Superresistance against hypoxia after preliminary adaptation to repeated stress

1994 ◽  
Vol 76 (5) ◽  
pp. 1856-1861 ◽  
Author(s):  
F. Meerson ◽  
V. Pozharov ◽  
T. Minyailenko

The study investigated the influence of adaptation to stress on resistance to hypoxia. After rats were adaptated to moderate restraint stress, they were anesthetized and exposed to 6% O2. Adaptation increased tidal volume by 2.6-fold, lung and alveolar ventilation by 1.6- and 1.8-fold, respectively, and O2 consumption by 1.6-fold; limited lactate accumulation in the liver by 2-fold, in the heart by 34%, in the lung by 36%, and in the blood by 36%; and elevated pH. At the same time, preliminary adaptation to stress inhibited the hypoxic activation of lipolysis and peroxidation in all tissues. The concentration of lipid peroxides decreased after adaptation by 1.3- to 1.5-fold in different organs, whereas the content of free fatty acids diminished by 1.7- to 2.3-fold. Finally, after adaptation, mortality decreased under severe hypoxia by 6.5-fold. Thus, the data suggest that the cross-protective effect of adaptation was achieved by the economization of respiration and circulation, by marked augmentation in the ability of tissue to utilize blood O2, and by the limitation of processes that are able to damage tissue membranes, namely, acidosis, lipolysis, and lipid peroxidation.

2017 ◽  
Vol 216 (12) ◽  
pp. 4287-4297 ◽  
Author(s):  
Caitlin W. Brown ◽  
John J. Amante ◽  
Hira Lal Goel ◽  
Arthur M. Mercurio

Increases in lipid peroxidation can cause ferroptosis, a form of cell death triggered by inhibition of glutathione peroxidase 4 (GPX4), which catalyzes the reduction of lipid peroxides and is a target of ferroptosis inducers, such as erastin. The α6β4 integrin protects adherent epithelial and carcinoma cells from ferroptosis induced by erastin. In addition, extracellular matrix (ECM) detachment is a physiologic trigger of ferroptosis, which is evaded by α6β4. The mechanism that enables α6β4 to evade ferroptosis involves its ability to protect changes in membrane lipids that are proferroptotic. Specifically, α6β4-mediated activation of Src and STAT3 suppresses expression of ACSL4, an enzyme that enriches membranes with long polyunsaturated fatty acids and is required for ferroptosis. Adherent cells lacking α6β4 require an inducer, such as erastin, to undergo ferroptosis because they sustain GPX4 expression, despite their increase in ACSL4. In contrast, ECM detachment of cells lacking α6β4 is sufficient to trigger ferroptosis because GPX4 is suppressed. This causal link between α6β4 and ferroptosis has implications for cancer biology and therapy.


1968 ◽  
Vol 106 (2) ◽  
pp. 515-522 ◽  
Author(s):  
B. O. Christophersen

1. GSH efficiently inhibited the ascorbate-stimulated lipid peroxidation of the unsaturated fatty acids in the fresh microsomal fraction and mitochondria of rat liver, whereas the peroxidation in heat-denatured particles was little inhibited. 2. Cysteamine and diethyldithiocarbamate inhibited the peroxidation in both fresh and boiled particles. Thioglycollate and 2-mercaptoethanol had no inhibiting effect. Cysteine and homocysteine both stimulated the lipid peroxidation even in the absence of ascorbate. 3. The added GSH disappeared at nearly the same rate in the presence of fresh and of boiled particles to which ascorbate had been added, although considerably more malonaldehyde was formed in the boiled particles. In the absence of ascorbate little GSH disappeared. 4. It is suggested that the protective effect of GSH against lipid peroxidation depends on the preservation of heat-labile structures in the microsomal fraction and mitochondria.


2019 ◽  
Vol 09 ◽  
Author(s):  
Vitaly A. Bekenev ◽  
Anatoly A. Arishin ◽  
Sergei N. Mager ◽  
Izolda V. Bolshakova ◽  
Natalia L. Tretyakova ◽  
...  

Background: Studies were carried out on two breeds of pigs - Pietrain (P), and Kemerovo (K), contrasting in composition of carcasses, and their hybrids. Objective: The purpose of this work was to establish the characteristics of the composition of lipids of intramuscular fat (IMF), back fat and serum, organoleptic qualities in animals of these breeds. Methods: Animals of 10 individuals in each group were fed on a standard feed and slaughtered with a live weight of 95-100 kg. The quality of carcasses, the biochemical characteristics of blood, the composition of fatty acids and cholesterol in meat and fat, and blood lipid peroxidation were determined. Results: Thickness on the back fat (BF) at the level of 6-7 thoracic vertebrae with a live weight of 100 kg was 35.8 ± 1.65 mm in pigs of breed K, in hybrids - 27.6 ± 1.06, and in breed P - 19, 6 ± 1.43 mm. IMF in pigs of breed K was almost 4.5 times greater than that of breed P. IMF K breed contained 2 times less cholesterol than in P (2.34 vs. 4.68%). In the IMF, K was 2 times less polyunsaturated fatty acids (PUFA), than P, 7.82 and 15.22%, linoleic acid, 6.74% and 12.42% respectively (p <0.005).The organoleptic properties of meat and salted back fat were significantly higher in breed K (P = 0.05). Conclusion: The data obtained allow us to establish priorities in the use of products of specific breeds of pigs, depending on medical requirements.


