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.

Protective effects of polysaccharide from Euphorbia kansui (Euphorbiaceae) on the swimming exercise-induced oxidative stress in mice

2006 ◽  
Vol 84 (10) ◽  
pp. 1071-1079 ◽  
Author(s):  
Farong Yu ◽  
Shunqing Lu ◽  
Fahong Yu ◽  
Shutao Feng ◽  
Peter M. McGuire ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Antioxidant Activities ◽  
Oral Treatment ◽  
Swimming Exercise ◽  
Strenuous Exercise ◽  
Antioxidant Enzyme Activities ◽  
Protective Effects ◽  
Euphorbia Kansui ◽  
Exercise Induced

The present study examined the effects of derivatives of galactosides and glucosides in a polysaccharide extract from Euphorbia kansui (Euphorbiaceae) on exercise-induced oxidative stress in mice. Exhaustive swimming exercise significantly increases the degree of lipid peroxidation in terms of malondialdehyde content and reduces the antioxidant activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx). Our findings revealed that chronic oral treatment with the extract elevates enzymatic activities of SOD and GPx accompanied by a corresponding decrease in malondialdehyde. The antioxidative activities of these compounds against exercise-induced oxidative stress are correlated with various activities such as reducing the production of superoxide and hydroxyl radicals, inhibiting lipid peroxidation, enhancing antioxidative defenses, and increasing the production of SOD and GPx activity and expression in different tissues. These compounds may be involved in glycogen metabolism to meet the requirement of working skeletal muscles and act as antioxidants by terminating the chain reaction of lipid peroxidation to maintain the morphological stability of mitochondria in spinal motor neurons. These observations suggest that E. kansui has antioxidative and antifatigue properties and can be given as prophylactic and (or) therapeutic supplements for increasing antioxidant enzyme activities and preventing lipid peroxidation during strenuous exercise.

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

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.

scholarly journals Effect of hydroethanolic extract of Piper betle in isoproterenol induced cardiac hypertrophy

2019 ◽  
Vol 10 (4) ◽  
pp. 3055-3062
Author(s):  
Doss VA ◽  
Sreeja Jeevan ◽  
Madhumitha Paranjothi ◽  
Dharaniyambigai Kuberapandian
Keyword(s):  
Cardiac Hypertrophy ◽  
Plant Extract ◽  
Ethanolic Extract ◽  
Myocardial Damage ◽  
Heart Tissue ◽  
Piper Betle ◽  
Histopathological Analysis ◽  
Standard Drug ◽  
Cell Layers ◽  
Enzymic Antioxidants

Cardiac hypertrophy (CH) is a condition in which myocardial mass is increased beyond the normal range due to irreversible fibrotic events that lead to various complication like ventricular chamber dilation, thinning of the internal walls and extensive myocardial damage. In this study, the cardioprotective potential of the hydro-ethanolic extract of Piper betle (P. betle) was evaluated against cardiac hypertrophy induced by isoproterenol in male albino Wistar rats. Isoproterenol (10 mg/kg b.w., i.p., 7 days) induced cardiac hypertrophy in experimental rats which were simultaneously treated with the standard drug losartan (50 mg/ kg b.w., oral., 7 days) and hydro-ethanolic extract of P. betle (200 mg/kg b.w., oral., 7 days). Biochemical estimations revealed increased levels of glucose, protein, cholesterol, serum creatinine, cardiac maker enzymes (SGOT; SGPT and LDH), reduced enzymic antioxidants (SOD, CAT, GPx) and serum were observed during CH which were reciprocated to normal when treated with plant extract. Histopathological analysis of the heart tissue (left ventricles) showed repairment of cellular architecture with reduced stiffened cell layers and necrosis in plant extract administered rats thereby indicating the anti-hypertrophic potential of P. betle.

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.

Hepato-renal protective effects of gallic acid and p-coumaric acid in nicotinamide/streptozotocin-induced diabetic rats

2016 ◽  
Vol 5 (06) ◽  
pp. 4641 ◽  
Author(s):  
Adel Abdel Moneim* ◽  
Sanaa M. Abd El-Twab ◽  
Mohamed B. Ashour ◽  
Ahmed I. Yousef
Keyword(s):  
Body Weight ◽  
Gallic Acid ◽  
Protein Profile ◽  
Serum Glucose ◽  
Diabetic Rats ◽  
Hypoglycemic Agents ◽  
Protective Effects ◽  
Coumaric Acid ◽  
Experimental Type

