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13 pages, 12391 KiB

Open AccessArticle

Resveratrol Protects against Cerebral Ischemic Injury via Restraining Lipid Peroxidation, Transition Elements, and Toxic Metal Levels, but Enhancing Anti-Oxidant Activity

by Ming-Cheng Lin, Chien-Chi Liu, Yu-Chen Lin and Chin-Sheng Liao

Antioxidants 2021, 10(10), 1515; https://doi.org/10.3390/antiox10101515 - 24 Sep 2021

Cited by 16 | Viewed by 1925

Abstract

Cerebral ischemia is related to increased oxidative stress. Resveratrol displays anti-oxidant and anti-inflammatory properties. The transition elements iron (Fe) and copper (Cu) are indispensable for the brain but overload is deleterious to brain function. Aluminum (Al) and arsenic (As) are toxic metals that [...] Read more.

Cerebral ischemia is related to increased oxidative stress. Resveratrol displays anti-oxidant and anti-inflammatory properties. The transition elements iron (Fe) and copper (Cu) are indispensable for the brain but overload is deleterious to brain function. Aluminum (Al) and arsenic (As) are toxic metals that seriously threaten brain health. This study was conducted to elucidate the correlation of the neuroprotective mechanism of resveratrol to protect cerebral ischemic damage with modulation of the levels of lipid peroxidation, anti-oxidants, transition elements, and toxic metals. Experimentally, 20 mg/kg of resveratrol was given once daily for 10 days. The cerebral ischemic operation was performed via occlusion of the right common carotid artery together with the right middle cerebral artery for 60 min followed by homogenization of the brain cortex and collection of supernatants for biochemical analysis. In the ligation group, levels of malondialdehyde, Fe, Cu, Al, and As increased but those of the anti-oxidants superoxide dismutase and catalase decreased. Pretreating rats with resveratrol before ischemia significantly reversed these effects. Our findings highlight the association of overload of Fe, Cu, As, and Al with the pathophysiology of cerebral ischemia. In conclusion, resveratrol protects against cerebral ischemic injury via restraining lipid peroxidation, transition elements, and toxic metals, but increasing anti-oxidant activity. Full article

(This article belongs to the Special Issue Oxidative/Nitrosative Stress-Related Mechanisms and Antioxidant Therapy in Cardiovascular Diseases)

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11 pages, 2556 KiB

Open AccessArticle

Mitochondrial Oxidation of the Cytoplasmic Reducing Equivalents at the Onset of Oxidant Stress in the Isoproterenol-Induced Rat Myocardial Infarction

by Olivia Vázquez-Martínez, Mauricio Díaz-Muñoz, Fernando López-Barrera and Rolando Hernández-Muñoz

Antioxidants 2021, 10(9), 1444; https://doi.org/10.3390/antiox10091444 - 11 Sep 2021

Cited by 2 | Viewed by 2204

Abstract

We have developed and characterized a model of isoproterenol (ISO)-induced myocardial necrosis, identifying three stages of cardiac damage: a pre-infarction (0–12 h), infarction (24 h), and post-infarction period (48–96 h). Using this model, we have previously found alterations in calcium homeostasis and their [...] Read more.

We have developed and characterized a model of isoproterenol (ISO)-induced myocardial necrosis, identifying three stages of cardiac damage: a pre-infarction (0–12 h), infarction (24 h), and post-infarction period (48–96 h). Using this model, we have previously found alterations in calcium homeostasis and their relationship with oxidant stress in mitochondria, which showed deficient oxygen consumption and coupled ATP synthesis. Therefore, the present study was aimed at assessing the mitochondrial ability to transport and oxidize cytoplasmic reducing equivalents (NADH), correlating the kinetic parameters of the malate-aspartate shuttle, oxidant stress, and mitochondrial functionality. Our results showed only discreet effects during the cardiotoxic ISO action on the endogenous malate-aspartate shuttle activity, suggesting that endogenous mitochondrial NADH oxidation capacity (Nohl dehydrogenase) was not affected by the cellular stress. On the contrary, the reconstituted system showed significant enhancement in maximal capacity of the malate-aspartate shuttle activity only at later times (post-infarction period), probably as a compensatory part of cardiomyocytes’ response to the metabolic and functional consequences of the infarcted tissue. Therefore, these findings support the notion that heart damage associated with myocardial infarction suffers a set of sequential biochemical and metabolic modifications within cardiomyocytes, where mitochondrial activity, controlling the redox state, could play a relevant role. Full article

