scholarly journals Mitochondrial Dysfunctions and Altered Metals Homeostasis: New Weapons to Counteract HCV-Related Oxidative Stress

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Mario Arciello ◽  
Manuele Gori ◽  
Clara Balsano
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Metabolic Pathways ◽  
Energy Production ◽  
Power Plants ◽  
Focal Point ◽  
Antioxidant Defenses ◽  
Host Organism ◽  
Mitochondrial Dysfunctions

The hepatitis C virus (HCV) infection produces several pathological effects in host organism through a wide number of molecular/metabolic pathways. Today it is worldwide accepted that oxidative stress actively participates in HCV pathology, even if the antioxidant therapies adopted until now were scarcely effective. HCV causes oxidative stress by a variety of processes, such as activation of prooxidant enzymes, weakening of antioxidant defenses, organelle damage, and metals unbalance. A focal point, in HCV-related oxidative stress onset, is the mitochondrial failure. These organelles, known to be the “power plants” of cells, have a central role in energy production, metabolism, and metals homeostasis, mainly copper and iron. Furthermore, mitochondria are direct viral targets, because many HCV proteins associate with them. They are the main intracellular free radicals producers and targets. Mitochondrial dysfunctions play a key role in the metal imbalance. This event, today overlooked, is involved in oxidative stress exacerbation and may play a role in HCV life cycle. In this review, we summarize the role of mitochondria and metals in HCV-related oxidative stress, highlighting the need to consider their deregulation in the HCV-related liver damage and in the antiviral management of patients.

scholarly journals Mitochondrial Sirtuins in Reproduction

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1047
Author(s):  
Giovanna Di Emidio ◽  
Stefano Falone ◽  
Paolo Giovanni Artini ◽  
Fernanda Amicarelli ◽  
Anna Maria D’Alessandro ◽  
...  
Keyword(s):  
Stress Responses ◽  
Metabolic Pathways ◽  
Redox Balance ◽  
Antioxidant Defenses ◽  
Metabolic Abnormalities ◽  
Female Reproduction ◽  
Mitochondrial Dysfunctions ◽  
Early Embryos ◽  
The Relationship

Mitochondria act as hubs of numerous metabolic pathways. Mitochondrial dysfunctions contribute to altering the redox balance and predispose to aging and metabolic alterations. The sirtuin family is composed of seven members and three of them, SIRT3-5, are housed in mitochondria. They catalyze NAD+-dependent deacylation and the ADP-ribosylation of mitochondrial proteins, thereby modulating gene expression and activities of enzymes involved in oxidative metabolism and stress responses. In this context, mitochondrial sirtuins (mtSIRTs) act in synergistic or antagonistic manners to protect from aging and aging-related metabolic abnormalities. In this review, we focus on the role of mtSIRTs in the biological competence of reproductive cells, organs, and embryos. Most studies are focused on SIRT3 in female reproduction, providing evidence that SIRT3 improves the competence of oocytes in humans and animal models. Moreover, SIRT3 protects oocytes, early embryos, and ovaries against stress conditions. The relationship between derangement of SIRT3 signaling and the imbalance of ROS and antioxidant defenses in testes has also been demonstrated. Very little is known about SIRT4 and SIRT5 functions in the reproductive system. The final goal of this work is to understand whether sirtuin-based signaling may be taken into account as potential targets for therapeutic applications in female and male infertility.

scholarly journals The Role of Oxidative Stress, Mitochondrial Function, and Autophagy in Diabetic Polyneuropathy

2017 ◽  
Vol 2017 ◽  
pp. 1-15 ◽  
Author(s):  
Sonia Sifuentes-Franco ◽  
Fermín Paul Pacheco-Moisés ◽  
Adolfo Daniel Rodríguez-Carrizalez ◽  
Alejandra Guillermina Miranda-Díaz
Keyword(s):  
Oxidative Stress ◽  
Metabolic Pathways ◽  
Metabolic Diseases ◽  
Mitochondrial Fission ◽  
Diabetic Polyneuropathy ◽  
Stress Factors ◽  
Antioxidant Defenses ◽  
Stress Hyperglycemia ◽  
Antioxidant Agents

