Application of postmortem lipid peroxidation in heart tissue to the diagnosis of myocardial damage

2004 ◽  
Vol 118 (1) ◽  
pp. 19-23 ◽  
Author(s):  
P. Dom�nech ◽  
L. Carbonell ◽  
M. D. P�rez C�rceles ◽  
M. Falc�n ◽  
A. Luna ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Myocardial Damage ◽  
Heart Tissue

Oral treatment with gallic acid and quercetin alleviates lindane-induced cardiotoxicity in rats

2013 ◽  
Vol 91 (2) ◽  
pp. 134-140 ◽  
Author(s):  
Viswanadha Vijaya Padma ◽  
Paramasivan Poornima ◽  
Chermakani Prakash ◽  
Ramachandran Bhavani
Keyword(s):  
Lipid Peroxidation ◽  
Gallic Acid ◽  
Oral Treatment ◽  
Myocardial Damage ◽  
Heart Tissue ◽  
Serum Marker ◽  
Protective Effects ◽  
Membrane Bound ◽  
Enzymic Antioxidants ◽  
Endogenous Antioxidant

Lindane is a man-made organochlorine pesticide used for agricultural purposes. Since lindane-induced toxicity is mediated by free radical generation, this investigation was carried out to study the protective effects of gallic acid and quercetin against lindane-induced cardiotoxicity. Lindane (100 mg·(kg body mass)−1) was administered orally to rats for 30 days. Histological analysis revealed pathological changes in the heart of lindane-treated rats. Biochemical analysis of the lindane-treated animals showed elevated activity for serum marker enzymes, lipid peroxidation (LPO), and membrane-bound Ca2+ ATPase, with a concomitant decrease in the level of non-enzymic antioxidant (GSH), enzymic antioxidants such as superoxide dismutase, catalase, glutathione peroxidase (GPx), and glutathione-S-transferase (GST), and membrane-bound ATPases like Na+/K+ ATPase and Mg2+ ATPase in heart tissue. The results suggest that gallic acid and quercetin offer protection against lindane-induced myocardial damage, possibly through maintaining levels of endogenous antioxidant enzymes and membrane bound ATPase activity, as well as inhibiting lipid peroxidation.

Menthol exposure induces reversible cardiac depression and reduces lipid peroxidation in the heart tissue of tambaqui Colossoma macropomum

Aquaculture ◽  
2021 ◽  
Vol 541 ◽  
pp. 736847
Author(s):  
Sildiane Martins Cantanhêde ◽  
Lílian Lund Amado ◽  
Brenda Maria P. Alho da Costa ◽  
Luis André L. Barbas ◽  
Marcelo Ferreira Torres ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Heart Tissue ◽  
Colossoma Macropomum ◽  
Cardiac Depression

Abstract 229: Determination of Phase-specific Biomarkers of Viral Myocarditis Induced by Theiler’s virus Using Multivariate Analyses of Viral Genome, Troponin, Transcriptome and Echocardiography Data

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Eiichiro Kawai ◽  
Seiichi Omura ◽  
Fumitaka Sato ◽  
Nicholas E Martinez ◽  
Viromi Fernando ◽  
...  
Keyword(s):  
Immune Responses ◽  
Viral Replication ◽  
Microarray Data ◽  
Viral Genome ◽  
Troponin I ◽  
Multivariate Analyses ◽  
Viral Myocarditis ◽  
Myocardial Damage ◽  
Heart Tissue ◽  
Viral Rna

