Interactions between cellular respiration and thermoregulation in the paramecium

1994 ◽  
Vol 267 (1) ◽  
pp. R349-R352 ◽  
Author(s):  
G. M. Malvin ◽  
P. Havlen ◽  
C. Baldwin

An important adaptation to hypoxia is a regulated reduction in body temperature because it lowers metabolic rate when oxygen supply is limited. Although this beneficial response occurs in organisms ranging from protozoans to mammals, little is known of the cellular mechanisms responsible for the hypoxia-induced reduction in temperature. Using the unicellular protozoan, Paramecium caudatum, we showed that inhibition of oxidative phosphorylation with sodium azide (NaN3) under normoxic conditions mimics the thermoregulatory effects of hypoxia, causing this species to select a lower temperature in a thermal gradient (P < 0.0001). Under control conditions, selected temperature (Tsel) was 28.3 +/- 0.3 degrees C. NaN3 concentrations of 0.1 mM and above significantly reduced Tsel (P < 0.0001). Ten millimolar NaN3 produced the maximal reduction in Tsel, 11.4 degrees C, and the dose that produced 50% of the maximal response was 0.7 mM. The reduction in temperature was beneficial because both O2 consumption and survival were significantly less affected by NaN3 at lower temperatures. These results suggest that O2 does not directly affect thermoregulation in the paramecium. Rather, the hypoxia-induced reduction in Tsel results from inhibition of oxidative phosphorylation.

1996 ◽  
Vol 270 (1) ◽  
pp. R169-R173 ◽  
Author(s):  
L. G. Branco ◽  
G. M. Malvin

An important adaptation to hypoxia is a regulated reduction in body temperature (Tb; anapyrexia), presumably because it lowers metabolic rate when oxygen supply is limited. Although this beneficial response occurs in organisms ranging from protozoans to mammals, little is known of the cellular mechanisms involved. We showed previously that inhibition of oxidative phosphorylation mediates hypoxia-induced anapyrexia in the paramecium. In this study, we tested the hypothesis that inhibition of oxidative phosphorylation also causes anapyrexia in a vertebrate, Bufo marinus. Tb in toads was measured in a thermal gradient 24 h before and 24 h after administration of either NaCN or NaN3, both inhibitors of oxidative phosphorylation. Subcutaneous NaCN (0.6 mmol/kg) reduced Tb from 29.1 +/- 0.8 to 19.6 +/- 0.6 degree C (P = 0.002). Infusion of NaCN (0.6 mumol/kg) into the fourth ventricle of the brain reduced Tb from 30.0 +/- 0.9 to 24.8 +/- 1.2 degrees C (P = 0.01). Responses to NaN3 were similar to the NaCN responses. Control injections and subcutaneous injections of 0.6 mumol/kg NaCN and NaN3 had no significant effect on Tb (P > 0.32). Neither NaCN nor NaN3 had significant effects on arterial PO2, PCO2, or pH at 26 degrees C. These results indicate that inhibition of oxidative phosphorylation in the central nervous system leads to the selection of cooler temperatures. Thus reduced oxidative phosphorylation within the brain may be an important factor eliciting hypoxia-induced anapyrexia.


1991 ◽  
Vol 159 (1) ◽  
pp. 203-215 ◽  
Author(s):  
S. C. Wood ◽  
G. M. Malvin

