Electrophysiological derangements induced by lipid peroxidation in cardiac tissue

1987 ◽  
Vol 253 (5) ◽  
pp. H1089-H1097 ◽  
Author(s):  
H. Nakaya ◽  
N. Tohse ◽  
M. Kanno
Keyword(s):  
Lipid Peroxidation ◽  
Guinea Pig ◽  
Cardiac Tissue ◽  
Membrane Lipids ◽  
Cumene Hydroperoxide ◽  
Butylated Hydroxytoluene ◽  
Cardiac Tissues ◽  
Conduction Disturbances ◽  
Tert Butyl Hydroperoxide ◽  
Mda Content

Recently it has been postulated that oxygen-derived free radicals may be involved in reperfusion-induced arrhythmias. This study was undertaken to evaluate cellular electrophysiological alterations produced by peroxidation of membrane lipids in isolated cardiac tissues. In retrogradely perfused guinea pig hearts, perfusion of organic hydroperoxides, cumene hydroperoxide (CH), and tert-butyl hydroperoxide (TBH) caused conduction disturbances and arrhythmias, concomitantly with an increase in malondialdehyde (MDA) content of the myocardium. The hydroperoxides decreased the maximum diastolic potential, action potential amplitude, and maximum upstroke velocity of phase 0 in both canine Purkinje fibers and guinea pig papillary muscles. They also induced abnormal automaticity, such as depolarization-induced automaticity, delayed afterdepolarizations, and triggered activity. Mechanical abnormalities including increased resting tension and aftercontractions, presumably resulting from intracellular Ca2+ overload, were produced by the hydroperoxides. Pretreatment with butylated hydroxytoluene, an antioxidant, significantly inhibited the hydroperoxide-induced electrophysiological derangements and MDA accumulation in the myocardium. These results suggest that lipid peroxidation of membranes causes various electrophysiological and mechanical abnormalities and may play a role in the genesis of reperfusion-induced arrhythmias.

Molecular distribution of volume-regulated chloride channels (ClC-2 and ClC-3) in cardiac tissues

2000 ◽  
Vol 279 (5) ◽  
pp. H2225-H2233 ◽  
Author(s):  
Fiona C. Britton ◽  
William J. Hatton ◽  
Charles F. Rossow ◽  
Dayue Duan ◽  
Joseph R. Hume ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Chloride Channels ◽  
Cardiac Tissue ◽  
Immunohistochemical Localization ◽  
Ventricular Wall ◽  
Mrna Levels ◽  
Cardiac Tissues ◽  
Cardiac Electrical Activity ◽  
Actin Expression ◽  
Molecular Expression

The molecular identification of cardiac chloride channels has provided probes to investigate their distribution and abundance in heart. In this study, the molecular expression and distribution of volume-regulated chloride channels ClC-2 and ClC-3 in cardiac tissues were analyzed and quantified. Total RNA was isolated from atria and ventricles of several species (dog, guinea pig, and rat) and subjected to a quantitative RT-PCR strategy. ClC-2 and ClC-3 mRNA expression were calculated relative to β-actin expression within these same tissues. The transcriptional levels of ClC-3 mRNA were between 1.8 and 10.2% of β-actin expression in atria and between 3.4 and 8.6% of β-actin in ventricles ( n= 3 for each tissue). The levels of ClC-2 in both atria and ventricles were significantly less than those measured for ClC-3 ( n = 3; P < 0.05). ClC-2 mRNA levels were between 0.04–0.08% and 0.03–0.18% of β-actin expression in atria and ventricles, respectively ( n = 3 for each tissue). Immunoblots of atrial and ventricular wall protein extracts demonstrated ClC-2- and ClC-3-specific immunoreactivity at 97 and 85 kDa, respectively. Immunohistochemical localization in guinea pig cardiac muscle demonstrates a ubiquitous distribution of ClC-2 and ClC-3 channels in the atrial and ventricular wall. Confocal analysis detected colocalization of ClC-2 and ClC-3 in sarcolemmal membranes and distinct ClC-3 immunoreactivity in cytoplasmic regions. The molecular expression of ClC-2 and ClC-3 in cardiac tissue is consistent with the proposed role of these chloride channels in the regulation of cardiac cell volume and the modulation of cardiac electrical activity.

