Heart Thiobarbituric Acid Reactive Substances Research Articles

Protective effects of 3, 4-dihydroxybenzoic acid on myocardial infarction induced by isoproterenol in rats.

Despite considerable advances in interventions and treatment, there is a high mortality rate in patients with myocardial infarction (MI). This is the first study to investigate the protective effects of 3, 4-dihydroxybenzoic acid against isoproterenol induced MI in rats. MI was induced by isoproterenol (100-mg/kg body weight) in rats. Then, rats were treated with 3, 4-dihydroxybenzoic acid (16-mg/kg body weight) for 2 weeks. Serum creatine kinase-MB, cardiac troponin-T, cardiac troponin-I, and heart thiobarbituric acid reactive substances were significantly (p < 0.05) increased and heart superoxide dismutase and catalase activities were significantly (p < 0.05) reduced in isoproterenol-induced myocardial infarcted rats. Isoproterenol induction significantly (p < 0.05) elevated the plasma homocysteine and serum high sensitivity-C-reactive protein levels. Furthermore, an enzyme-linked immunosorbent assay, reverse transcription polymerase chain study, and immunohistochemical (IHC) staining revealed significantly (p < 0.05) elevated levels and expression of serum/myocardial nuclear factor-κB, tumor necrosis factor-alpha, interleukin-1 beta, and Interleukin-6 and significantly (p < 0.05) reduced levels/expression of serum/myocardial interleukin-10 in myocardial infarcted rats. Nevertheless, isoproterenol-induced rats treated with 3, 4-dihydroxybenzoic acid considerably (p < 0.05) attenuated all the biochemical, molecular, and IHC parameters investigated and inhibited oxidative stress and inflammation and protected the heart, through its antioxidant and anti-inflammatory mechanisms.

Effects of chronic quercetin treatment on antioxidant defence system and oxidative status of deoxycorticosterone acetate-salt-hypertensive rats.

We investigated the potential of chronic administration of an oral daily dose (10 mg/kg) of the dietary flavonoid quercetin to prevent hypertension and oxidative stress induced by deoxycorticosterone acetate (DOCA)-salt in rats. We have compared its effects to those produced by the well-known anti-hypertensive drug verapamil, administered orally (20 mg/kg/day). Quercetin and verapamil treatments reduced systolic blood pressure of DOCA-salt rats in approximately 67.6 and 63.3% respectively, producing no effect in control animals. Both drugs reduced significantly hepatic and renal hypertrophy induced by DOCA-salt administration, while only quercetin prevented cardiac hypertrophy. Decreased endothelium-dependent relaxation to acetylcholine of aortic rings from DOCA-salt-treated rats was improved by quercetin, but verapamil only enhanced it in the presence of superoxide dismutase (SOD) plus catalase. Increased plasma and heart thiobarbituric acid reactive substances (TBARS) and total glutathione (GSH) levels in liver and heart, decreased liver glutathione peroxidase (GPX) and liver and kidney glutathione transferase (GST) activities were observed in DOCA-salt-treated rats compared to the control animals. The antihypertensive effect of quercetin was accompanied by normalisation of plasma TBARS values, improvement of the antioxidant defences system in heart and liver, restoring total GSH levels in both organs and altered liver GST and GPX activities, and improving kidney GST activity. Verapamil treatment only restored GSH levels in heart, having no effect on other alterations induced by DOCA-salt chronic administration in the antioxidant defences analysed. In conclusion, quercetin shows both antihypertensive and antioxidant properties in this model of mineralocorticoid hypertension, while verapamil exhibits only antihypertensive effects.

Evidence that dimethyl sulfoxide inhibits defects of copper deficiency by inhibition of glycation

Prior studies have indicated that dimethyl sulfoxide (DMSO), when fed to rats, can inhibit the cardiac enlargement and anemia of a concurrent dietary copper (Cu) deficiency. Because DMSO is capable of chemically destroying the hydroxyl radical, its inhibition of defects of Cu deficiency was taken as evidence that those defects resulted from oxidative stress. To examine this conclusion further, rats were fed Cu-adequate (6.4 μg/g) and -deficient (0.5 μg/g) diets and given water with or without 5% DMSO. Two additional groups of rats were pair-fed to test for the effects of reduced food intake caused by DMSO. To test for mechanism of action of DMSO, indices of lipid peroxidation and nonenzymatic glycosylation of protein (glycation) were measured. Compared to Cu-adequate rats, Cu-deficient rats were anemic and had enlarged hearts, increased serum malondialdehyde (MDA), increased heart thiobarbituric acid reactive substances (TBARS) and an enhanced percentage of glycated hemoglobin (Hb A 1). Both DMSO administration and pair feeding ameliorated the anemia of Cu deficiency; pair feeding reduced the cardiac enlargement of Cu deficiency. Neither DMSO nor pair feeding inhibited the rise in serum MDA or heart TBARS, but both caused a similar degree of inhibition of the rise in Hb A 1. Although dietary Cu deficiency is associated with an increase in products of peroxidation, the inhibition of defects by DMSO appears to be related to food restriction and inhibition of glycation.

Vitamin E attenuates myocardial oxidative stress induced by DHEA in rested and exercised rats.