(This article belongs to the Special Issue Oxidative/Nitrosative Stress-Related Mechanisms and Antioxidant Therapy in Cardiovascular Diseases)

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14 pages, 1136 KiB

Open AccessArticle

Association of Particulate Matter from Cooking Oil Fumes with Heart Rate Variability and Oxidative Stress

by Chang-Chuan Chan, Lian-Yu Lin, Ching-Huang Lai, Kai-Jen Chuang, Ming-Tsang Wu and Chih-Hong Pan

Antioxidants 2021, 10(8), 1323; https://doi.org/10.3390/antiox10081323 - 23 Aug 2021

Cited by 6 | Viewed by 2295

Abstract

Many studies have reported various cardiovascular autonomic responses to ambient particulate matter (PM) pollution, but few have reported such responses to occupational PM exposures. Even fewer have demonstrated a relationship between PM pollution and oxidative stress in humans. This panel study evaluates the [...] Read more.

Many studies have reported various cardiovascular autonomic responses to ambient particulate matter (PM) pollution, but few have reported such responses to occupational PM exposures. Even fewer have demonstrated a relationship between PM pollution and oxidative stress in humans. This panel study evaluates the association between occupational exposure to PM in cooking oil fumes (COFs), and changes in both heart rate variability (HRV) and oxidative stress responses in 54 male Chinese cooks. Linear mixed-effects regression models were adopted to estimate the strength of the association between PM and HRV. Participants’ pre- and post-workshift urine samples were analyzed for 8-hydroxy-2′-deoxyguanosine (8-OHdG) and malondialdehyde (MDA). Exposure to PM in COFs from 15 min to 2 h were associated with a decrease in HRV and an increase in heart rate among cooks. The urinary 8-OHdG levels of cooks were significantly elevated after workshift exposure to COFs. The levels of PM_2.5, PM_1.0, and particulate benzo(a)pyrene in COFs were all positively correlated with cross-workshift urinary 8-OHdG levels. Furthermore, the levels of benzo(a)pyrene in COFs were positively correlated with cross-workshift urinary MDA levels. The effects of COFs on HRV were independent of cross-workshift urinary 8-OHdG levels. Exposure to COFs leads to disturbed autonomic function and an increased risk of oxidative DNA injury among cooks in Chinese restaurants. Full article

(This article belongs to the Special Issue Oxidative/Nitrosative Stress-Related Mechanisms and Antioxidant Therapy in Cardiovascular Diseases)

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13 pages, 2251 KiB

Open AccessArticle

Pharmacological Inhibition of S-Nitrosoglutathione Reductase Reduces Cardiac Damage Induced by Ischemia–Reperfusion

by Oscar Arriagada Castillo, Gustavo Herrera, Carlos Manriquez, Andrea F. Rojas and Daniel R. González

Antioxidants 2021, 10(4), 555; https://doi.org/10.3390/antiox10040555 - 02 Apr 2021

Cited by 4 | Viewed by 2014

Abstract

The cardioprotective effects of nitric oxide (NO) have been described through S-nitrosylation of several important proteins in the mitochondria of the cardiomyocyte. S-nitrosoglutathione reductase (GSNOR) is an enzyme involved in the metabolism of S-nitrosothiols by producing denitrosylation, thus limiting the cardioprotective effect of [...] Read more.

The cardioprotective effects of nitric oxide (NO) have been described through S-nitrosylation of several important proteins in the mitochondria of the cardiomyocyte. S-nitrosoglutathione reductase (GSNOR) is an enzyme involved in the metabolism of S-nitrosothiols by producing denitrosylation, thus limiting the cardioprotective effect of NO. The effect of GSNOR inhibition on the damage by cardiac ischemia–reperfusion is still unclear. We tested the hypothesis that pharmacological inhibition of GSNOR promotes cardioprotection by increasing the levels of protein S-nitrosylation. In a model of ischemia–reperfusion in isolated rat heart, the effect of a GSNOR inhibitor, 5-chloro-3-(2-[4-ethoxyphenyl) (ethyl) amino]-2-oxoethyl)-1H-indole-2-carboxylic acid (C2), was investigated. Ventricular function and hemodynamics were determined, in addition to tissue damage and S-nitrosylation of mitochondrial proteins. Hearts treated with C2 showed a lower release of myocardial damage marker creatine kinase and a reduction in the infarcted area. It also improved post-ischemia ventricular function compared to controls. These results were associated with increasing protein S-nitrosylation, specifically of the mitochondrial complexes III and V. The pharmacological inhibition of GSNOR showed a concentration-dependent cardioprotective effect, being observed in functional parameters and myocardial damage, which was maximal at 1 µmol/L, associated with increased S-nitrosylation of mitochondrial proteins. These data suggest that GSNOR is an interesting pharmacological target for cardiac reperfusion injury. Full article