Melatonin reduces high levels of lipid peroxidation induced by potassium iodate in porcine thyroid

2019 ◽  
pp. 1-7 ◽  
Author(s):  
Paulina Iwan ◽  
Jan Stepniak ◽  
Malgorzata Karbownik-Lewinska
Keyword(s):  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Membrane Lipids ◽  
Chemical Properties ◽  
Iodine Concentration ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Protective Effects ◽  
Potassium Iodate ◽  
Hormone Synthesis

Abstract. Iodine is essential for thyroid hormone synthesis. Under normal iodine supply, calculated physiological iodine concentration in the thyroid is approx. 9 mM. Either potassium iodide (KI) or potassium iodate (KIO3) are used in iodine prophylaxis. KI is confirmed as absolutely safe. KIO3 possesses chemical properties suggesting its potential toxicity. Melatonin (N-acetyl-5-methoxytryptamine) is an effective antioxidant and free radical scavenger. Study aims: to evaluate potential protective effects of melatonin against oxidative damage to membrane lipids (lipid peroxidation, LPO) induced by KI or KIO3 in porcine thyroid. Homogenates of twenty four (24) thyroids were incubated in presence of either KI or KIO3 without/with melatonin (5 mM). As melatonin was not effective against KI-induced LPO, in the next step only KIO3 was used. Homogenates were incubated in presence of KIO3 (200; 100; 50; 25; 20; 15; 10; 7.5; 5.0; 2.5; 1.25 mM) without/with melatonin or 17ß-estradiol. Five experiments were performed with different concentrations of melatonin (5.0; 2.5; 1.25; 1.0; 0.625 mM) and one with 17ß-estradiol (1.0 mM). Malondialdehyde + 4-hydroxyalkenals (MDA + 4-HDA) concentration (LPO index) was measured spectrophotometrically. KIO3 increased LPO with the strongest damaging effect (MDA + 4-HDA level: ≈1.28 nmol/mg protein, p < 0.05) revealed at concentrations of around 15 mM, thus corresponding to physiological iodine concentrations in the thyroid. Melatonin reduced LPO (MDA + 4-HDA levels: from ≈0.97 to ≈0,76 and from ≈0,64 to ≈0,49 nmol/mg protein, p < 0.05) induced by KIO3 at concentrations of 10 mM or 7.5 mM. Conclusion: Melatonin can reduce very strong oxidative damage to membrane lipids caused by KIO3 used in doses resulting in physiological iodine concentrations in the thyroid.

Penconazole and calcium ameliorate drought stress in canola by upregulating the antioxidative enzymes

2020 ◽  
Vol 47 (9) ◽  
pp. 825 ◽  
Author(s):  
Maryam Rezayian ◽  
Vahid Niknam ◽  
Hassan Ebrahimzadeh
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Drought Stress ◽  
Drought Tolerance ◽  
Antioxidative Enzymes ◽  
Proline Content ◽  
Fresh Weight ◽  
Negative Effects ◽  
Mda Content ◽  
Effects Of Drought

The aim of this research was to gauge the alternations in the lipid peroxidation and antioxidative enzyme activity in two cultivars (cv. RGS003 and cv. Sarigol) of canola under drought stress and drought tolerance amelioration by penconazole (PEN) and calcium (Ca). Plants were treated with different polyethylene glycol (PEG) concentrations (0, 5, 10 and 15%) without or with PEN (15 mg L–1) and Ca (15 mM). The Ca treatment prevented the negative effects of drought on fresh weight (FW) in RGS003 and Sarigol at 5 and 15% PEG respectively. Ca and PEN/Ca treatments caused significant induction in the proline content in Sarigol at 15% PEG; the latter treatment was accompanied by higher glycine betaine (GB), lower malondialdehyde (MDA) and growth recovery. Hydrogen peroxide (HO2) content in Sarigol was proportional to the severity of drought stress and all PEN, Ca and PEN/Ca treatments significantly reduced the H2O2 content. PEN and PEN/Ca caused alleviation of the drought-induced oxidative stress in RGS003. RGS003 cultivar exhibited significantly higher antioxidative enzymes activity at most levels of drought, which could lead to its drought tolerance and lower MDA content. In contrast to that of Sarigol, the activity of catalase and superoxide dismutase (SOD) increased with Ca and PEN/Ca treatments in RGS003 under low stress. The application of PEN and Ca induced significantly P5CS and SOD expression in RGS003 under drought stress after 24 h. Overall, these data demonstrated that PEN and Ca have the ability to enhance the tolerance against the drought stress in canola plants.

scholarly journals Endurance Training Regulates Expression of Some Angiogenesis-Related Genes in Cardiac Tissue of Experimentally Induced Diabetic Rats

Biomolecules ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 498
Author(s):  
Mojdeh Khajehlandi ◽  
Lotfali Bolboli ◽  
Marefat Siahkuhian ◽  
Mohammad Rami ◽  
Mohammadreza Tabandeh ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endurance Training ◽  
Molecular Mechanisms ◽  
Cardiac Tissue ◽  
Critical Role ◽  
Diabetic Rats ◽  
Moderate Intensity ◽  
Pcr Analysis ◽  
Cardiac Tissues ◽  
The Impact