Viral myocarditis has been proposed to be initiated by viral replication in the heart (acute phase), followed by immune-mediated damage (subacute phase), where each phase requires anti-viral and immunomodulatory treatments, respectively. There are no specific biomarkers to distinguish acute from subacute phases of myocarditis while serum troponin, echocardiography, and myocardial biopsy data have been used for diagnosis clinically. To determine the phase-specific biomarkers, we used a mouse model for myocarditis induced by Theiler’s murine encephalomyelitis virus (TMEV), which belongs to the genus Cardiovirus, the family Picornaviridae. We conducted multivariate analyses of viral genome, serum cardiac troponin I, echocardiography, histology, and transcriptome using microarray data of the heart tissue harvested on 4 (acute) and 7 (subacute) days post infection (dpi). The level of viral RNA semi-quantified by RT-PCR was 10-fold higher on 4 dpi (ΔCt = 2.5×10-2 ± 4.9×10-3) than 7 dpi (ΔCt = 2.6×10-3 ± 3.0×10-4) (P < 0.05). Serum troponin was undetectable in 4 of 10 mice on 4 dpi and only in 1 of 10 mice on 7 dpi; the serum troponin levels (ng/ml) on 4 dpi (42.9 ± 15.6) were significantly lower than 7 dpi (249.9 ± 62.8) (P < 0.05). The levels of viral RNA and troponin were strongly correlated on 4 dpi (r = 0.79, P < 0.05), but not 7 dpi (P = 0.12), suggesting that viral replication could be a major cause of myocardial damage only on 4 dpi. We found multiple high intensity cardiac lesions using echocardiography with histological myocarditis on 7 dpi, but not 4 dpi. Transcriptome analyses of microarray data showed upregulation of genes associated with innate immune responses in samples from 4 and 7 dpi, compared with controls. Samples from 7 dpi showed upregulation of genes associated with T, B, and antigen presenting cells and downregulation of cardiac myosin-related genes (Myl4, Myl7, and Mybphl), compared with 4 dpi, suggesting that acquired immune responses contribute to cardiomyocyte damage on 7 dpi. In summary, the chronological order of emergence of biomarker candidates was 1) viral genome and innate immunity, 2) troponin, and 3) acquired immunity and echo and histological changes.

Application of high-dose propofol during ischemia improves postischemic function of rat hearts: effects on tissue antioxidant capacity

2004 ◽  
Vol 82 (10) ◽  
pp. 919-926 ◽  
Author(s):  
Zhengyuan Xia ◽  
David V Godin ◽  
David M Ansley
Keyword(s):  
Lipid Peroxidation ◽  
Antioxidant Capacity ◽  
Functional Recovery ◽  
Isolated Heart ◽  
Cardiac Mechanics ◽  
Heart Tissue ◽  
Global Ischemia ◽  
High Dose ◽  
High Concentration ◽  
Heart Preparation

Previous studies have shown that reactive oxygen species mediated lipid peroxidation in patients undergoing cardiac surgery occurs primarily during cardiopulmonary bypass. We examined whether application of a high concentration of propofol during ischemia could effectively enhance postischemic myocardial functional recovery in the setting of global ischemia and reperfusion in an isolated heart preparation. Hearts were subjected to 40 min of global ischemia followed by 90 min of reperfusion. During ischemia, propofol (12 µg/mL in saline) was perfused through the aorta at 60 µL/min. We found that application of high-concentration propofol during ischemia combined with low-concentration propofol (1.2 µg/mL) administered before ischemia and during reperfusion significantly improved postischemic myocardial functional recovery without depressing cardiac mechanics before ischemia, as is seen when high-concentration propofol was applied prior to ischemia and during reperfusion. The functional enhancement is associated with increased heart tissue antioxidant capacity and reduced lipid peroxidation. We conclude that high-concentration propofol application during ischemia could be a potential therapeutic and anesthetic strategy for patients with preexisting myocardial dysfunction.Key words: propofol, ischemia, heart, rat, oxidative stress.

Comparative study of the protective effect between deferoxamine and deferiprone on chronic iron overload induced cardiotoxicity in rats

2006 ◽  
Vol 25 (7) ◽  
pp. 375-385 ◽  
Author(s):  
A M Emara ◽  
R S El Kelany ◽  
K A Moustafa
Keyword(s):  
Vitamin C ◽  
Iron Overload ◽  
Protective Effect ◽  
Histopathological Examination ◽  
Binding Capacity ◽  
Myocardial Damage ◽  
Heart Tissue ◽  
Albino Rats ◽  
Beneficial Effects ◽  
Iron Binding Capacity

Patients with iron overload frequently suffer from hemochromatosis of major organs, such as the heart and liver. Heart affection is the most common cause of death in patients with iron overload. Although the beneficial effects of deferoxamine (DFO) on iron-associated mortality are well documented, the role of deferiprone in the management of transfusional iron overload is controversial. The aim of this study was to compare the protective effect of iron chelators (DFO and deferiprone) individually and in combination with the anti-oxidant (vitamin C) in the prevention of myocardial damage. Sixty albino rats were divided into six groups: two control groups (noniron-loaded and iron-loaded) and four iron-loaded groups classified as follows: DFO group, DFO combined with vitamin C group, deferiprone group and deferiprone combined with vitamin C group. Heart tissue and blood samples were taken for histopathological examination of the heart, determination of total iron-binding capacity, 8-OH-deoxyguanosine (8-OH-dG), myocardial lipid peroxidation and glutathione (GSH) content. Less histopathological cardiac changes and a significant decrease in all biochemical parameters, except myocardial GSH, were observed in the deferiprone group. The addition of vitamin C improves the biochemical and histopathological changes in comparison to those rats administered DFO or deferiprone individually.