(This article belongs to the Special Issue Oxidative/Nitrosative Stress-Related Mechanisms and Antioxidant Therapy in Cardiovascular Diseases)

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16 pages, 1740 KiB

Open AccessArticle

The Hypoxia Tolerance of the Goldfish (Carassius auratus) Heart: The NOS/NO System and Beyond

by Mariacristina Filice, Rosa Mazza, Serena Leo, Alfonsina Gattuso, Maria Carmela Cerra and Sandra Imbrogno

Antioxidants 2020, 9(6), 555; https://doi.org/10.3390/antiox9060555 - 26 Jun 2020

Cited by 12 | Viewed by 3366

Abstract

The extraordinary capacity of the goldfish (Carassius auratus) to increase its cardiac performance under acute hypoxia is crucial in ensuring adequate oxygen supply to tissues and organs. However, the underlying physiological mechanisms are not yet completely elucidated. By employing an ex [...] Read more.

The extraordinary capacity of the goldfish (Carassius auratus) to increase its cardiac performance under acute hypoxia is crucial in ensuring adequate oxygen supply to tissues and organs. However, the underlying physiological mechanisms are not yet completely elucidated. By employing an ex vivo working heart preparation, we observed that the time-dependent enhancement of contractility, distinctive of the hypoxic goldfish heart, is abolished by the Nitric Oxide Synthase (NOS) antagonist L-NMMA, the Nitric Oxide (NO) scavenger PTIO, as well as by the PI3-kinase (PI3-K) and sarco/endoplasmic reticulum Ca²⁺-ATPase 2a (SERCA2a) pumps’ inhibition by Wortmannin and Thapsigargin, respectively. In goldfish hearts exposed to hypoxia, an ELISA test revealed no changes in cGMP levels, while Western Blotting analysis showed an enhanced expression of the phosphorylated protein kinase B (pAkt) and of the NADPH oxidase catalytic subunit Nox2 (gp91phox). A significant decrease of protein S-nitrosylation was observed by Biotin Switch assay in hypoxic hearts. Results suggest a role for a PI3-K/Akt-mediated activation of the NOS-dependent NO production, and SERCA2a pumps in the mechanisms conferring benefits to the goldfish heart under hypoxia. They also propose protein denitrosylation, and the possibility of nitration, as parallel intracellular events. Full article

(This article belongs to the Special Issue Oxidative/Nitrosative Stress-Related Mechanisms and Antioxidant Therapy in Cardiovascular Diseases)

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Review

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19 pages, 1291 KiB

Open AccessReview

Glutathione Participation in the Prevention of Cardiovascular Diseases

by Deyamira Matuz-Mares, Héctor Riveros-Rosas, María Magdalena Vilchis-Landeros and Héctor Vázquez-Meza

Antioxidants 2021, 10(8), 1220; https://doi.org/10.3390/antiox10081220 - 29 Jul 2021

Cited by 59 | Viewed by 12138

Abstract

Cardiovascular diseases (CVD) (such as occlusion of the coronary arteries, hypertensive heart diseases and strokes) are diseases that generate thousands of patients with a high mortality rate worldwide. Many of these cardiovascular pathologies, during their development, generate a state of oxidative stress that [...] Read more.