We tested the hypotheses that hypoxic toads (Bufo marinus) in a thermal gradient would select a lower than normal temperature and that this behavioral response would be beneficial. Under normoxic conditions, selected body temperature was 24.2 +/− 3.6 degrees C. When inspired O2 was 10% or less, mean selected temperature decreased to 15.3 +/− 2.4 degrees C. The theoretical advantages of hypoxia-induced hypothermia we tested include (1) a reduction of oxygen uptake (VO2) by a Q10 effect; (2) increased arterial saturation (SaO2), (3) a decreased ventilatory response, and (4) a decreased stress response. Gas exchange, hematocrit, hemoglobin, SaO2, PaO2 and pH were measured at 25 degrees C (normal preferred temperature) and 15 degrees C (hypoxia preferred temperature) in toads breathing normoxic or hypoxic gas mixtures. During graded hypoxia at 15 degrees C, SaO2 was significantly increased and VO2 was significantly reduced compared with 25 degrees C. Graded hypoxia did not significantly affect VO2 at 25 degrees C, despite evidence for increased ventilation at that temperature (increased pH and respiratory exchange ratio, RE). At 15 degrees C, graded hypoxia had a significant effect on VO2 only at an inspired O2 of 4%. Increased RE with hypoxia was significant at 25 degrees C but not at 15 degrees C. Hematocrit and [hemoglobin] rose significantly during graded hypoxia at 25 degrees C but did not change at 15 degrees C. Toads exposed to 10% O2 (the value that elicits behavioral hypothermia) showed a significant respiratory alkalosis at 25 degrees C but not at 15 degrees C. Likewise, hypoxia caused a significant drop in SaO2 and PO2 at 25 degrees C. Cooling to 15 degrees C during hypoxia caused a significant rise in SaO2 but no change in PaO2. In conclusion, behavioral hypothermia is a beneficial response to hypoxia in Bufo marinus.


2016 ◽  
Vol 40 (4) ◽  
pp. 511-520 ◽  
Author(s):  
Chun-Lang Yeh

The effects of choke ring dimension on the thermal and fluid flow in a practical SRU (sulfur recovery unit) thermal reactor are investigated numerically. It is found that zone 1 is a higher temperature region. In contrast, zone 2 is a lower temperature region. The average temperature for the rich oxygen supply is higher than that of normal oxygen supply. Without a choke ring, the temperature difference between zone 1 and zone 2 is smaller and the temperature in zone 1 becomes lower while the temperature in zone 2 becomes higher. In addition, the average temperature in zone 1 and the sulfur concentration at exit are the lowest without a choke ring. The reactor with a choke ring height of 0.74 m has the lowest peak temperature and the largest sulfur concentration at exit. Finally, with a choke ring height of 1.11 m, the blockage effect of the choke ring leads to the largest peak skin friction coefficient.


2013 ◽  
Vol 280 (1768) ◽  
pp. 20131314 ◽  
Author(s):  
Geoffrey E. Hill ◽  
James D. Johnson

Why females assess ornaments when choosing mates remains a central question in evolutionary biology. We hypothesize that the imperative for a choosing female to find a mate with nuclear oxidative phosphorylation (OXPHOS) genes that are compatible with her mitochondrial OXPHOS genes drives the evolution of ornaments. Indicator traits are proposed to signal the efficiency of OXPHOS function thus enabling females to select mates with nuclear genes that are compatible with maternal mitochondrial genes in the formation of OXPHOS complexes. Species-typical pattern of ornamentation is proposed to serve as a marker of mitochondrial type ensuring that females assess prospective mates with a shared mitochondrial background. The mitonuclear compatibility hypothesis predicts that the production of ornaments will be closely linked to OXPHOS pathways, and that sexual selection for compatible mates will be strongest when genes for nuclear components of OXPHOS complexes are Z-linked. The implications of this hypothesis are that sexual selection may serve as a driver for the evolution of more efficient cellular respiration.


2021 ◽  
Author(s):  
Julia Maria Torres-Velarde ◽  
Sree Rohit Raj Kolora ◽  
Jane I. Khudyakov ◽  
Daniel E. Crocker ◽  
Peter H. Sudmant ◽  
...  

AbstractElephant seals experience natural periods of prolonged food deprivation while breeding, molting, and undergoing postnatal development. Prolonged food deprivation in elephant seals increases circulating glucocorticoids without inducing muscle atrophy, but the cellular mechanisms that allow elephant seals to cope with such conditions remain elusive. We generated a cellular model and conducted transcriptomic, metabolic, and morphological analyses to study how seal cells adapt to sustained glucocorticoid exposure. Seal muscle progenitor cells differentiate into contractile myotubes with a distinctive morphology, gene expression profile, and metabolic phenotype. Exposure to dexamethasone at three ascending concentrations for 48h modulated the expression of 6 clusters of genes related to structural constituents of muscle and pathways associated with energy metabolism and cell survival. Knockdown of the glucocorticoid receptor (GR) and downstream expression analyses corroborated that GR mediates the observed effects. Dexamethasone also decreased cellular respiration, shifted the metabolic phenotype towards glycolysis, and induced mitochondrial fission and dissociation of mitochondria-ER interactions without decreasing cell viability. Knockdown of DDIT4, a GR target involved in the dissociation of mitochondria-ER membranes, recovered respiration and modulated antioxidant gene expression. These results show that adaptation to sustained glucocorticoid exposure in elephant seal myotubes involves a metabolic shift toward glycolysis, which is supported by alterations in mitochondrial morphology and a reduction in mitochondria-ER interactions, resulting in decreased respiration without compromising cell survival.