On the benefit of magnetic magnesium nanocarrier in cardiovascular toxicity of aluminum phosphide

2011 ◽  
Vol 29 (2) ◽  
pp. 126-135 ◽  
Author(s):  
Maryam Baeeri ◽  
Marjan Shariatpanahi ◽  
Amir Baghaei ◽  
Seyedeh Farnaz Ghasemi-Niri ◽  
Hamidreza Mohammadi ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Considerable Increase ◽  
Lethal Dose ◽  
Heart Tissue ◽  
Cardiac Cells ◽  
Intragastric Administration ◽  
Aluminum Phosphide ◽  
Antioxidant Power ◽  
Effective Combination ◽  
Study Support

The present study was designed to determine the effect of a new 25Mg2+-carrying nanoparticle (25MgPMC16) on energy depletion, oxidative stress, and electrocardiographic (ECG) parameters on heart tissue of the rats poisoned by aluminum phosphide (AlP). 25MgPMC16 at doses of 0.025, 0.05, and 0.1 median lethal dose (LD50 = 896 mg/kg) was administered intravenously (iv) 30 min after a single intragastric administration of AlP (0.25 LD50). Sodium bicarbonate (Bicarb; 2 mEq/kg, iv) was used as the standard therapy. After anesthesia, the animals were rapidly connected to an electronic cardiovascular monitoring device for monitoring of ECG, blood pressure (BP), and heart rate (HR). Later lipid peroxidation, antioxidant power, ATP/ADP ratio, and Mg concentration in the heart were evaluated. Results indicated that after AlP administration, BP and HR decreased while R-R duration increased. 25MgPMC16 significantly increased the BP and HR at all doses used. We found a considerable increase in antioxidant power, Mg level in the plasma and the heart and a reduction in lipid peroxidation and ADP/ATP ratio at various doses of 25MgPMC16, but 25MgPMC16-0.025 + Bicarb was the most effective combination therapy. The results of this study support that 25MgPMC16 can increase heart energy by active transport of Mg inside the cardiac cells.25MgPMC16 seems ameliorating AlP-induced toxicity and cardiac failure necessitating further studies.

Metabolic Syndrome in the Rat: Females are Protected Against the Pro-Oxidant Effect of a High Sucrose Diet

2002 ◽  
Vol 227 (9) ◽  
pp. 837-842 ◽  
Author(s):  
Jérôme Busserolles ◽  
Andrzej Mazur ◽  
Elyett Gueux ◽  
Edmond Rock ◽  
Yves Rayssiguier
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Lipid Peroxidation ◽  
Heart Tissue ◽  
Female Rats ◽  
Hormonal Status ◽  
Sucrose Diet ◽  
High Sucrose Diet ◽  
Oxidant Effect ◽  
High Sucrose

Metabolic syndrome is more prevalent in men than in women. In an experimental dietary model of metabolic syndrome, the high-fructose–fed rat, oxidative stress has been observed in males. Given that estradiol has been documented to exert an antioxidant effect, we investigated whether female rats were better protected than males against the adverse effects of a high-sucrose diet, and we studied the influence of hormonal status in female rats. Males and females were first fed a sucrose-based or starch-based diet for 2 weeks. In the males, the plasma triglyceride (TG)-raising effect of sucrose was accompanied by significantly lowered plasma α-tocopherol and a significantly lowered α-tocopherol/TG ratio (30%), suggesting that vitamin E depletion may predispose lipoproteins to subsequent oxidative stress. In males, after exposure of heart tissue homogenate to iron-induced lipid peroxidation, thiobarbituric reactive substances were significantly higher in the sucrose-fed than in the starch-fed rats. In contrast, in sucrose-fed females, neither a decrease in vitamin E/TG ratio nor an increased susceptibility of heart tissue to peroxidation was observed, despite both a significantly decreased heart superoxide dismutase activity (14%) and a significant 3-fold increase in plasma nitric oxide concentration compared with starch-fed females. The influence of hormonal status in female rats was then assessed using intact, ovariectomized, or estradlol-supplemented ovariectomized female rats fed the sucrose or starch diet for 2 weeks. After exposure of heart tissue to iron-induced lipid peroxidation, higher susceptibility to peroxidation was found only in ovariectomized females fed the sucrose diet compared with the starch group and not in intact females or ovariectomized females supplemented with estradiol. Thus, estrogens, by their effects on antioxidant capacity, might explain the sexual difference in the pro-oxidant effect of sucrose diet resulting in metabolic syndrome in rats.