Cardiovascular diseases (CVD) (such as occlusion of the coronary arteries, hypertensive heart diseases and strokes) are diseases that generate thousands of patients with a high mortality rate worldwide. Many of these cardiovascular pathologies, during their development, generate a state of oxidative stress that leads to a deterioration in the patient’s conditions associated with the generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS). Within these reactive species we find superoxide anion (O₂^•–), hydroxyl radical (^•OH), nitric oxide (NO^•), as well as other species of non-free radicals such as hydrogen peroxide (H₂O₂), hypochlorous acid (HClO) and peroxynitrite (ONOO^–). A molecule that actively participates in counteracting the oxidizing effect of reactive species is reduced glutathione (GSH), a tripeptide that is present in all tissues and that its synthesis and/or regeneration is very important to be able to respond to the increase in oxidizing agents. In this review, we will address the role of glutathione, its synthesis in both the heart and the liver, and its importance in preventing or reducing deleterious ROS effects in cardiovascular diseases. Full article

(This article belongs to the Special Issue Oxidative/Nitrosative Stress-Related Mechanisms and Antioxidant Therapy in Cardiovascular Diseases)

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17 pages, 783 KiB

Open AccessReview

Roles and Therapeutic Implications of Endoplasmic Reticulum Stress and Oxidative Stress in Cardiovascular Diseases

by Yan Zhou, Dharmani Devi Murugan, Haroon Khan, Yu Huang and Wai San Cheang

Antioxidants 2021, 10(8), 1167; https://doi.org/10.3390/antiox10081167 - 22 Jul 2021

Cited by 33 | Viewed by 4281

Abstract

In different pathological states that cause endoplasmic reticulum (ER) calcium depletion, altered glycosylation, nutrient deprivation, oxidative stress, DNA damage or energy perturbation/fluctuations, the protein folding process is disrupted and the ER becomes stressed. Studies in the past decade have demonstrated that ER stress [...] Read more.

In different pathological states that cause endoplasmic reticulum (ER) calcium depletion, altered glycosylation, nutrient deprivation, oxidative stress, DNA damage or energy perturbation/fluctuations, the protein folding process is disrupted and the ER becomes stressed. Studies in the past decade have demonstrated that ER stress is closely associated with pathogenesis of obesity, insulin resistance and type 2 diabetes. Excess nutrients and inflammatory cytokines associated with metabolic diseases can trigger or worsen ER stress. ER stress plays a critical role in the induction of endothelial dysfunction and atherosclerosis. Signaling pathways including AMP-activated protein kinase and peroxisome proliferator-activated receptor have been identified to regulate ER stress, whilst ER stress contributes to the imbalanced production between nitric oxide (NO) and reactive oxygen species (ROS) causing oxidative stress. Several drugs or herbs have been proved to protect against cardiovascular diseases (CVD) through inhibition of ER stress and oxidative stress. The present article reviews the involvement of ER stress and oxidative stress in cardiovascular dysfunction and the potential therapeutic implications. Full article

(This article belongs to the Special Issue Oxidative/Nitrosative Stress-Related Mechanisms and Antioxidant Therapy in Cardiovascular Diseases)

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23 pages, 1292 KiB

Open AccessReview

Implications of Oxidative and Nitrosative Post-Translational Modifications in Therapeutic Strategies against Reperfusion Damage

by Mabel Buelna-Chontal, Wylly R. García-Niño, Alejandro Silva-Palacios, Cristina Enríquez-Cortina and Cecilia Zazueta

Antioxidants 2021, 10(5), 749; https://doi.org/10.3390/antiox10050749 - 08 May 2021

Cited by 10 | Viewed by 2528

Abstract

Post-translational modifications based on redox reactions “switch on-off” the biological activity of different downstream targets, modifying a myriad of processes and providing an efficient mechanism for signaling regulation in physiological and pathological conditions. Such modifications depend on the generation of redox components, such [...] Read more.

Post-translational modifications based on redox reactions “switch on-off” the biological activity of different downstream targets, modifying a myriad of processes and providing an efficient mechanism for signaling regulation in physiological and pathological conditions. Such modifications depend on the generation of redox components, such as reactive oxygen species and nitric oxide. Therefore, as the oxidative or nitrosative milieu prevailing in the reperfused heart is determinant for protective signaling, in this review we defined the impact of redox-based post-translational modifications resulting from either oxidative/nitrosative signaling or oxidative/nitrosative stress that occurs during reperfusion damage. The role that cardioprotective conditioning strategies have had to establish that such changes occur at different subcellular levels, particularly in mitochondria, is also presented. Another section is devoted to the possible mechanism of signal delivering of modified proteins. Finally, we discuss the possible efficacy of redox-based therapeutic strategies against reperfusion damage. Full article

(This article belongs to the Special Issue Oxidative/Nitrosative Stress-Related Mechanisms and Antioxidant Therapy in Cardiovascular Diseases)

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