scholarly journals Improvement of Oxidative Stress and Mitochondrial Dysfunction by β-Caryophyllene: A Focus on the Nervous System

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 546
Author(s):  
Hammad Ullah ◽  
Alessandro Di Minno ◽  
Cristina Santarcangelo ◽  
Haroon Khan ◽  
Maria Daglia
Keyword(s):  
Oxidative Stress ◽  
Electron Transport ◽  
Mitochondrial Dysfunction ◽  
Neurodegenerative Disorders ◽  
Cannabinoid Receptor ◽  
Neuronal Loss ◽  
Food Plants ◽  
Active Principle ◽  
Atp Production ◽  
Anticancer Properties

Mitochondrial dysfunction results in a series of defective cellular events, including decreased adenosine triphosphate (ATP) production, enhanced reactive oxygen species (ROS) output, and altered proteastasis and cellular quality control. An enhanced output of ROS may damage mitochondrial components, such as mitochondrial DNA and elements of the electron transport chain, resulting in the loss of proper electrochemical gradient across the mitochondrial inner membrane and an ensuing shutdown of mitochondrial energy production. Neurons have an increased demand for ATP and oxygen, and thus are more prone to damage induced by mitochondrial dysfunction. Mitochondrial dysfunction, damaged electron transport chains, altered membrane permeability and Ca2+ homeostasis, and impaired mitochondrial defense systems induced by oxidative stress, are pathological changes involved in neurodegenerative disorders. A growing body of evidence suggests that the use of antioxidants could stabilize mitochondria and thus may be suitable for preventing neuronal loss. Numerous natural products exhibit the potential to counter oxidative stress and mitochondrial dysfunction; however, science is still looking for a breakthrough in the treatment of neurodegenerative disorders. β-caryophyllene is a bicyclic sesquiterpene, and an active principle of essential oils derived from a large number of spices and food plants. As a selective cannabinoid receptor 2 (CB2) agonist, several studies have reported it as possessing numerous pharmacological activities such as antibacterial (e.g., Helicobacter pylori), antioxidant, anti-inflammatory, analgesic (e.g., neuropathic pain), anti-neurodegenerative and anticancer properties. The present review mainly focuses on the potential of β-caryophyllene in reducing oxidative stress and mitochondrial dysfunction, and its possible links with neuroprotection.

Mitochondrial Dysfunction in Aging and Neurodegeneration

2019 ◽  
pp. 76-101
Author(s):  
Vaibhav Walia ◽  
Munish Garg
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Mitochondrial Dysfunction ◽  
Neurodegenerative Disorders ◽  
Electron Transport Chain ◽  
Tricarboxylic Acid ◽  
Atp Production ◽  
Important Target ◽  
Transport Chain ◽  
Cellular Apoptosis

Mitochondria are a dynamic organelle of the cell involved in the various biological processes. Mitochondria are the site of the adenosine triphosphate (ATP) production, electron transport chain (ETC), oxidation of fatty acids, tricarboxylic acid (TCA), and cellular apoptosis. Besides these, mitochondria are the site of production of reactive oxygen species (ROS), which further disrupts the normal functioning of this organelle also making mitochondria itself as an important target of oxidative stress. Thus, mitochondria serve as an important target in the process of neurodegeneration. In the present chapter, the authors describe mitochondria and its functioning, dynamics, and the mitochondrial dysfunction in aging and neurodegenerative disorders (NDs).

scholarly journals Honeybush Extracts (Cyclopia spp.) Rescue Mitochondrial Functions and Bioenergetics against Oxidative Injury

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Anastasia Agapouda ◽  
Veronika Butterweck ◽  
Matthias Hamburger ◽  
Dalene de Beer ◽  
Elizabeth Joubert ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Hot Water ◽  
Human Neuroblastoma ◽  
Atp Production ◽  
Physiological Conditions ◽  
Age Related ◽  
Mitochondrial Functions ◽  
Scientific Attention

