Lipid Peroxidation In Rat Heart Research Articles

Phytochemical profiling and antioxidant activities of monodora myristica and dennettia tripetala against lipid peroxidation in rat heart

Phytochemical profiling and antioxidant activities of monodora myristica and dennettia tripetala against lipid peroxidation in rat heart

Influence of Moringa (Moringa oleifera) leaf extracts on the antioxidant and angiotensin-1 converting enzyme inhibitory properties of lisinopril

This study investigated the in vitro effect of various combinations of aqueous extracts of moringa (Moringa oleifera) leaves on the ACE inhibitory and antioxidant properties of lisinopril, which is a popular synthetic ACE inhibitor. Moringa leaves were air-dried and blended into powdery form. Thereafter, the aqueous extract was prepared and freeze-dried. The following sample mixtures were prepared: L = 100% lisinopril (1 mg/ml); M = 100% moringa extract (1 mg/ml); 1L + 3M = 25% lisinopril + 75% moringa extract; L + M = 50% lisinopril + 50% moringa extract; 3L + 1M = 75% lisinopril + 25% moringa extract. The results revealed that 100% moringa and the various combinations showed higher ACE inhibition than 100% lisinopril in both rat heart and lung homogenates. Furthermore, all the samples caused the inhibition of Fe2+-induced lipid peroxidation in rat heart and lung tissue homogenates, with moringa leaf extract having the highest inhibitory ability. All the samples also showed antioxidant properties (ferric reducing antioxidant property, 2,2’-azino-bis (-3-ethylbenzthiazoline-6-sulphonate [ABTS*] and 1,1-diphenyl-2-picrylhydrazyl [DPPH] free radicals scavenging abilities, and Fe2+ chelating ability). This study revealed that moringa leaf extracts could improve the antioxidant and ACE inhibitory properties of lisinopril. However, further in vivo experiments and clinical trials are recommended.

Effect of Different Processing Methods on Antihypertensive Property and Antioxidant Activity of Sandpaper Leaf (Ficus exasperata) Extracts

ABSTRACTSandpaper leaf (Ficus exasperata) is commonly used in folk medicine to manage high blood pressure. However, different methods such as soaking, boiling, hand maceration, and blending have been employed for preparing sandpaper leaf extracts for hypertensive patients. This study sought to investigate and compare the influence of different processing methods on the antihypertensive properties of sandpaper leaf as well as its effect on Fe2+ and sodium nitroprusside– (SNP-) induced lipid peroxidation in rat heart in vitro. Sandpaper leaf extracts were prepared using different methods and the resulting solutions were freeze-dried. Effect of the extracts on angiotensin-1-converting enzymes (ACE) and arginase activity was assessed. Thereafter, antioxidant activities of the extracts were determined using in vitro antioxidant assays, and the total phenolic content and flavonoid content of the extracts were determined. The results revealed that sandpaper leaf extracts from different processing methods inhibited ACE and arginase activity in a dose-dependent manner. However, the soaking method had significantly (p < .05) higher inhibitory effect on angiotensin converting (ACE) and arginase activity than hand maceration, boiling, and blending methods. Sandpaper leaf extracts also exhibited high antioxidant activities as typified by their iron-chelating ability, 2, 2′-azino-bis (3-ethylbenzthiazoline-6-sulphonic acid) (ABTS) radical–scavenging and iron-chelating ability as well as inhibition of Fe2+- and SNP-induced lipid peroxidation in rat heart in vitro. Processing methods alter the inhibitory effect of sandpaper leaf extracts on ACE and arginase activities. Thus, inhibition of ACE and arginase coupled with antioxidant properties could offer protective mechanisms against hypertension. However, the soaking method appears to be the most promising among methods considered.

A comparative study on antihypertensive and antioxidant properties of phenolic extracts from fruit and leaf of some guava (Psidium guajava L.) varieties

Investigation of antihypertensive and antioxidant properties of fruit and leaf extracts from four varieties (giant white, small white, stripped and pink) of guava (Psidium guajava L.) in vitro was the focus of this study. Consequently, methanol/1 M HCl (20:1 v/v) extraction of fruit and leaf of the guava varieties were carried out. Thereafter, the extracts were assayed for their angiotensin I converting enzyme (ACE) inhibitory effect, total phenol and flavonoid contents, reducing property, radicals (DPPH, ABTS•+, hydroxyl and nitric oxide) scavenging ability, Fe2+ chelating ability, and inhibition of Fe2+ and Sodium nitroprusside (SNP) induced lipid peroxidation reactions (in vitro). Furthermore, the phenolic constituents of the extracts were characterised with gas chromatography (GC). The results showed that all the extracts significantly (P < 0.05) inhibited ACE activity, scavenged (DPPH, ABTS•+, nitric oxide and hydroxyl) radicals, chelated Fe2+ and also inhibited Fe2+ and SNP induced lipid peroxidation in rat heart (in vitro). Nevertheless, the pink guava variety had the highest ACE inhibitory and antioxidant properties. In addition, Rosmarinic acid, eugenol, carvacrol, catechin and caffeic acid were the dominant phenolics found in the extracts. The ACE inhibitory effects and antioxidant properties of the guava extracts, which correlates significantly with their phenolic constituents, could largely contribute to their antihypertensive properties as obtained in traditional medicine.

