scholarly journals Reduced lactate dehydrogenase activity in the heart and suppressed sex hormone levels are associated with female-biased mortality during thermal stress in Pacific salmon

2020 ◽  
Vol 223 (14) ◽  
pp. jeb214841
Author(s):  
A. G. Little ◽  
E. Hardison ◽  
K. Kraskura ◽  
T. Dressler ◽  
T. S. Prystay ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Thermal Stress ◽  
Lactate Dehydrogenase ◽  
Citrate Synthase ◽  
Coho Salmon ◽  
Pacific Salmon ◽  
Field Studies ◽  
Liver Size ◽  
Lactate Dehydrogenase Activity ◽  
Gonad Size

ABSTRACTFemale-biased mortality has been repeatedly reported in Pacific salmon during their upriver migration in both field studies and laboratory holding experiments, especially in the presence of multiple environmental stressors, including thermal stress. Here, we used coho salmon (Oncorhynchus kisutch) to test whether females exposed to elevated water temperatures (18°C) (i) suppress circulating sex hormones (testosterone, 11-ketotestosterone and estradiol), owing to elevated cortisol levels, (ii) have higher activities of enzymes supporting anaerobic metabolism (e.g. lactate dehydrogenase, LDH), (iii) have lower activities of enzymes driving oxidative metabolism (e.g. citrate synthase, CS) in skeletal and cardiac muscle, and (iv) have more oxidative stress damage and reduced capacity for antioxidant defense [lower catalase (CAT) activity]. We found no evidence that a higher susceptibility to oxidative stress contributes to female-biased mortality at warm temperatures. We did, however, find that females had significantly lower cardiac LDH and that 18°C significantly reduced plasma levels of testosterone and estradiol, especially in females. We also found that relative gonad size was significantly lower in the 18°C treatment regardless of sex, whereas relative liver size was significantly lower in females held at 18°C. Further, relative spleen size was significantly elevated in the 18°C treatments across both sexes, with larger warm-induced increases in females. Our results suggest that males may better tolerate bouts of cardiac hypoxia at high temperature, and that thermal stress may also disrupt testosterone- and estradiol-mediated protein catabolism, and the immune response (larger spleens), in migratory female salmon.

scholarly journals Simulated maternal stress reduces offspring aerobic swimming performance in Pacific salmon

2019 ◽  
Vol 7 (1) ◽  
Author(s):  
Amanda I Banet ◽  
Stephen J Healy ◽  
Erika J Eliason ◽  
Edward A Roualdes ◽  
David A Patterson ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Citrate Synthase ◽  
Maternal Stress ◽  
Pacific Salmon ◽  
Swimming Performance ◽  
Haemoglobin Concentration ◽  
Aerobic Performance ◽  
Aerobic Scope ◽  
Lactate Dehydrogenase Activity ◽  
Treatment Groups

Abstract Pacific salmon routinely encounter stressors during their upriver spawning migration, which have the potential to influence offspring through hormonally-mediated maternal effects. To disentangle genetic vs. hormonal effects on offspring swimming performance, we collected gametes from three species of Pacific salmon (Chinook, pink and sockeye) at the end of migration and exposed a subset of eggs from each female to cortisol baths to simulate high levels of maternal stress. Fertilised eggs were reared to fry and put through a series of aerobic swim trials. Results show that exposure to cortisol early in development reduces maximum oxygen consumption while swimming, and decreases aerobic scope in all three species. Resting oxygen consumption did not differ between cortisol and control treatment groups. We also examined several metrics that could influence aerobic performance, and found no differences between treatment groups in haematocrit%, haemoglobin concentration, heart mass, citrate synthase activity or lactate dehydrogenase activity. Though it was not the focus of this study, an interesting discovery was that pink salmon had a higher MO2max and aerobic scope relative to the other species, which was supported by a greater haematocrit, haemoglobin, a larger heart and higher CS activity. Some management and conservation practices for Pacific salmon focus efforts primarily on facilitating adult spawning. However, if deleterious effects of maternal stress acquired prior to spawning persist into the next generation, consideration will need to be given to sub-lethal effects that could be imparted onto offspring from maternal stress.