Mitochondrial dysfunction plays a major role not only in the pathogenesis of many oxidative stress or age-related diseases such as neurodegenerative as well as mental disorders but also in normal aging. There is evidence that oxidative stress and mitochondrial dysfunction are the most upstream and common events in the pathomechanisms of neurodegeneration. Cyclopia species are endemic South African plants and some have a long tradition of use as herbal tea, known as honeybush tea. Extracts of the tea are gaining more scientific attention due to their phenolic composition. In the present study, we tested not only the in vitro mitochondria-enhancing properties of honeybush extracts under physiological conditions but also their ameliorative properties under oxidative stress situations. Hot water and ethanolic extracts of C. subternata, C. genistoides, and C. longifolia were investigated. Pretreatment of human neuroblastoma SH-SY5Y cells with honeybush extracts, at a concentration range of 0.1-1 ng/ml, had a beneficial effect on bioenergetics as it increased ATP production, respiration, and mitochondrial membrane potential (MMP) after 24 hours under physiological conditions. The aqueous extracts of C. subternata and C. genistoides, in particular, showed a protective effect by rescuing the bioenergetic and mitochondrial deficits under oxidative stress conditions (400 μM H2O2 for 3 hours). These findings indicate that honeybush extracts could constitute candidates for the prevention of oxidative stress with an impact on aging processes and age-related neurodegenerative disorders potentially leading to the development of a condition-specific nutraceutical.

Mitochondrial Dysfunction and Oxidative Stress in Bipolar Disorder

2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1 ◽  
Author(s):  
A. Andreazza
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Bipolar Disorder ◽  
Oxidative Damage ◽  
Mitochondrial Dysfunction ◽  
Frontal Cortex ◽  
Meta Analysis ◽  
Therapeutic Interventions ◽  
Atp Production ◽  
And Oxidative Stress

While we continue to refine our understanding of the pathophysiology of bipolar disorder (BD), several hypotheses have been postulated including a role for monoamines, gamma-amino butyric acid, glutamate, and second messenger signaling pathways. Recently, mitochondrial dysfunction and oxidative stress have been identified by a number of studies, as an important etiological factor in this disorder. Mitochondria play a crucial role in ATP production through oxidative phosphorylation, a process carried out by the electron transport chain (ETC) complexes. During the transfer of electrons along this ETC, the ROS can be generated, especially in complex I and III4. Growing body of evidence suggests the association of mitochondrial dysfunction and BD. Recent DNA microarray analysis in post-mortem frontal cortex and hippocampus revealed that the expression of several mRNAs coding for ETC complexes I-V subunits was decreased in subjects with BD. Supporting the key involvement of oxidative damage in BD, assays conducted with peripheral blood samples have demonstrated that BD is associated with alterations in antioxidant enzymes and increased lipid peroxidation. Recently we found that oxidative damage to lipid is present in the frontal cortex of BD subjects. A meta-analysis suggested that the levels of lipid peroxidation are elevated in BD providing support for oxidative stress hypothesis of BD. Furthermore, BD subjects showed increased DNA damage, as well as, upregulation of apoptotic genes. These data not only suggest that oxidative mechanisms may form unifying common pathogenic pathways in psychiatric disorders, but also introduce new targets for the development of therapeutic interventions.

scholarly journals Oxidative stress-mediated mitochondrial dysfunction facilitates mesenchymal stem cell senescence in ankylosing spondylitis

2020 ◽  
Vol 11 (9) ◽  
Author(s):  
Guiwen Ye ◽  
Zhongyu Xie ◽  
Huiqiong Zeng ◽  
Peng Wang ◽  
Jinteng Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stem Cell ◽  
Ankylosing Spondylitis ◽  
Mitochondrial Dysfunction ◽  
Chronic Inflammatory Disease ◽  
Atp Production ◽  
Cycle Arrest ◽  
Markers Of Oxidative Stress ◽  
Cellular Dysfunction

