Liver and heart mitochondria in rats submitted to chronic hypobaric hypoxia

Costa, Lidia E.; Boveris, Alberto; Koch, Osvaldo R.; Taquini, Alberto C.

doi:10.1152/ajpcell.1988.255.1.c123

Cited by 88 publications

(50 citation statements)

References 9 publications

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“…The mechanisms behind this reduction in Complex V activity are not known, but in preconditioning models it has been proposed that Complex V is directly inhibited either through the binding of the inhibitory factor (Vander Heide et al, 1996) or through S-nitrosylation (Sun et al, 2007). These results are in contrast to the results observed in hypobaric hypoxia-exposed rats, where mitochondrial properties were not changed, but mitochondrial density increased (Costa et al, 1988); however, the present study used complete anoxia versus hypoxia, therefore it is not surprising that the results differ. Whatever the mechanism is for a reduction in Complex V activity, its beneficial effects on the anoxic cell are clear.…”

Section: Complex V Activity Is Reduced By Long-term Anoxia Exposure Imentioning

confidence: 81%

Beating oxygen: chronic anoxia exposure reduces mitochondrial F1FO-ATPase activity in turtle (Trachemys scripta) heart

Galli

Lau

Richards

2013

Journal of Experimental Biology

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SUMMARYThe freshwater turtle Trachemys scripta can survive in the complete absence of O 2 (anoxia) for periods lasting several months. In mammals, anoxia leads to mitochondrial dysfunction, which culminates in cellular necrosis and apoptosis. Despite the obvious clinical benefits of understanding anoxia tolerance, little is known about the effects of chronic oxygen deprivation on the function of turtle mitochondria. In this study, we compared mitochondrial function in hearts of T. scripta exposed to either normoxia or 2weeks of complete anoxia at 5°C and during simulated acute anoxia/reoxygenation. Mitochondrial respiration, electron transport chain activities, enzyme activities, proton conductance and membrane potential were measured in permeabilised cardiac fibres and isolated mitochondria. Two weeks of anoxia exposure at 5°C resulted in an increase in lactate, and decreases in ATP, glycogen, pH and phosphocreatine in the heart. Mitochondrial proton conductance and membrane potential were similar between experimental groups, while aerobic capacity was dramatically reduced. The reduced aerobic capacity was the result of a severe downregulation of the F 1 F O -ATPase (Complex V), which we assessed as a decrease in enzyme activity. Furthermore, in stark contrast to mammalian paradigms, isolated turtle heart mitochondria endured 20min of anoxia followed by reoxygenation without any impact on subsequent ADP-stimulated O 2 consumption (State III respiration) or State IV respiration. Results from this study demonstrate that turtle mitochondria remodel in response to chronic anoxia exposure and a reduction in Complex V activity is a fundamental component of mitochondrial and cellular anoxia survival.

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Section: Complex V Activity Is Reduced By Long-term Anoxia Exposure Imentioning

confidence: 81%

Beating oxygen: chronic anoxia exposure reduces mitochondrial F1FO-ATPase activity in turtle (Trachemys scripta) heart

Galli

Lau

Richards

2013

Journal of Experimental Biology

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“…For the first category of studies, research has shown that there is either no change or a decrease in aerobic indicators of the heart and liver (Kayar and Banchero, 1987;Costa et al, 1988;Lewis et al, 1999;Kennedy et al, 2001). For studies of the second type, CS (Hochachka et al, 1982) and LDH activities of the heart were increased (Vergnes, 1971;Penney, 1974;Barrie and Harris, 1976;Ohtsuka and Gilbert, 1995).…”

Section: Discussionmentioning

confidence: 99%

“…When scaled for RMR, seal liver VV(mt) was even greater (6.6× and 2.3×) than in rat and dog liver, respectively. As with the seal heart, we hypothesize that this increase in VV(mt) decreases the intracellular distance for oxygen diffusion and effectively increases diffusive conductance to maintain aerobic metabolism and organ function during periods of hypoxia while diving (Costa et al, 1988). Based on the hepatic clearance of indocyanine green (ICG) from the blood during voluntary dives, Davis et al (1983) showed that hepatic function was maintained in subadult Weddell seals during voluntary dives, even though hepatic arterial and portal blood flow were reduced as a result of the dive response.…”

Section: Interspecies Comparison Of the Livermentioning

confidence: 99%

Adaptations to diving hypoxia in the heart, kidneys and splanchnic organs of harbor seals (Phoca vitulina)