Effect of pretreatment with coenzyme Q 10 on isoproterenol-induced cardiotoxicity and cardiac hypertrophy in rats

Background: Coenzyme Q 10 (CoQ 10) is a lipid-soluble, vitamin-like substance found in the hydrophobic interior of the phospholipid bilayer of most cellular membranes. It appears to be involved in the coordinated regulation between oxidative stress and antioxidant capacity of heart tissue when the heart is subjected to oxidative stress in various pathogenic conditions. Objective: The objective of the present study was to investigate the effect of pretreatment with CoQ 10 (100 mg/kg) on isoproterenol (ISO)-induced cardiotoxicity and cardiac hypertrophy in rats. Methods: Albino male Wistar rats (250–300 g) were evenly divided by lottery method into 1 of the following 3 groups: the ISO group (olive oil 2 mL/kg orally for 18 days and ISO 1 mg/kg IP from days 9–18); the CoQ 10 + ISO group (CoQ 10 100 mg/kg orally for 18 days and ISO 1 mg/kg IP from days 9–18); and the control group (olive oil 2 mL/kg orally for 18 days and water IP from days 9–18). Twenty-four hours after the last dose of water or ISO, the rats were anesthetized and an ECG was recorded. Blood was withdrawn by retro-orbital puncture for estimation of serum creatine kinase-MB (CK-MB) isoenzyme levels, lactate dehydrogenase (LDH) levels, and aspartate aminotransferase activities. The animals were euthanized using an overdose of ether. The hearts of 6 animals from each group were used for estimation of superoxide dismutase (SOD) activity, reduced glutathione (GSH) concentration, lipid peroxidation (LPO), malondialdehyde (MDA), and total protein concentration. Histopathology of the 2 remaining hearts in each group was carried out by a blinded technician. Results: A total of 24 rats (8 in each group) were used in this study; all rats survived to study end. Compared with the control group, the ISO-treated rats had a significant change in heart to body weight ratio ( P < 0.001); significant changes in the endogenous antioxidants (ie, significantly higher myocardial MDA concentration [ P < 0.001]; significantly lower myocardial GSH concentration [ P < 0.001] and SOD activity [ P < 0.01]); and significantly higher serum activities of marker enzymes (eg, CK-MB [ P < 0.001] and LDH [ P < 0.001]). Compared with the ISO group, the CoQ 10 + ISO group had a significant change in heart to body weight ratio ( P < 0.001); significant changes in the endogenous antioxidants (ie, significantly lower MDA concentration [ P < 0.05]; significantly higher myocardial GSH concentration [ P < 0.001] and SOD activity [ P < 0.05]); and significantly lower serum activities of marker enzymes (eg, CK-MB [ P < 0.05] and LDH [ P < 0.01]). Conclusion: Pretreatment with CoQ 10 (100 mg/kg) for 18 days was associated with moderate protection against ISO-induced cardiotoxicity and cardiac hypertrophy, and with lower myocardial injury by preserving endogenous antioxidants and reducing LPO in rat heart.

Effects of endurance training and acute exhaustive exercise on antioxidant defense mechanisms in rat heart

We investigated whether 8-week treadmill training strengthens antioxidant enzymes and decreases lipid peroxidation in rat heart. The effects of acute exhaustive exercise were also investigated. Male rats ( Rattus norvegicus, Sprague-Dawley strain) were divided into trained and untrained groups. Both groups were further divided equally into two groups where the rats were studied at rest and immediately after exhaustive exercise. Endurance training consisted of treadmill running 1.5 h day − 1 , 5 days week − 1 for 8 weeks. For acute exhaustive exercise, graded treadmill running was conducted. Malondialdehyde level in heart tissue was not affected by acute exhaustive exercise in untrained and trained rats. The activities of glutathione peroxidase and glutathione reductase enzymes decreased by both acute exercise and training. Glutathione S-transferase and catalase activities were not affected. Total and non-enzymatic superoxide scavenger activities were not affected either. Superoxide dismutase activity decreased by acute exercise in untrained rats; however, this decrease was not observed in trained rats. Our results suggested that rat heart has sufficient antioxidant enzyme capacity to cope with exercise-induced oxidative stress, and adaptive changes in antioxidant enzymes due to endurance training are limited.