Abstract Ankylosing spondylitis (AS) is a chronic inflammatory disease possessing a morbid serum microenvironment with enhanced oxidative stress. Long-term exposure to an oxidative environment usually results in cellular senescence alone with cellular dysfunction. Mesenchymal stem cells (MSCs) are a kind of stem cell possessing strong capabilities for immunoregulation, and senescent MSCs may increase inflammation and participate in AS pathogenesis. The objective of this study was to explore whether and how the oxidative serum environment of AS induces MSC senescence. Here, we found that AS serum facilitated senescence of MSCs in vitro, and articular tissues from AS patients exhibited higher expression levels of the cell cycle arrest-related proteins p53, p21 and p16. Importantly, the levels of advanced oxidative protein products (AOPPs), markers of oxidative stress, were increased in AS serum and positively correlated with the extent of MSC senescence induced by AS serum. Furthermore, MSCs cultured with AS serum showed decreased mitochondrial membrane potential and ATP production together with a reduced oxygen consumption rate. Finally, we discovered that AS serum-induced mitochondrial dysfunction resulted in elevated reactive oxygen species (ROS) in MSCs, and ROS inhibition successfully rescued MSCs from senescence. In conclusion, our data demonstrated that the oxidative serum environment of AS facilitated MSC senescence through inducing mitochondrial dysfunction and excessive ROS production. These results may help elucidate the pathogenesis of AS and provide potential targets for AS treatment.

scholarly journals Melatonin in Mitochondrial Dysfunction and Related Disorders

2011 ◽  
Vol 2011 ◽  
pp. 1-16 ◽  
Author(s):  
Venkatramanujam Srinivasan ◽  
D. Warren Spence ◽  
Seithikurippu R. Pandi-Perumal ◽  
Gregory M. Brown ◽  
Daniel P. Cardinali
Keyword(s):  
Septic Shock ◽  
Electron Transport ◽  
Mitochondrial Dysfunction ◽  
Neurodegenerative Disorders ◽  
Nitrosative Stress ◽  
Mitochondrial Permeability Transition ◽  
Ischemia Reperfusion ◽  
No Production ◽  
Lethal Effects ◽  
Respiratory Complex

Mitochondrial dysfunction is considered one of the major causative factors in the aging process, ischemia/reperfusion (I/R), septic shock, and neurodegenerative disorders like Parkinson's disease (PD), Alzheimer's disease (AD), and Huntington's disease (HD). Increased free radical generation, enhanced mitochondrial inducible nitric oxide (NO) synthase activity, enhanced NO production, decreased respiratory complex activity, impaired electron transport system, and opening of mitochondrial permeability transition pore all have been suggested as factors responsible for impaired mitochondrial function. Melatonin, the major hormone of the pineal gland, also acts as an antioxidant and as a regulator of mitochondrial bioenergetic function. Both in vitro and in vivo, melatonin was effective for preventing oxidative stress/nitrosative stress-induced mitochondrial dysfunction seen in experimental models of PD, AD, and HD. In addition, melatonin is known to retard aging and to inhibit the lethal effects of septic shock or I/R lesions by maintaining respiratory complex activities, electron transport chain, and ATP production in mitochondria. Melatonin is selectively taken up by mitochondrial membranes, a function not shared by other antioxidants. Melatonin has thus emerged as a major potential therapeutic tool for treating neurodegenerative disorders such as PD or AD, and for preventing the lethal effects of septic shock or I/R.

scholarly journals Transcriptomic and Functional Analyses of Mitochondrial Dysfunction in Pressure Overload‐Induced Right Ventricular Failure