Sixty-four male Sprague-Dawley rats were randomly assigned to one of eight treatment groups to determine whether vitamin E (VitE) could help protect the heart from oxidative stress induced by either dehydroepiandrosterone (DHEA) or exercise. Oxidative stress was indicated by lipid peroxidation [i.e., thiobarbituric acid-reactive substances (TBARS)] and two scavenger enzymes. VitE supplementation (250 IU VitE/kg of diet) was given to one-half of the rats. DHEA acetate (0.35 mol/kg body wt) was injected intraperitoneally to one-half of the animals while the others were injected with corn oil vehicle. All treatments lasted for 5 wk. Next, 32 rats were randomly assigned to run for 1 h on a motorized rodent treadmill at 21 m/min up a 12% grade and then were killed. The remaining rats were killed at rest. Exercise increased TBARS in heart independent of treatment (1.94 +/- 0.12 vs. 2.43 +/- 0.11 nmol/mg protein). VitE attenuated the amount of TBARS in heart when DHEA was given. DHEA significantly increased TBARS in heart. Total and selenium-dependent glutathione peroxidase activities in heart were unaffected by any treatment. DHEA increased catalase activity at rest. Exercise increased catalase activity (71.5 +/- 7.9 vs. 97.4 +/- 9.5 mu mol x min-1 x mg protein-1); however, when VitE was given, the response to exercise was attenuated (74.1 +/- 8.4 vs. 80.9 +/- 9.9 mu mol center dot min-1 x mg protein-1). These results suggest that aerobic exercise and DHEA are mild oxidative stressors on the heart and that VitE supplementation can be beneficial in attenuating these combined stressors on the heart.

Influence of 12-week nicotine treatment and dietary copper on blood pressure and indices of the antioxidant system in male spontaneous hypertensive rats.

Nicotine treatment and copper (Cu) deficiency have been associated with an increased production of reactive oxygen species that may contribute to the development and/or progression of cardiovascular diseases (CVD). The present study investigated the influence of dietary Cu intake on the response to chronic nicotine treatment in spontaneous hypertensive rats (SHR) with respect to tissue trace mineral levels, several components of the oxidant defense system, and lipid peroxidation rates. SHR weighing 100-110 g were fed a Cu deficient diet (-Cu) (0.5 microgram Cu/g) for 14 d prior to nicotine treatment. SHR were inserted with tablets that released nicotine at a rate of 75 micrograms/h or placebo (control). Following tablet insertion, rats were fed a control diet (+Cu) (12.0 micrograms Cu/g) or the -Cu diet. Nicotine treatment lasted for 12 wk. Blood pressure (BP) was higher in nicotine-treated SHR than in control SHR at wk 3; BP was unaffected by diet. BP was higher in +Cu nicotine-treated SHR at wk 6 compared to -Cu nicotine and control rats. BP was not affected by nicotine or diet at wk 2. Liver, heart, and brain Cu levels and liver, heart, and red cell CuZn superoxide dismutase and plasma ceruloplasmin oxidase activities were lower in the -Cu SHR than in the +Cu SHR. Liver Fe levels were higher and plasma Fe levels were lower in the -Cu rats than in the +Cu rats. Liver selenium-dependent-glutathione peroxidase (Se-GSH-Px) activity was lower in the -Cu rats than in the +Cu rats; heart and thoracic aorta Se-GSH-Px activity was unaffected by -Cu diet. Thoracic aorta, liver, and heart GSH-reductase activities were unaffected by treatments. Plasma thiobarbituric acid reactive substances (TBARS) were higher in the -Cu than in the +Cu SHR. Liver and heart TBARS production was similar among the groups. These data show that nicotine can exacerbate the development of high BP in susceptible individuals; Cu deficiency did not exacerbate the effects of nicotine.

Cystine feeding enhances defects of dietary copper deficiency by a mechanism not involving oxidative stress

Dietary cystine supplementation exacerbates the effects of dietary copper deficiency. We examined the possibilities that this exacerbation is caused by an oxidative mechanism or by an effect on copper status. Male Sprague-Dawley rats (∼ 120 g) were fed copper-adequate or copper-deficient diets (0.5 or 16 mg/kg diet) that were supplemented with combinations of l-cystine (20 g/kg diet), vitamin E (37 mg/kg diet), and sodium tungstate (360 mg/L in drinking water). Dietary copper deficiency depressed serum and organ copper concentrations; increased heart size; caused anemia; reduced heart and liver superoxide dismutase and cytochrome c oxidase activities; and increased serum, heart, and liver thiobarbituric acid reactive substances. Cystine feeding exacerbated the cardiac enlargement and anemia of copper deficiency and reduced liver cytochrome oxidase and superoxide dismutase activities, but had no effect on organ copper content. Cystine feeding had no effect on serum or heart thiobarbituric acid reactive substances but depressed liver thiobarbituric acid reactive substances production. Neither vitamin E nor tungsten, which was used to inhibit sulfite oxidase and its potential production of free radicals, had an effect on the copper- or cystine-dependent changes in heart size, hematocrit, or hemoglobin. Dietary vitamin E and tungsten had variable beneficial effects on copper- and cystine-dependent changes in variables related to red blood cell size, but these effects could not be consistently related to the inhibition of TBARS production caused by vitamin E and tungsten. We conclude that, while cystine feeding enhanced signs of copper deficiency, it did not do so by an oxidative mechanism or by altering copper status.