scholarly journals Effect of the MPT Pore Inhibitor Alisporivir on the Development of Mitochondrial Dysfunction in the Heart Tissue of Diabetic Mice

Biology ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 839 ◽  
Author(s):  
Natalia V. Belosludtseva ◽  
Vlada S. Starinets ◽  
Irina B. Mikheeva ◽  
Dmitriy A. Serov ◽  
Maxim E. Astashev ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Lipid Peroxidation ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Permeability Transition ◽  
Permeability Transition ◽  
Tolerance Test ◽  
Heart Tissue ◽  
Heart Mitochondria ◽  
Diabetic Mice ◽  
Pore Opening

Diabetes mellitus is a systemic metabolic disorder associated with mitochondrial dysfunction, with the mitochondrial permeability transition (MPT) pore opening being considered as one of its possible mechanisms. The effect of alisporivir, a non-immunosuppressive cyclosporin derivative and a selective inhibitor of the MPT pore opening, on the ultrastructure and functions of the heart mitochondria of mice with diabetes mellitus induced by a high-fat diet combined with streptozotocin injections was studied. The treatment of diabetic animals with alisporivir (2.5 mg/kg ip for 20 days) increased the rate of glucose clearance during the glucose tolerance test. The blood glucose level and the indicator of heart rate in alisporivir-treated diabetic mice tended to restore. An electron microscopy analysis showed that alisporivir prevented mitochondrial swelling and ultrastructural alterations in cardiomyocytes of diabetic mice. Alisporivir canceled the diabetes-induced increases in the susceptibility of heart mitochondria to the MPT pore opening and the level of lipid peroxidation products, but it did not affect the decline in mitochondrial oxidative phosphorylation capacity. The mRNA expression levels of Pink1 and Parkin in the heart tissue of alisporivir-treated diabetic mice were elevated, suggesting the stimulation of mitophagy. In parallel, alisporivir decreased the level of mtDNA in the heart tissue. These findings suggest that targeting the MPT pore opening by alisporivir alleviates the development of mitochondrial dysfunction in the diabetic heart. The cardioprotective effect of the drug in diabetes can be mediated by the induction of mitophagy and the inhibition of lipid peroxidation in the organelles.

scholarly journals Syringic Acid Attenuates Cardiomyopathy in Streptozotocin-Induced Diabetic Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Zahra Sabahi ◽  
Mohammad Javad Khoshnoud ◽  
Sara Hosseini ◽  
Fatemeh Khoshraftar ◽  
Marzieh Rashedinia
Keyword(s):  
Lipid Peroxidation ◽  
Diabetic Cardiomyopathy ◽  
Protective Factor ◽  
Cardiac Injury ◽  
Heart Tissue ◽  
Syringic Acid ◽  
Diabetic Rats ◽  
Protein Carbonylation ◽  
Protective Effects

Objectives. Diabetic cardiomyopathy (DC) has become one of the serious complications in diabetic cases. In this study, we aimed to explore the syringic acid (SYR) protective effect against diabetes-induced cardiac injury in experimental rats. Methods. Rats were divided in control and streptozotocin-induced diabetic rats which were subdivided into diabetic controls, and three test groups (SYR at 25, 50, and 100 mg/kg) and the nondiabetic group received 100 mg/kg of SYR. All treatments were given SYR for 6 weeks. SYR effects on cardiac diagnostic markers, heart lipid peroxidation, protein carbonylation, antioxidant system, and changes of the heart mitochondrial mass and biogenesis were measured. Results. Diabetes induction prompted CK-MB, LDH levels in serum, cardiac catalase, and superoxide dismutase activity, as well as cardiac TBARs and carbonylated protein. SYR administration (100 m/kg) attenuated CK-MB and LDH levels. Also, 50 and 100 mg/kg of SYR reduced cardiac TBARs and carbonylated protein in diabetic rats. These treatments did not show any effects on GSH content, mtDNA, and mitochondrial biogenesis indices (PGC1- α, NRF1, NRF2, and TFAM) in heart tissue. Conclusions. SYR treatment showed protective effects on diabetic cardiomyopathy in rats by reducing lipid peroxidation and protein carbonylation. The possible mechanisms could be related to antioxidant activity of this phenolic acid. SYR might play a role of a protective factor in cardiac challenges in diabetes.

Sign in / Sign up

Export Citation Format

Share Document