Diabetic polyneuropathy (DPN) is the most frequent and prevalent chronic complication of diabetes mellitus (DM). The state of persistent hyperglycemia leads to an increase in the production of cytosolic and mitochondrial reactive oxygen species (ROS) and favors deregulation of the antioxidant defenses that are capable of activating diverse metabolic pathways which trigger the presence of nitro-oxidative stress (NOS) and endoplasmic reticulum stress. Hyperglycemia provokes the appearance of micro- and macrovascular complications and favors oxidative damage to the macromolecules (lipids, carbohydrates, and proteins) with an increase in products that damage the DNA. Hyperglycemia produces mitochondrial dysfunction with deregulation between mitochondrial fission/fusion and regulatory factors. Mitochondrial fission appears early in diabetic neuropathy with the ability to facilitate mitochondrial fragmentation. Autophagy is a catabolic process induced by oxidative stress that involves the formation of vesicles by the lysosomes. Autophagy protects cells from diverse stress factors and routine deterioration. Clarification of the mechanisms involved in the appearance of complications in DM will facilitate the selection of specific therapeutic options based on the mechanisms involved in the metabolic pathways affected. Nowadays, the antioxidant agents consumed exogenously form an adjuvant therapeutic alternative in chronic degenerative metabolic diseases, such as DM.

scholarly journals Oxidative Stress Levels in Orthodontic Patients and Efficacy of Antioxidant Supplements in Combating Its Effects- A Randomized Clinical Study

2019 ◽  
Vol 9 (2) ◽  
pp. 29-34
Author(s):  
Sheetal Yamyar ◽  
Suchita Daokar
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Orthodontic Appliances ◽  
Randomized Clinical Study ◽  
Gingival Health ◽  
Orthodontic Patients ◽  
Group A ◽  
Antioxidant Supplements ◽  
Group B

Introduction: Orthodontic appliances are considered to be biocompatible although adverse effects attributed to release of nickel ion which are free radicals in oral cavity. These free radical produce damages both in cellular and extracellular components phospholipid membrane, proteins, mitochondrial and nuclear DNA leading to Oxidative stress which is normally counter balanced by the action antioxidant mechanisms. However in higher concentrations of free radicals resulting in cellular death and apoptosis Orthodontic appliances such as brackets, wire, resins has considered as potential allergen leading to release of free radicals. The study was conducted to determine and compare the role of oxidative stress and role of antioxidants in saliva of patients undergoing fixed orthodontic appliances therapy at different time intervals. Materials & Method: A double-blinded, parallel, randomized clinical study was designed consisting of 40 healthy participants, aged 15-30yrs. The samples were divided into two groups Group A without antioxidants supplements and Group B with antioxidants supplements. Salivary MDA levels and gingival health index was recorded at different time intervals from each group. Salivary Lipid peroxidation (Malondialdehyde) level was estimated using Thiobarbituric acid (TBA) method and gingival status was investigated using Silness & Loe gingival index. Intragroup and intergroup comparison was statistically analyzed using student’s paired T test. Result: Increased salivary MDA levels and mild to moderate amount of gingivitis is seen in both groups. This is more pronounced after 24 hours of appliance placement. Improvement in salivary MDA levels and gingival health status is observed during the course of treatment, In Group B the salivary MDA levels and gingival health index score reached below their pretreatment values. However even after a span of 3 months the levels remained higher to their base values in Group A. Conclusion: Improvement in salivary MDA levels and gingival health status is observed following antioxidant therapy during course of treatment, indicating combating nature of antioxidant supplements in orthodontic patients.

scholarly journals Curcumin Ameliorates Lead-Induced Hepatotoxicity by Suppressing Oxidative Stress and Inflammation, and Modulating Akt/GSK-3β Signaling Pathway

Biomolecules ◽  
2019 ◽  
Vol 9 (11) ◽  
pp. 703 ◽  
Author(s):  
Ahlam Alhusaini ◽  
Laila Fadda ◽  
Iman H. Hasan ◽  
Enas Zakaria ◽  
Abeer M. Alenazi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caspase 3 ◽  
Tissue Injury ◽  
Elevated Serum ◽  
Antioxidant Defenses ◽  
Exact Role ◽  
Toxic Heavy Metal ◽  
Tnf Α ◽  
Gsk 3Β