1981 ◽  
Vol 22 (5) ◽  
pp. 763-769
Author(s):  
V C Gavino ◽  
J S Miller ◽  
S O Ikharebha ◽  
G E Milo ◽  
D G Cornwell

Molecules ◽  
2021 ◽  
Vol 26 (11) ◽  
pp. 3089
Author(s):  
Lukas M. Müller-Wirtz ◽  
Daniel Kiefer ◽  
Sven Ruffing ◽  
Timo Brausch ◽  
Tobias Hüppe ◽  
...  

Exhaled aliphatic aldehydes were proposed as non-invasive biomarkers to detect increased lipid peroxidation in various diseases. As a prelude to clinical application of the multicapillary column–ion mobility spectrometry for the evaluation of aldehyde exhalation, we, therefore: (1) identified the most abundant volatile aliphatic aldehydes originating from in vitro oxidation of various polyunsaturated fatty acids; (2) evaluated emittance of aldehydes from plastic parts of the breathing circuit; (3) conducted a pilot study for in vivo quantification of exhaled aldehydes in mechanically ventilated patients. Pentanal, hexanal, heptanal, and nonanal were quantifiable in the headspace of oxidizing polyunsaturated fatty acids, with pentanal and hexanal predominating. Plastic parts of the breathing circuit emitted hexanal, octanal, nonanal, and decanal, whereby nonanal and decanal were ubiquitous and pentanal or heptanal not being detected. Only pentanal was quantifiable in breath of mechanically ventilated surgical patients with a mean exhaled concentration of 13 ± 5 ppb. An explorative analysis suggested that pentanal exhalation is associated with mechanical power—a measure for the invasiveness of mechanical ventilation. In conclusion, exhaled pentanal is a promising non-invasive biomarker for lipid peroxidation inducing pathologies, and should be evaluated in future clinical studies, particularly for detection of lung injury.


2000 ◽  
Vol 352 (1) ◽  
pp. 27-36 ◽  
Author(s):  
Lixia TANG ◽  
Yong ZHANG ◽  
Zhongming QIAN ◽  
Xun SHEN

The mechanism of Fe2+-initiated lipid peroxidation in a liposomal system was studied. It was found that a second addition of ferrous ions within the latent period lengthened the time lag before lipid peroxidation started. The apparent time lag depended on the total dose of Fe2+ whenever the second dose of Fe2+ was added, which indicates that Fe2+ has a dual function: to initiate lipid peroxidation on one hand and suppress the species responsible for the initiation of the peroxidation on the other. When the pre-existing lipid peroxides (LOOH) were removed by incorporating triphenylphosphine into liposomes, Fe2+ could no longer initiate lipid peroxidation and the acceleration of Fe2+ oxidation by the liposomes disappeared. However, when extra LOOH were introduced into liposomes, both enhancement of the lipid peroxidation and shortening of the latent period were observed. When the scavenger of lipid peroxyl radicals (LOOP), N,N´-diphenyl-p-phenylene-diamine, was incorporated into liposomes, neither initiation of the lipid peroxidation nor acceleration of the Fe2+ oxidation could be detected. The results may suggest that both the pre-existing LOOH and LOOP are necessary for the initiation of lipid peroxidation. The latter comes initially from the decomposition of the pre-existing LOOH by Fe2+ and can be scavenged by its reaction with Fe2+. Only when Fe2+ is oxidized to such a degree that LOOP is no longer effectively suppressed does lipid peroxidation start. It seems that by taking the reactions of Fe2+ with LOOH and LOOP into account, the basic chemistry in lipid peroxidation can explain fairly well the controversial phenomena observed in Fe2+-initiated lipid peroxidation, such as the existence of a latent period, the critical ratio of Fe2+ to lipid and the required oxidation of Fe2+.


1964 ◽  
Vol 19 (2) ◽  
pp. 360-362 ◽  
Author(s):  
Leonard I. Kleinman ◽  
Edward P. Radford

Ventilation standards for small mammals have been prepared on the basis of the relationship between alveolar ventilation and metabolism. On the assumptions of an average respiratory quotient of 0.85 and physiological dead space directly proportional to tidal volume, the relationship between tidal volume, breathing frequency, and body weight has been derived. The standards are presented in a graphic form and as a slide rule. animal ventilation; artificial respiration; tidal volume, breathing frequency and body weight relationship Submitted on August 15, 1963


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