The goal of diabetes treatment is primarily to save life and alleviate symptoms and secondary to prevent long-term diabetic complications resulting from hyperglycemia. Thus, our present investigation was designed to evaluate the hepato-renal protective effects of gallic acid and p-coumaric acid in nicotinamide/streptozotocin (NA/STZ)-induced diabetic rats. Experimental type 2 diabetes was induced by a single intraperitoneal (i.p.) injection of STZ (65 mg/kg b.wt.), after 15 min of i.p. injection of NA (120 mg/kg b.wt.). Gallic acid and p-coumaric acid were orally administered to diabetic rats at a dose of 20, 40 mg/kg b.wt./day, respectively, for 6 weeks. Body weight, serum glucose, protein profile, liver function enzymes and kidney function indicators was assayed. Treatment with either gallic acid or p-coumaric acid significantly ameliorated the elevated levels of glucose, alanine aminotransferase (ALT), aspartate aminotransferase (AST), urea and uric acid. Both compounds were also found to restore total protein, albumin, and globulin as well as body weight of diabetic rats to near normal values. It can conclude that both gallic acid and p-coumaric acid have potent hypoglycemic and hepato-renal protective effects in diabetic rats. Therefore, our results suggest promising hypoglycemic agents that can attenuate the progression of diabetic hepatopathy and nephropathy.

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

scholarly journals Analysis of Lipid Peroxidation by UPLC-MS/MS and Retinoprotective Effects of the Natural Polyphenol Pterostilbene

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 168
Author(s):  
Isabel Torres-Cuevas ◽  
Iván Millán ◽  
Miguel Asensi ◽  
Máximo Vento ◽  
Camille Oger ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Diabetic Retinopathy ◽  
Redox Homeostasis ◽  
Ultra Performance Liquid Chromatography ◽  
Protective Effects ◽  
Diabetic Retina ◽  
Key Factor ◽  
Adrenic Acid ◽  
Diabetic Rabbits ◽  
High Level

The loss of redox homeostasis induced by hyperglycemia is an early sign and key factor in the development of diabetic retinopathy. Due to the high level of long-chain polyunsaturated fatty acids, diabetic retina is highly susceptible to lipid peroxidation, source of pathophysiological alterations in diabetic retinopathy. Previous studies have shown that pterostilbene, a natural antioxidant polyphenol, is an effective therapy against diabetic retinopathy development, although its protective effects on lipid peroxidation are not well known. Plasma, urine and retinas from diabetic rabbits, control and diabetic rabbits treated daily with pterostilbene were analyzed. Lipid peroxidation was evaluated through the determination of derivatives from arachidonic, adrenic and docosahexaenoic acids by ultra-performance liquid chromatography coupled with tandem mass spectrometry. Diabetes increased lipid peroxidation in retina, plasma and urine samples and pterostilbene treatment restored control values, showing its ability to prevent early and main alterations in the development of diabetic retinopathy. Through our study, we are able to propose the use of a derivative of adrenic acid, 17(RS)-10-epi-SC-Δ15-11-dihomo-IsoF, for the first time, as a suitable biomarker of diabetic retinopathy in plasmas or urine.

scholarly journals Kaempferol Ameliorates Oxygen-Glucose Deprivation/Reoxygenation-Induced Neuronal Ferroptosis by Activating Nrf2/SLC7A11/GPX4 Axis

Biomolecules ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 923
Author(s):  
Yuan Yuan ◽  
Yanyu Zhai ◽  
Jingjiong Chen ◽  
Xiaofeng Xu ◽  
Hongmei Wang
Keyword(s):  
Lipid Peroxidation ◽  
Cell Death ◽  
Antioxidant Capacity ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Related Factor ◽  
Protective Effects

Kaempferol has been shown to protect cells against cerebral ischemia/reperfusion injury through inhibition of apoptosis. In the present study, we sought to investigate whether ferroptosis is involved in the oxygen-glucose deprivation/reperfusion (OGD/R)-induced neuronal injury and the effects of kaempferol on ferroptosis in OGD/R-treated neurons. Western blot, immunofluorescence, and transmission electron microscopy were used to analyze ferroptosis, whereas cell death was detected using lactate dehydrogenase (LDH) release. We found that OGD/R attenuated SLC7A11 and glutathione peroxidase 4 (GPX4) levels as well as decreased endogenous antioxidants including nicotinamide adenine dinucleotide phosphate (NADPH), glutathione (GSH), and superoxide dismutase (SOD) in neurons. Notably, OGD/R enhanced the accumulation of lipid peroxidation, leading to the induction of ferroptosis in neurons. However, kaempferol activated nuclear factor-E2-related factor 2 (Nrf2)/SLC7A11/GPX4 signaling, augmented antioxidant capacity, and suppressed the accumulation of lipid peroxidation in OGD/R-treated neurons. Furthermore, kaempferol significantly reversed OGD/R-induced ferroptosis. Nevertheless, inhibition of Nrf2 by ML385 blocked the protective effects of kaempferol on antioxidant capacity, lipid peroxidation, and ferroptosis in OGD/R-treated neurons. These results suggest that ferroptosis may be a significant cause of cell death associated with OGD/R. Kaempferol provides protection from OGD/R-induced ferroptosis partly by activating Nrf2/SLC7A11/GPX4 signaling pathway.

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