Lead (Pb) is a toxic heavy metal pollutant with adverse effects on the liver and other body organs. Curcumin (CUR) is the principal curcuminoid of turmeric and possesses strong antioxidant and anti-inflammatory activities. This study explored the protective effect of CUR on Pb hepatotoxicity with an emphasis on oxidative stress, inflammation and Akt/GSK-3β signaling. Rats received lead acetate and CUR and/or ascorbic acid (AA) for seven days and samples were collected for analyses. Pb(II) induced liver injury manifested by elevated serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH), as well as histopathological alterations, including massive hepatocyte degeneration and increased collagen deposition. Lipid peroxidation, nitric oxide, TNF-α and DNA fragmentation were increased, whereas antioxidant defenses were diminished in the liver of Pb(II)-intoxicated rats. Pb(II) increased hepatic NF-κB and JNK phosphorylation and caspase-3 cleavage, whereas Akt and GSK-3β phosphorylation was decreased. CUR and/or AA ameliorated liver function, prevented tissue injury, and suppressed oxidative stress, DNA damage, NF-κB, JNK and caspase-3. In addition, CUR and/or AA activated Akt and inhibited GSK-3β in Pb(II)-induced rats. In conclusion, CUR prevents Pb(II) hepatotoxicity via attenuation of oxidative injury and inflammation, activation of Akt and inhibition of GSK-3β. However, further studies scrutinizing the exact role of Akt/GSK-3β signaling are recommended.

scholarly journals The Role of Oxidative Stress in Myocardial Ischemia and Reperfusion Injury and Remodeling: Revisited

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Gino A. Kurian ◽  
Rashmi Rajagopal ◽  
Srinivasan Vedantham ◽  
Mohanraj Rajesh
Keyword(s):  
Oxidative Stress ◽  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Antioxidant Defenses ◽  
Common Denominator ◽  
Myocardial Ischemia And Reperfusion ◽  
Reductive Stress ◽  
Myocardial Infraction

Oxidative and reductive stress are dual dynamic phases experienced by the cells undergoing adaptation towards endogenous or exogenous noxious stimulus. The former arises due to the imbalance between the reactive oxygen species production and antioxidant defenses, while the latter is due to the aberrant increase in the reducing equivalents. Mitochondrial malfunction is the common denominator arising from the aberrant functioning of the rheostat that maintains the homeostasis between oxidative and reductive stress. Recent experimental evidences suggest that the maladaptation during oxidative stress could play a pivotal role in the pathophysiology of major cardiovascular diseases such as myocardial infraction, atherosclerosis, and diabetic cardiovascular complications. In this review we have discussed the role of oxidative and reductive stress pathways in the pathogenesis of myocardial ischemia/reperfusion injury and diabetic cardiomyopathy (DCM). Furthermore, we have provided impetus for the development of subcellular organelle targeted antioxidant drug therapy for thwarting the deterioration of the failing myocardium in the aforementioned cardiovascular conditions.

Oxidative Damage in the Liver of Rats Treated With Glycolaldehyde

2011 ◽  
Vol 30 (2) ◽  
pp. 253-258 ◽  
Author(s):  
Rodrigo Lorenzi ◽  
Michael Everton Andrades ◽  
Rafael Calixto Bortolin ◽  
Ryoji Nagai ◽  
Felipe Dal-Pizzol ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Failure ◽  
Protein Function ◽  
Liver Diseases ◽  
Protein Carbonyl ◽  
Antioxidant Defenses ◽  
Stress Markers ◽  
Glycation End Products ◽  
Carboxymethyl Lysine

Liver diseases are often associated with hyperglycemia, inflammation, and oxidative stress. These conditions, commonly associated with diabetes mellitus and obesity, facilitate the formation of advanced glycation end products (AGEs). These products are known to impair protein function and promote inflammation. Accumulation of AGEs such as Nε-(carboxymethyl)lysine (CML) is related to chronic liver diseases and their severity. Although several reports suggest a crucial role of AGEs in liver failure, there is little investigation on the direct effects of reducing sugars, precursors of AGEs, and on the onset and progression of liver failure. In this work, we investigate the effects of intravenously administrated glycolaldehyde (GA), a short-chain aldehyde, on oxidative parameters in the liver of Wistar rats. Animals received a single injection of GA (10, 50, or 100 mg/kg) and were sacrificed after 6, 12, or 24 hours. Levels of protein carbonyl, lipid peroxidation, and reduced thiol were quantified. The activities of catalase, superoxide dismutase, and glyoxalase I were also assessed. The amount of CML was quantified with specific antibody. There was an increase in oxidative stress markers in the liver of GA-treated rats. Glycolaldehyde induced a decrease in the activities of all enzymes assayed. Also, all tested doses led to an increase in CML content. Our data suggest that GA might play an important role in liver diseases through the impairment of antioxidant defenses and generation of AGEs.