Exercise can ameliorate cardiovascular dysfunctions in the diabetes condition, but its precise molecular mechanisms have not been entirely understood. The aim of the present study was to determine the impact of endurance training on expression of angiogenesis-related genes in cardiac tissue of diabetic rats. Thirty adults male Wistar rats were randomly divided into three groups (N = 10) including diabetic training (DT), sedentary diabetes (SD), and sedentary healthy (SH), in which diabetes was induced by a single dose of streptozotocin (50 mg/kg). Endurance training (ET) with moderate-intensity was performed on a motorized treadmill for six weeks. Training duration and treadmill speed were increased during five weeks, but they were kept constant at the final week, and slope was zero at all stages. Real-time polymerase chain reaction (RT-PCR) analysis was used to measure the expression of myocyte enhancer factor-2C (MEF2C), histone deacetylase-4 (HDAC4) and Calmodulin-dependent protein kinase II (CaMKII) in cardiac tissues of the rats. Our results demonstrated that six weeks of ET increased gene expression of MEF2C significantly (p < 0.05), and caused a significant reduction in HDAC4 and CaMKII gene expression in the DT rats compared to the SD rats (p < 0.05). We concluded that moderate-intensity ET could play a critical role in ameliorating cardiovascular dysfunction in a diabetes condition by regulating the expression of some angiogenesis-related genes in cardiac tissues.

Pygo1 regulates pathological cardiac hypertrophy via a β-catenin-dependent mechanism

2021 ◽  
Author(s):  
Li Lin ◽  
Wei Xu ◽  
Yongqing Li ◽  
Ping Zhu ◽  
Wuzhou Yuan ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Cardiac Tissue ◽  
Heart Weight ◽  
Dependent Manner ◽  
Tissue Specific ◽  
Cardiac Tissues ◽  
Pathological Cardiac Hypertrophy ◽  
Interaction Factor ◽  
Myocardial Remodelling

Wnt/β-catenin signalling plays a key role in pathological cardiac remodelling in adults. The identification of a tissue-specific Wnt/β-catenin interaction factor may realise a tissue-specific clinical targeting strategy. Drosophila Pygo codes for the core interaction factor of Wnt/β-catenin. Two Pygo homologs, Pygo1 and Pygo2, have been identified in mammals. Different from the ubiquitous expression profile of Pygo2, Pygo1is enriched in cardiac tissue. However, the role of Pygo1 in mammalian cardiac disease remains unelucidated. Here, we found that Pygo1 was upregulated in human cardiac tissues with pathological hypertrophy. Cardiac-specific overexpression of Pygo1 in mice spontaneously led to cardiac hypertrophy accompanied by declined cardiac function, increased heart weight/body weight and heart weight/tibial length ratios and increased cell size. The canonical β-catenin/T-cell transcription factor 4 complex was abundant in Pygo1-overexpressingtransgenic(Pygo1-TG) cardiac tissue,and the downstream genes of Wnt signaling, i.e., Axin2, Ephb3, and C-myc, were upregulated. A tail vein injection of β-catenin inhibitor effectively rescued the phenotype of cardiac failure and pathological myocardial remodelling in Pygo1-TG mice. Furthermore, in vivo downregulated pygo1 during cardiac hypertrophic condition antagonized agonist-induced cardiac hypertrophy. Therefore, our study is the first to present in vivo evidence demonstrating that Pygo1 regulates pathological cardiac hypertrophy in a canonical Wnt/β-catenin-dependent manner, which may provide new clues for a tissue-specific clinical treatment targeting this pathway.

Methomyl induced effect on fortilin and S100A1 in serum and cardiac tissue: Potential biomarkers of toxicity

2018 ◽  
Vol 38 (3) ◽  
pp. 371-377
Author(s):  
SD Nusair ◽  
AN Joukhan ◽  
AH Bani Rashaid ◽  
AM Rababa’h
Keyword(s):  
Toxic Effect ◽  
Cardiac Tissue ◽  
Cardiac Fibroblasts ◽  
Study Group ◽  
Sprague Dawley ◽  
Cardiac Tissues ◽  
Sprague Dawley Rats ◽  
Cervical Dislocation ◽  
Potential Biomarkers