Lipid peroxidation of rat myocardial tissue following daunomycin administration

Daunomycin-induced cardiotoxicity has been regarded to be the result of oxygen-mediated lipid peroxidation of cell membranes. The aim of the present work was to evaluate the extent of lipid peroxidation in rat heart after administration of this anticancer drug and, further, to examine possible activation of some endogenous antioxidant defense systems. Myocardial tissue from both control and drug-treated rats was tested for lipid peroxidation using a selective third-order derivative method that is based on the analysis of the free malondialdehyde produced. Determination of reduced/oxidized glutathione levels and measurement of the activity of DT-diaphorase, glutathione- S-transferase, glutathione reductase, glucose-6-phosphate dehydrogenase and NADPH-cytochrome P-450 reductase were also carried out using literature methods. Significant increase of malondialdehyde content, and DT-diaphorase and glutathione- S-transferase activities were found in myocardial tissue from daunomycin-treated rats. On the other hand, reduced and oxidized glutathione levels were significantly decreased while the activity of glutathione reductase, glucose-6-phosphate dehydrogenase and NADPH-cytochrome P-450 reductase remained unchanged after daunomycin administration. The results of the present study give further evidence that daunomycin can induce lipid peroxidation in heart. However, additional experimentation is needed in order to delineate the molecular details of this process as well as of the mechanisms evolved to limit it.

Dietary Vitamins A and E Affect Differently Lipid Peroxidation in Rat Heart and Testis.

This study examines the susceptibility to lipid peroxidation of rat heart and testis microsomes, in relation to dietary vitamin A and/or E status. Four groups of rats were fed different levels of the vitamins. After a period of 8 weeks, lipid peroxide levels estimated by thiobarbituric acid method, fatty acid composition and vitamins A and E were measured in serum or in microsomes. In heart, lipid peroxide levels were enhanced in dietary vitamin E deficiency; linoleic acid 18:2 (n-6), arachidonic acid 20:4 (n-6), and docosahexaenoic acid 22:6 (n-3) were significantly decreased. In testis, dietary vitamin A deficiency significantly increased lipid peroxide production and decreased docosapentaenoic acid 22:5 (n-6) and 20:4 (n-6). Supplementation of the diet with both vitamins A and E significantly decreased lipid peroxide production but did not change the fatty acid composition. Induced lipid peroxidation increased in the heart of vitamin E-deficient rats and in the testis of vitamin A-deficient ones. Both in heart and testis, we found a good correlation between spontaneous and induced lipid peroxides and also between lipid peroxides and polyunsaturated to saturated fatty acid ratio. Besides, lipid peroxide production was well correlated with polyunsaturated fatty acids/vitamin A in testis and with polyunsaturated fatty acids/vitamin E molar ratios in heart. Membrane susceptibility to lipid peroxidation varied greatly according to dietary status and organ. Vitamin E seemed to be a more effective antioxidant for heart, and vitamin A, for testis. Supplementation enhanced the beneficial role of each vitamin.

The effect of beta blocking drugs on lipid peroxidation in rat heart in vitro.

Beta-adrenergic receptor blocking drugs include a structurally related class of drugs that are employed clinically to treat a variety of cardiovascular disorders. Since these drugs exert additional nonspecific effects including membrane stabilization, representative samples including atenolol, dilevolol, labetalol, metoprolol and propranolol were studied to determine their influence on lipid peroxidation. Homogenates or liposomes of adult rat hearts were incubated in the presence of various concentrations of propranolol or equivalent concentrations of dilevolol, labetalol, metoprolol or atenolol. Lipid peroxidation was stimulated with 50 microM FeSO4, 5 microM t-butyl hydroperoxide (homogenates) or 0.2 mM citrate FeSO4 (liposomes) plus O2. Lipid peroxidation, as assessed by both the thiobarbituric acid reaction and chemiluminescence, was reduced in a dose-dependent manner as the propranolol concentration was increased from 1 to 10 mM. The five beta-adrenergic receptor blocking drugs reduced lipid peroxidation both in crude homogenates and in liposomes; their effectiveness was related to their lipophilicity. Dilevolol, propranolol, labetalol and metoprolol at a concentration of 20 mM reduced lipid peroxidation by 45%, 37%, 35% and 28%, respectively. The hydrophilic blocker atenolol was ineffective in reducing lipid peroxidation even at elevated concentrations. Lipophilic beta-blocking drugs apparently are capable of exerting an antioxidant effect in protecting membrane lipids against peroxidation.

Inhibition of rat heart and liver microsomal lipid peroxidation by nifedipine

Lipid peroxidation in rat heart and liver microsomes was induced by an NADPH-generating system or by ascorbate in the presence of an ADP-iron complex. Microsomal lipid peroxidation, as measured by malonaldehyde formation, was inhibited by nifedipine over a wide range of concentrations (47 μM to 6 μM). Nifedipine also decreased the oxygen consumption of cardiac and hepatic microsomes in a concentration-dependent manner. These results indicate that nifedipine may perturb microsomal electron transport systems. Nifedipine may have the potential to alter the sensitivity of cardiac and hepatic membranes to peroxidative damage.

Lipid peroxidation in rat heart: Effect of feeding coconut and sunflower seed oil: C.K. George, A.S. Balasubramaniam and G. Cherian. Christian Medical College Hospital, Vellore, India

Lipid peroxidation in rat heart: Effect of feeding coconut and sunflower seed oil: C.K. George, A.S. Balasubramaniam and G. Cherian. Christian Medical College Hospital, Vellore, India