scholarly journals Role of vitamin B6 status on antioxidant defenses, glutathione, and related enzyme activities in mice with homocysteine-induced oxidative stress

2015 ◽  
Vol 59 (1) ◽  
pp. 25702 ◽  
Author(s):  
Cheng-Chin Hsu ◽  
Chien-Hsiang Cheng ◽  
Chin-Lin Hsu ◽  
Wan-Ju Lee ◽  
Shih-Chien Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Enzyme Activities ◽  
Vitamin B6 ◽  
Antioxidant Defenses ◽  
Related Enzyme

scholarly journals Comparison of Oxidant-Antioxidant Status in Patients with Vitiligo and Healthy Population

2015 ◽  
Vol 12 (2) ◽  
pp. 132-136 ◽  
Author(s):  
S Agrawal ◽  
A Kumar ◽  
TK Dhali ◽  
SK Majhi
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Vitamin E ◽  
Vitamin C ◽  
Control Group ◽  
Healthy Population ◽  
Significant Difference ◽  
Destruction Of Melanocytes ◽  
And Control

Background Vitiligo is a well-recognized pigmentary disorder of the skin and /or mucous membrane characterized by circumscribed ivory or chalky white macules devoid of identifiable melanocytes. The pathogenesis of vitiligo is complex and still not well understood. According to autocytotoxic hypothesis, oxidative stress has been suggested to be the initial pathogenic event in melanocyte degeneration. The role of free radicals and oxidative damage in the pathophysiology of vitiligo has been documented in recent studies.Objective To evaluate the role of oxidative stress in patients with vitiligo and of healthy controls by measuring levels of the oxidant malondialdehyde (MDA) and antioxidants vitamin C and vitamin E in serum and catalase (CAT) in erythrocytes.Method A total of 80 clinically diagnosed cases of vitiligo and 80 control subjects were included in the study to assess the activity of MDA, vitamin C and vitamin E in serum and CAT in erythrocytes of patients and controls by using the spectrophotometric assay.Result There was statistically significant increase in the levels of MDA in patients with vitiligo compared to the control group (p<0.001). No significant difference was found in the levels of vitamin C (p=0.411) and vitamin E (p=0.771) between the patients with vitiligo and control group. The levels of CAT in the vitiligo patients were found to be significantly lower than those of controls (p<0.001).Conclusion Increased oxidative stress and decreased catalase have been observed in vitiligo patients and the data suggesting that the free radicals may be involved in the destruction of melanocytes or dysregulation of melanogenesis.Kathmandu University Medical Journal Vol.12(2) 2014: 132-136

scholarly journals Oxidative stress in dogs

2016 ◽  
Vol 37 (3) ◽  
pp. 1431 ◽  
Author(s):  
Claudia Russo ◽  
Ana Paula F. Rodrigues Loureiro Bracarense
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Free Radicals ◽  
Cell Membrane ◽  
The Body ◽  
Antioxidant Defenses ◽  
Cellular Respiration ◽  
Bodily Fluids ◽  
Cellular Components ◽  
Harmful Effects

Reactive oxygen species (ROS), also known as free radicals, are generated during cellular respiration. Under normal conditions, the body has the ability to neutralize the effects of free radicals by using its antioxidant defenses. In the case of an imbalance between oxidants and antioxidants, free radical production exceeds the capacity of organic combustion, resulting in oxidative stress. Of all the cellular components compromised by the harmful effects of ROS, the cell membrane is the most severely affected owing to lipid peroxidation, which invariably leads to changes in the membrane structure and permeability. With lipid peroxidation of the cell membrane, some by-products can be detected and measured in tissues, blood, and other bodily fluids. The measurement of biomarkers of oxidative stress is commonly used to quantify lipid peroxidation of the cell membrane in humans, a species in which ROS can be considered as a cause or consequence of oxidative stress-related diseases. In dogs, few studies have demonstrated this correlation. The present review aims to identify current literature knowledge relating to oxidative stress diseases and their detection in dogs.

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