Changes in the metabolic profile of equine muscle from birth through 1 yr of age

1990 ◽  
Vol 68 (4) ◽  
pp. 1399-1404 ◽  
Author(s):  
K. H. Kline ◽  
P. J. Bechtel
Keyword(s):  
Lactate Dehydrogenase ◽  
Citrate Synthase ◽  
Fiber Type ◽  
Gluteus Medius ◽  
Fiber Types ◽  
Superficial Fascia ◽  
Muscle Enzyme ◽  
Lactate Dehydrogenase Activity ◽  
Hydroxyacyl Coa Dehydrogenase ◽  
Fast Twitch

The purpose of this study was to investigate metabolic changes in equine muscle from birth to 1 yr of age. Duplicate biopsies from the middle portion of the gluteus medius were obtained from a depth of 2 cm beneath the superficial fascia at 1 day, 7 days, 1 mo, 3 mo, 6 mo, and 1 yr of age in 11 quarter horses and at 1 day, 3 mo, 6 mo, and 1 yr of age in 5 Standardbreds. Muscle enzyme activities determined were citrate synthase, 3-hydroxyacyl-CoA dehydrogenase, phosphorylase, and lactate dehydrogenase. Percent fast-twitch, fast-twitch high oxidative, and slow-twitch oxidative fiber types were determined using succinate dehydrogenase and myosin adenosinetriphosphatase (pH 9.4) histochemical stains. Histochemically determined muscle fiber-type percents did not change dramatically with increasing age. However, lactate dehydrogenase activity increased threefold in quarter horses and twofold in Standardbreds, and phosphorylase activity increased sixfold in quarter horses and sevenfold in Standardbreds from 1 day to 6 mo of age. Citrate synthase and 3-hydroxyacyl-CoA dehydrogenase activities decreased during the first 3 mo of age in quarter horses.

scholarly journals The study of cardiomyocytes mitochondrial dysfunction in hyperhomocysteinemia and nitric oxyde deficiency

2015 ◽  
Vol 96 (5) ◽  
pp. 837-843
Author(s):  
D V Medvedev ◽  
V I Zvyagina
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Superoxide Dismutase ◽  
Lactate Dehydrogenase ◽  
Atpase Activity ◽  
Mitochondrial Dysfunction ◽  
Dehydrogenase Activity ◽  
Tween 80 ◽  
Lactate Dehydrogenase Activity ◽  
Nitric Oxide Deficiency

Aim. To study the influence of nitric oxide metabolism disturbance on the development of mitochondrial dysfunction in case of hyperhomocysteinemia. Methods. The research was conducted on 32 Wistar male rats. Hyperhomocysteinemia was simulated by intragastric injection of methionine suspension prepared using starch and Tween-80 with addition of this amino acid into the drinking water. The nitric oxide deficiency was induced by intraperitoneal injection of L-Nω-nitroarginine methyl ester (L-NAME) solution. Results. Hyperhomocysteinemia is accompanied by dysfunction of cardiac cells mitochondria, manifesting in growth of cytoplasmic lactate level and development of oxidative stress with increased mitochondrial proteins carbonylation. Oxidative stress is largely compensated by the activation of the antioxidant defense system (including superoxide dismutase), as evidenced by a slight decrease of succinate dehydrogenase and H+-ATPase activity, the absence of statistically significant changes of cytoplasmic lactate dehydrogenase activity. Tween-80 showed antioxidant properties, reducing the content of protein carbonyl derivatives and superoxide dismutase activity. Nitric oxide deficiency caused by the L-NAME injection was accompanied by an inhibition of aerobic oxidation processes in cardiomyocytes mitochondria, which was proved by a significant decrease in succinate dehydrogenase activity as well as slight reduction of lactate dehydrogenase activity and lactate accumulation in the cytoplasm, and an oxidative phosphorylation reduction which manifested with a decrease of H+-ATPase activity. One reason for these changes is increased carbonylation of proteins due to high production of reactive oxygen species, which is not sufficiently compensated by increased activity of superoxide dismutase. Conclusion. Since hyperhomocysteinemia is associated with reduced concentrations of nitric oxide metabolites in cardiomyocytes mitochondria, and changes in these organelles after the administering of methionine have some similarities with those after injection of L-NAME, it can be argued that nitric oxide deficiency plays an important role in the pathogenesis of mitochondrial dysfunction of cardiomyocytes in case of hyperhomocysteinemia.