Methomyl toxicity has been reported as a cause of several accidental and suicidal fatalities. The study is evaluating the effect of lethal methomyl toxicity on fortilin and S100A1 in serum and cardiac tissues. Adult 96 female Sprague-Dawley rats were divided equally into a control (euthanized by cervical dislocation) and a study group (overdosed with methomyl). The levels of fortilin and S100A1 in serum were measured antemortem (to establish the basal levels in serum) and postmortem (to evaluate changes after methomyl exposure) using enzyme-linked immunoassay. S100A1 was immunostained in sections from cardiac tissues. Both proteins in the control were not significantly different ( p > 0.05) compared with the antemortem levels. On the contrast, both biomarkers levels in the intoxicated group were remarkably higher ( p < 0.001) than the control and the antemortem levels. Ventricular tissues from the intoxicated rats presented depleted S100A1 immunostain in cardiomyocytes localized mainly in the epicardium with deeply stained adjacent cardiac fibroblasts. The cardiomyocytes were damaged with a prominent loss of striations compared to normal cardiac tissues from the control. The present outcomes explain to a certain degree the potential toxic effect of methomyl poisoning on the cardiac tissue. Both proteins could be added to the currently available battery of markers for assessing methomyl toxicity.

scholarly journals Defense Mechanisms of Two Pioneer Submerged Plants during Their Optimal Performance Period in the Bioaccumulation of Lead: A Comparative Study

2018 ◽  
Vol 15 (12) ◽  
pp. 2844 ◽  
Author(s):  
Dian Li ◽  
Linglei Zhang ◽  
Min Chen ◽  
Xiaojia He ◽  
Jia Li ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Protein Content ◽  
Defense Mechanisms ◽  
Hydrilla Verticillata ◽  
Optimal Performance ◽  
Ceratophyllum Demersum ◽  
Contaminated Water ◽  
Submerged Plants ◽  
Significant Difference ◽  
Mda Content

Ceratophyllum demersum L. and Hydrilla verticillata (L.f.) Royle, two pioneer, submerged plants, effectively remove heavy metals from contaminated water. The present work evaluates the bioaccumulation and defense mechanisms of these plants in the accumulation of lead from contaminated water during their optimal performance period. C. demersum and H. verticillata were investigated after 14 days of exposure to various lead concentrations (5–80 μM). The lead accumulation in both C. demersum and H. verticillata increased with an increasing lead concentration, reaching maximum values of 2462.7 and 1792 mg kg−1 dw, respectively, at 80 μM. The biomass and protein content decreased significantly in C. demersum when exposed to lead. The biomass of H. verticillata exposed to lead had no significant difference from that of the controls, and the protein content increased for the 5–10 μM exposure groups. The malondialdehyde (MDA) content and superoxide dismutase (SOD), peroxidase (POD), and polyphenol oxidase (PPO) activities were much higher in C. demersum, suggesting considerable damage from lipid peroxidation and sensitivity to lead stress. Enzyme inhibition and inactivation were also observed in C. demersum at high lead concentrations (40–80 μM). The excellent growth status, low damage from lipid peroxidation, and high activity of catalase (CAT) and phenylalanine ammonia-lyase (PAL) observed in H. verticillata illustrate its better tolerance under the same lead stress.

Bitter Melon Protects Against Lipid Peroxidation Caused by Immobilization Stress in Albino Rats

2009 ◽  
Vol 79 (1) ◽  
pp. 48-56 ◽  
Author(s):  
Chaturvedi
Keyword(s):  
Lipid Peroxidation ◽  
Immobilization Stress ◽  
Reduced Glutathione ◽  
Cumene Hydroperoxide ◽  
Liver Homogenate ◽  
Thiobarbituric Acid ◽  
Albino Rats ◽  
Bitter Melon ◽  
Protective Effects

In the present study, protective effects of bitter melon (Momordica charantia) extract on lipid peroxidation induced by immobilization stress in rats have been assessed. Graded doses of extract (50, 100, and 150 mg/kg body weight) were administered orally to rats subjected to immobilization stress for two hours for seven consecutive days. Stress was applied by keeping the rats in a cage where no movement was possible. After seven days, rats were killed by decapitation after ether anesthesia. Blood and liver were collected to measure thiobarbituric acid reactive substances, reduced glutathione, and catalase. In vitro effects of M. charantia extract on lipid peroxidation in liver homogenate of normal, control, and rats pretreated with extract were carried out against cumene hydroperoxide-induced lipid peroxidation. Results reveal that in vivo M. charantia inhibited stress-induced lipid peroxidation by increasing the levels of reduced glutathione and activities of catalase. These results were further supported by in vitro results. In vitro inhibition of lipid peroxidation was indicated by low levels of thiobarbituric acid in the liver homogenate from pretreated rats and normal rats when incubated with both cumene hydroperoxide and extract. Inhibition was also noted in the homogenate where the rats were pretreated but the mixture contained no extract. Thus this plant provides protection by strengthening the antioxidants like reduced glutathione and catalase. Inclusion of this plant in the daily diet would be beneficial.

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