Fuson

Cowan

Kanatous

et al. 2003

Journal of Experimental Biology

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Based on forced submergence studies conducted from the 1940s to the early 1970s, it was believed that marine mammals relied primarily on anaerobic metabolism during diving (Elsner and Gooden, 1983;Butler and Jones, 1997). After a forced submergence, there was a net accumulation of lactic acid in the plasma, indicating that anaerobic glycolysis had provided ATP as the organs and tissues became hypoxic. Therefore, it was assumed that marine mammals might have enhanced enzyme activities for anaerobic glycolysis. However, showed that, on average, marine mammals do not posses significantly elevated anaerobic enzyme activities when compared with terrestrial mammals. These results were difficult to reconcile with the apparent reliance of marine mammals on anaerobic metabolism during forced submergence. In the early 1980s, Kooyman et al. (1981) established the concept of the aerobic dive limit (ADL) by measuring the post-dive blood lactate concentration in Weddell seals (Leptonycotes weddellii) following voluntary dives from an isolated ice hole in Antarctica. The ADL is defined as the longest dive that a marine mammal can make while relying principally on oxygen stored in the lungs, blood and muscles to maintain aerobic metabolism. They found that dives shorter in duration than the ADL showed no post-dive increase in blood lactic acid, indicating that metabolism had remained aerobic. By attaching time-depth recorders to free-ranging Weddell seals, they showed that most voluntary dives were within the ADL. Similar results have been dehydrogenase (HOAD) activities in their swimming muscles to maintain an aerobic, fat-based metabolism during diving. The goal of this study was to determine whether the heart, kidneys and splanchnic organs have an elevated VV(mt) and CS and HOAD activities as parallel adaptations for sustaining aerobic metabolism and normal function during hypoxia in harbor seals (Phoca vitulina).Samples of heart, liver, kidney, stomach and small intestine were taken from 10 freshly killed harbor seals and fixed in glutaraldehyde for transmission electron microscopy or frozen in liquid nitrogen for enzymatic analysis. Samples from dogs and rats were used for comparison. Within the harbor seal, the liver and stomach had the highest VV(mt). The liver also had the highest CS activity. The kidneys and heart had the highest HOAD activities, and the liver and heart had the highest lactate dehydrogenase (LDH) activities. Mitochondrial volume densities scaled to tissue-specific resting metabolic rate [VV(mt)/RMR] in the heart, liver, kidneys, stomach and small intestine of harbor seals were elevated (range 1.2-6.6×) when compared with those in the dog and/or rat. In addition, HOAD activity scaled to tissue-specific RMR in the heart and liver of harbor seals was elevated compared with that in the dog and rat (3.2× and 6.2× in the heart and 8.5× and 5.5× in the liver, respectively). These data suggest that organs such as the liver, kidneys and stomach possess a heightened ability for aerobic, fatbased metabolism dur...

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“…As shown in in vitro and in vivo experiments, hypobaric pressure increases cellular oxidative stress and to promote hypoxia suggests that especially impairs function in mitochondria (Costa et al, 1988). As a result of this lipids, proteins and DNA damaged and irreversible damage occurs for cells frequently (Magalhaes et al, 2005).…”

Section: Discussionmentioning

confidence: 98%

Effects of Hypobaric Conditions on Apoptosis Signalling Pathways in HeLa Cells

Arıcan

Khalilia²,

Serbes³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Nowadays increasing effectiveness in cancer therapy and investigation of formation of new strategies that enhance antiproliferative activity against target organs has become a subject of interest. Although the molecular mechanisms of apoptosis can not be fully explained, it is known that cell suicide program existing in their memory genetically is activated by pathophysiological conditions and events such as oxidative stress. Low pressure (hypobaric) conditions that create hypoxia promote apoptosis by inhibiting cell cycling. In this study, determination of the effects of fractional hypobaric applications at different times on HeLa cells at cellular and molecular levels were targeted. Experiments were carried out under hypobaric conditions (35.2 kPa) in a specially designed hypobaric cabin including 2% O 2 and 98% N. Application of fractional hypobaric conditions was repeated two times for 3 hours with an interval of 24 hours. At the end of the implementation period cells were allowed to incubate for 24 hours for activation of repair mechanisms. Cell kinetic parameters such as growth rate (MTT) and apoptotic index were used in determination of the effect of hypobaric conditions on HeLa cells. Also in our study expression levels of the Bcl-2 gene family that have regulatory roles in apoptosis were determined by the RT-PCR technique to evaluate molecular mechanisms. The results showed that antiproliferative effect of hypobaric conditions on HeLa cells started three hours from the time of application and increased depending on the period of exposure. While there was a significant decrease in growth rate values, there was a significant increase in apoptotic index values (p<0.01). Also molecular studies showed that hypobaric conditions caused a significant increase in expression level of proapoptotic gene Bax and significant decrease in antiapoptotic Bfl-1. Consequently fractional application of hypobaric conditions on HeLa cell cultures increased both antiproliferative and apoptotic effects and these effects were triggered by the Bax gene.

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Liver and heart mitochondria in rats submitted to chronic hypobaric hypoxia

Cited by 88 publications

References 9 publications

Beating oxygen: chronic anoxia exposure reduces mitochondrial F1FO-ATPase activity in turtle (Trachemys scripta) heart

Beating oxygen: chronic anoxia exposure reduces mitochondrial F1FO-ATPase activity in turtle (Trachemys scripta) heart

Adaptations to diving hypoxia in the heart, kidneys and splanchnic organs of harbor seals (Phoca vitulina)

Effects of Hypobaric Conditions on Apoptosis Signalling Pathways in HeLa Cells

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