scholarly journals 145 President Oral Presentation Pick: Prenatal stress increases skeletal muscle mitochondrial volume density and function in yearling Brahman calves

2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 120-121
Author(s):  
Chloey P Guy ◽  
Catherine L Wellman ◽  
David G Riley ◽  
Charles R Long ◽  
Ron D Randel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Creatine Kinase ◽  
Muscle Damage ◽  
Prenatal Stress ◽  
Citrate Synthase ◽  
Volume Density ◽  
Assembly Factor ◽  
Mitochondrial Volume ◽  
Mitochondrial Volume Density ◽  
And Function

Abstract We previously determined that prenatal stress (PNS) differentially affected methylation of DNA from leukocytes of 28-d-old calves. Specifically, COX14 (cytochrome c oxidase (COX) assembly factor) and CKMT1B (mitochondrial creatine kinase U-type) were hypomethylated and COA5 (COX assembly factor 5), COX5A (COX subunit 5A), NRF1 (nuclear respiratory factor 1), and GSST1 (glutathione S-transferase theta-1) were hypermethylated in PNS compared to non-PNS calves (P ≤ 0.05). Our current objective was to test the hypothesis that PNS exhibit impaired mitochondrial function and greater oxidative stress than non-PNS calves. Blood and longissimus dorsi muscle samples were collected from yearling Brahman calves whose mothers were stressed by 2 h transportation at 60, 80, 100, 120, and 140 days of gestation (PNS; 8 bulls, 6 heifers) and non-PNS calves (4 bulls, 6 heifers). Serum was evaluated for the stress hormone, cortisol, and muscle damage marker, creatine kinase; muscle was analyzed for mitochondrial volume density and function by citrate synthase (CS) and COX activities, respectively, concentration of malondialdehyde, a lipid peroxidation marker, and activity of the antioxidant, superoxide dismutase (SOD). Data were analyzed using mixed linear models with treatment and sex as fixed effects. Serum cortisol was numerically higher in PNS than non-PNS calves but was not statistically different. Muscle CS and COX activities relative to protein were greater in PNS than non-PNS calves (P ≤ 0.03), but COX relative to CS activity was similar between groups. Activity of COX was greater in bulls than heifers (P = 0.03), but no other measure was affected by sex. All other measures were unaffected by PNS. Prenatal stress did not affect markers of muscle damage and oxidative stress in yearling Brahman calves at rest but mitochondrial volume density and function were greater in PNS calves. Acute stressors induce oxidative stress, so implications of differences in mitochondria in PNS calves following a stressor should be investigated.

Nrf2 mediates the neuroprotective effect of isoflurane preconditioning in cortical neuron injury induced by oxygen-glucose deprivation

2021 ◽  
pp. 096032712198941
Author(s):  
X-S Liu ◽  
X-L Bai ◽  
Z-X Wang ◽  
S-Y Xu ◽  
Y Ma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cortical Neuron ◽  
Cortical Neurons ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Lactate Dehydrogenase Activity ◽  
Primary Mouse ◽  
Ldh Release ◽  
Neuron Injury ◽  
And Oxidative Stress

