demonstrates that...
Pacific hagfish, Eptatretus stoutii, can recover from 36 h of anoxia and their systemic hearts continue to work throughout the exposure. Recent work demonstrates that glycogen stores are utilized in the E. stoutii heart during anoxia but that these are not sufficient to support the measured rate of ATP production. One metabolic fuel that could supplement glycogen during anoxia is glycerol. This substrate can be derived from lipid stores, stored in the heart, or delivered via the blood. The purpose of this study was to determine the effect of glycerol on the contractile function of the excised E. stoutii heart during anoxia exposure. When excised hearts, perfused with metabolite free saline (mf-saline), were exposed to anoxia for 12 h, there was no difference in heart rate, pressure generation (max-dP), rate of contraction (max-dP/dt), or rate of relaxation (max-dP/dt) compared to hearts perfused with mf-saline in normoxia. However, hearts perfused with saline containing glycerol (gly-saline) in anoxia had higher max-dP, max-dP/dt, and max-dP/dt than hearts perfused with mf-saline in anoxia. Tissue levels of glycerol increased when hearts were perfused with gly-saline in normoxia, but not when perfused with gly-saline in anoxia. Anoxia exposure did not affect the activities of triglyceride lipase, glycerol kinase, or glycerol-3-phosphate dehydrogenase. This study suggests that glycerol stimulates cardiac function in the hagfish but that it is not derived from stored lipids. How glycerol may stimulate contraction is not known. This could be as an energy substrate, as an allosteric factor, or a combination of the two.
Topics: Animals; Glucose; Glycerol; Hagfishes; Heart; Hypoxia; Myocardial Contraction; Myocardium; Triglycerides
PubMed: 30725175
DOI: 10.1007/s00360-019-01208-w -
Antioxidants & Redox Signaling Sep 2007The mechanisms underlying anoxia (0-0.5% oxygen)-induced cell death are not fully understood. Here we discuss the mechanisms by which cells undergo apoptosis in the... (Review)
Review
The mechanisms underlying anoxia (0-0.5% oxygen)-induced cell death are not fully understood. Here we discuss the mechanisms by which cells undergo apoptosis in the absence of oxygen. Cell death during anoxia occurs via the intrinsic pathway of apoptosis. Key regulators of apoptosis during anoxia are the Bcl-2 family of proteins. The pathway is initiated by the loss of function of the prosurvival Bcl-2 family members Mcl-1 and Bcl-2/Bcl-XL, resulting in Bax- or Bak-dependent release of cytochrome c and subsequent caspase-9-dependent cell death.
Topics: Apoptosis; Cell Death; Homeostasis; Hypoxia; Models, Biological; Proto-Oncogene Proteins c-bcl-2
PubMed: 17627475
DOI: 10.1089/ars.2007.1731