Cells ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 2620
Author(s):  
Alba Timón-Gómez ◽  
Emma L. Bartley-Dier ◽  
Flavia Fontanesi ◽  
Antoni Barrientos

The biogenesis and function of eukaryotic cytochrome c oxidase or mitochondrial respiratory chain complex IV (CIV) undergo several levels of regulation to adapt to changing environmental conditions. Adaptation to hypoxia and oxidative stress involves CIV subunit isoform switch, changes in phosphorylation status, and modulation of CIV assembly and enzymatic activity by interacting factors. The latter include the Hypoxia Inducible Gene Domain (HIGD) family yeast respiratory supercomplex factors 1 and 2 (Rcf1 and Rcf2) and two mammalian homologs of Rcf1, the proteins HIGD1A and HIGD2A. Whereas Rcf1 and Rcf2 are expressed constitutively, expression of HIGD1A and HIGD2A is induced under stress conditions, such as hypoxia and/or low glucose levels. In both systems, the HIGD proteins localize in the mitochondrial inner membrane and play a role in the biogenesis of CIV as a free unit or as part as respiratory supercomplexes. Notably, they remain bound to assembled CIV and, by modulating its activity, regulate cellular respiration. Here, we will describe the current knowledge regarding the specific and overlapping roles of the several HIGD proteins in physiological and stress conditions.


2018 ◽  
Author(s):  
Pablo Hernansanz-Agustín ◽  
Carmen Choya-Foces ◽  
Susana Carregal-Romero ◽  
Elena Ramos ◽  
Tamara Oliva ◽  
...  

All metazoans depend on O2 delivery and consumption by the mitochondrial oxidative phosphorylation (OXPHOS) system to produce energy. A decrease in O2 availability (hypoxia) leads to profound metabolic rewiring. In addition, OXPHOS uses O2 to produce reactive oxygen species (ROS) that can drive cell adaptations through redox signalling, but also trigger cell damage1–4, and both phenomena occur in hypoxia4–8. However, the precise mechanism by which acute hypoxia triggers mitochondrial ROS production is still unknown. Ca2+ is one of the best known examples of an ion acting as a second messenger9, yet the role ascribed to Na+ is to serve as a mere mediator of membrane potential and collaborating in ion transport10. Here we show that Na+ acts as a second messenger regulating OXPHOS function and ROS production by modulating fluidity of the inner mitochondrial membrane (IMM). We found that a conformational shift in mitochondrial complex I during acute hypoxia11 drives the acidification of the matrix and solubilization of calcium phosphate precipitates. The concomitant increase in matrix free-Ca2+ activates the mitochondrial Na+/Ca2+ exchanger (NCLX), which imports Na+ into the matrix. Na+ interacts with phospholipids reducing IMM fluidity and mobility of free ubiquinone between complex II and complex III, but not inside supercomplexes. As a consequence, superoxide is produced at complex III, generating a redox signal. Inhibition of mitochondrial Na+ import through NCLX is sufficient to block this pathway, preventing adaptation to hypoxia. These results reveal that Na+ import into the mitochondrial matrix controls OXPHOS function and redox signalling through an unexpected interaction with phospholipids, with profound consequences in cellular metabolism.