Objective: To investigate how nuclear factor-E2-related factor 2 (Nrf2) involved in the protective effect of isoflurane (Iso) preconditioning in oxygen glucose deprivation (OGD)-induced cortical neuron injury. Methods: Primary mouse cortical neurons were divided into Control, ML385 (an Nrf2 inhibitor), Iso, Iso + ML385, OGD, ML385 + OGD, Iso + OGD, and Iso + ML385 + OGD groups. Lactate dehydrogenase activity (LDH) release and oxidative stress indexes were quantified. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to detect cell viability, Annexin V-FITC/propidium iodide (PI) staining to measure cell apoptosis, dichloro-dihydro-fluorescein diacetate (DCFH-DA) method to test reactive oxygen species (ROS), and quantitative reverse-transcription polymerase chain reaction (qRT-PCR) and Western blotting to evaluate genes and protein expression. Results: Iso preconditioning reduced LDH release and inhibited cell cytotoxicity in OGD-induced cortical neurons, which was abolished by ML385. Iso preconditioning increased the Nrf2 nuclear translocation in cortical neurons. Meanwhile, Iso decreased the OGD-induced apoptosis with the down-regulations of Bax and Caspase-3 and the up-regulation of Bcl-2, which was reversed by ML385. OGD enhanced the level of ROS and malondialdehyde (MDA) in cortical neurons, but reduced the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), which were aggravated in ML385 + OGD group and mitigated in Iso + OGD group. No observable difference was found between OGD group and Iso + ML385 + OGD group regarding apoptosis-related proteins and oxidative stress-related indexes. Conclusion: Iso preconditioning up-regulated Nrf2 level to play its protective role in OGD-induced mouse cortical neuron injury.

scholarly journals Cardioprotective Effects of PPARβ/δ Activation against Ischemia/Reperfusion Injury in Rat Heart Are Associated with ALDH2 Upregulation, Amelioration of Oxidative Stress and Preservation of Mitochondrial Energy Production

2021 ◽  
Vol 22 (12) ◽  
pp. 6399
Author(s):  
Ioanna Papatheodorou ◽  
Eleftheria Galatou ◽  
Georgios-Dimitrios Panagiotidis ◽  
Táňa Ravingerová ◽  
Antigone Lazou
Keyword(s):  
Oxidative Stress ◽  
Mrna Expression ◽  
Energy Production ◽  
Citrate Synthase ◽  
Ischemia Reperfusion Injury ◽  
Ex Vivo ◽  
Uncoupling Protein ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Isocitrate Dehydrogenase 2

Accumulating evidence support the cardioprotective properties of the nuclear receptor peroxisome proliferator activated receptor β/δ (PPARβ/δ); however, the underlying mechanisms are not yet fully elucidated. The aim of the study was to further investigate the mechanisms underlying PPARβ/δ-mediated cardioprotection in the setting of myocardial ischemia/reperfusion (I/R). For this purpose, rats were treated with PPARβ/δ agonist GW0742 and/or antagonist GSK0660 in vivo and hearts were subjected to ex vivo global ischemia followed by reperfusion. PPARβ/δ activation improved left ventricular developed pressure recovery, reduced infarct size (IS) and incidence of reperfusion-induced ventricular arrhythmias while it also up-regulated superoxide dismutase 2, catalase and uncoupling protein 3 resulting in attenuation of oxidative stress as evidenced by the reduction in 4-hydroxy-2-nonenal protein adducts and protein carbonyl formation. PPARβ/δ activation also increased both mRNA expression and enzymatic activity of aldehyde dehydrogenase 2 (ALDH2); inhibition of ALDH2 abrogated the IS limiting effect of PPARβ/δ activation. Furthermore, upregulation of PGC-1α and isocitrate dehydrogenase 2 mRNA expression, increased citrate synthase activity as well as mitochondrial ATP content indicated improvement in mitochondrial content and energy production. These data provide new mechanistic insight into the cardioprotective properties of PPARβ/δ in I/R pointing to ALDH2 as a direct downstream target and suggesting that PPARβ/δ activation alleviates myocardial I/R injury through coordinated stimulation of the antioxidant defense of the heart and preservation of mitochondrial function.

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