2021 ◽  
Vol 10 (4) ◽  
Author(s):  
HyunTae V. Hwang ◽  
Nefthi Sandeep ◽  
Ramesh V. Nair ◽  
Dong‐Qing Hu ◽  
Mingming Zhao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Electron Transport ◽  
Mitochondrial Dysfunction ◽  
Electron Transport Chain ◽  
Mitochondrial Fission ◽  
Pressure Overload ◽  
Energy Generation ◽  
Complex Congenital Heart Disease ◽  
Chain Complexes ◽  
Transport Chain

Background In complex congenital heart disease patients such as those with tetralogy of Fallot, the right ventricle (RV) is subject to pressure overload, leading to RV hypertrophy and eventually RV failure. The mechanisms that promote the transition from stable RV hypertrophy to RV failure are unknown. We evaluated the role of mitochondrial bioenergetics in the development of RV failure. Methods and Results We created a murine model of RV pressure overload by pulmonary artery banding and compared with sham‐operated controls. Gene expression by RNA‐sequencing, oxidative stress, mitochondrial respiration, dynamics, and structure were assessed in pressure overload‐induced RV failure. RV failure was characterized by decreased expression of electron transport chain genes and mitochondrial antioxidant genes (aldehyde dehydrogenase 2 and superoxide dismutase 2) and increased expression of oxidant stress markers (heme oxygenase, 4‐hydroxynonenal). The activities of all electron transport chain complexes decreased with RV hypertrophy and further with RV failure (oxidative phosphorylation: sham 552.3±43.07 versus RV hypertrophy 334.3±30.65 versus RV failure 165.4±36.72 pmol/(s×mL), P <0.0001). Mitochondrial fission protein DRP1 (dynamin 1‐like) trended toward an increase, while MFF (mitochondrial fission factor) decreased and fusion protein OPA1 (mitochondrial dynamin like GTPase) decreased. In contrast, transcription of electron transport chain genes increased in the left ventricle of RV failure. Conclusions Pressure overload‐induced RV failure is characterized by decreased transcription and activity of electron transport chain complexes and increased oxidative stress which are associated with decreased energy generation. An improved understanding of the complex processes of energy generation could aid in developing novel therapies to mitigate mitochondrial dysfunction and delay the onset of RV failure.

scholarly journals Aging-Related Disorders and Mitochondrial Dysfunction: A Critical Review for Prospect Mitoprotective Strategies Based on Mitochondrial Nutrient Mixtures

2020 ◽  
Vol 21 (19) ◽  
pp. 7060
Author(s):  
Giovanni Pagano ◽  
Federico V. Pallardó ◽  
Alex Lyakhovich ◽  
Luca Tiano ◽  
Maria Rosa Fittipaldi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Clinical Trials ◽  
Mitochondrial Dysfunction ◽  
Neurodegenerative Disorders ◽  
Clinical Studies ◽  
Antioxidant Properties ◽  
Cardiovascular Disorders ◽  
Combined Administration

A number of aging-related disorders (ARD) have been related to oxidative stress (OS) and mitochondrial dysfunction (MDF) in a well-established body of literature. Most studies focused on cardiovascular disorders (CVD), type 2 diabetes (T2D), and neurodegenerative disorders. Counteracting OS and MDF has been envisaged to improve the clinical management of ARD, and major roles have been assigned to three mitochondrial cofactors, also termed mitochondrial nutrients (MNs), i.e., α-lipoic acid (ALA), Coenzyme Q10 (CoQ10), and carnitine (CARN). These cofactors exert essential–and distinct—roles in mitochondrial machineries, along with strong antioxidant properties. Clinical trials have mostly relied on the use of only one MN to ARD-affected patients as, e.g., in the case of CoQ10 in CVD, or of ALA in T2D, possibly with the addition of other antioxidants. Only a few clinical and pre-clinical studies reported on the administration of two MNs, with beneficial outcomes, while no available studies reported on the combined administration of three MNs. Based on the literature also from pre-clinical studies, the present review is to recommend the design of clinical trials based on combinations of the three MNs.

Sign in / Sign up

Export Citation Format

Share Document