1997 ◽  
Vol 272 (1) ◽  
pp. R1-R5 ◽  
Author(s):  
L. G. Branco

The present study was designed to test the hypothesis that hypoglycemia induces hypothermia in ectotherms and to elucidate the mechanisms responsible for behavioral hypothermia. Behavioral hypothermia is a stress response that occurs in organisms ranging from protozoans to mammals, but very little is known about the cellular mechanisms involved. Toads equipped with a temperature probe were tested in a thermal gradient (10-40 degrees C). Insulin was used to reduce plasma glucose levels, and an inhibitor of glucose utilization, 2-deoxy-D-glucose (2-DG), was used to cause intracellular glucopenia. Insulin injections into the dorsal lymph sac caused significant reductions of both plasma glucose levels and body temperature. To determine if the response was mediated by extracellular glucose receptors or an intracellular mechanism. 2-DG was also injected into the lymph sac. 2-DG caused a similar drop in body temperature and a marked increase in plasma glucose. To assess the role of central thermoregulatory mechanisms, a smaller dose of 2-DG was injected into the fourth cerebral ventricle or the lymph sac. Intracerebroventricular injection of 2-DG caused a decrease in body temperature despite elevated circulating glucose levels, whereas injection into the lymph sac caused no significant change. The data indicate that exclusion of glucose from central rather than peripheral sites plays a major role in the hypoglycemia-induced behavioral hypothermia and that intracellular mechanisms rather than extracellular glucose receptors are involved in this response. Hypothermia may be a beneficial response to hypoglycemia in toads because it dampens cellular oxidative demands during glucose deprivation.


1991 ◽  
Vol 261 (4) ◽  
pp. 30-38
Author(s):  
V. A. Saks ◽  
Y. O. Belikova ◽  
A. V. Kuznetsov ◽  
Z. A. Khuchua ◽  
T. H. Branishte ◽  
...  

Chemically skinned (by treatment with saponin, 40 μg/ml) isolated cardiomyocytes were used to study the intracellular diffusion of ADP and creatine (Cr). Stimulation of respiration was studied in these cardiomyocytes without intact sarcolemma and in isolated heart mitochondrial by addition of ADP and Cr in the presence of 0.2 mM ATP (via mitochondrial creatine kinase reaction: Cr + MgATP = MgADP + PCr). The Michaelis constant (Km) for Cr was similar in both cases, 5.67 ± 0.11 (SD) mM in skinned myocytes and 6.9 ± 0.2 mM in mitochondria, showing that there is no significant restriction to the diffusion of this substrate. However, the apparent Km for external ADP increased from 17.6 ± 1.0 μM for mitochondria to 250 ± 38 μM for skinned cardiomyocytes, showing decreased diffusivity of ADP as a result of binding to cellular structures. In the presence of 25 mM Cr, the Km for ADP for myocytes decreased to 35.6 ± 5.6 μM due to the coupling of the creatine kinase and oxidative phosphorylation reactions. Provision of substrate for the creatine kinase reaction amplified the weak ADP signal in the regulation of respiration. The activity of the mitochondrial creatine kinase was decreased by a factor of two in cardiomyopathic hamsters and human hearts and was associated with a twofold decrease in creatine-stimulated respiration. These data show a potentially key role of mitochondrial creatine kinase in the regulation of cellular respiration and the possible importance of changes in its activity for the functional disturbances of the cardiomyopathic heart. cellular respiration; creatine kinase; oxidative phosphorylation


1976 ◽  
Vol 54 (11) ◽  
pp. 1912-1917 ◽  
Author(s):  
T. Hamor ◽  
E. T. Garside

Embryos of Atlantic salmon. Salmo salur L., were incubated from fertilization to completion of hatching at 5 and 10 °C, at 20, 50, and 100% air-saturation, and at several rates of water exchange from 0.2 to 15 ml/s. Developmental rate to various structural stages, expressed as the reciprocal of time units, and hatching time were significantly controlled by temperature, oxygen supply, and rate of water exchange. Survival during embryogenesis and during the hatching period were limited primarily by oxygen supply and secondarily by water exchange, both having highly significant effects. The effect of temperature ranked third but was also statistically significant. Lower temperature reduced the rate of development and enhanced survival through hutching. Developmental rate and survival increased directly with increasing concentration of dissolved oxygen and with increasing rate of water exchange.


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