Considerations on the Ethiopathogenesis of Algae from the Primary Form of BMD

The study is motivated by the existence of a still controversial etiopathogen on Burning Mouth Syndrome. The objective of the study, which is carried out on a group of 103 sick of both sexes, presenting the Burning Mouth Disorder - the primary form, is to identify the prevalence of the disease and establish possible correlations with coexistence of age, gender and dyslipidemia as factors that can be considered as favoring the installation non-specific oral allergy. The conclusions of the research constitute an argument for admitting the hypothesis of the existence of a neuronal irrigation deficiency, manifested both at the conductive sensory fibers of the influx and, more preferably, at the sensory-sensorial cortex for pain and taste, or only at one of these levels. According to the hypothesis, neuronal suffering consists in a deficiency of energy production and use, induced by excessively local reactive oxygen species, through irrigation, developed by the presence of arteriosclerosis.

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Conjugation of Natural Triterpenic Acids with Delocalized Lipophilic Cations: Selective Targeting Cancer Cell Mitochondria

Journal of Personalized Medicine ◽

10.3390/jpm11060470 ◽

2021 ◽

Vol 11 (6) ◽

pp. 470

Author(s):

Anna Yu. Spivak ◽

Darya A. Nedopekina ◽

Rinat R. Gubaidullin ◽

Mikhail V. Dubinin ◽

Konstantin N. Belosludtsev

Keyword(s):

Reactive Oxygen Species ◽

Anticancer Agents ◽

Energy Production ◽

Reactive Oxygen ◽

Oxygen Species ◽

Pentacyclic Triterpenoids ◽

Cell Death Pathways ◽

Selective Targeting ◽

Triterpenic Acids ◽

Distinguishing Features

Currently, a new line of research on mitochondria-targeted anticancer drugs is actively developing in the field of biomedicine and medicinal chemistry. The distinguishing features of this universal target for anticancer agents include presence of mitochondria in the overwhelming majority, if not all types of transformed cells, crucial importance of these cytoplasmic organelles in energy production, regulation of cell death pathways, as well as generation of reactive oxygen species and maintenance of calcium homeostasis. Hence, mitochondriotropic anticancer mitocan agents, acting through mitochondrial destabilization, have good prospects in cancer therapy. Available natural pentacyclic triterpenoids are considered promising scaffolds for development of new mitochondria-targeted anticancer agents. These secondary metabolites affect the mitochondria of tumor cells and initiate formation of reactive oxygen species. The present paper focuses on the latest research outcomes of synthesis and study of cytotoxic activity of conjugates of pentacyclic triterpenoids with some mitochondria-targeted cationic lipophilic molecules and highlights the advantages of applying them as novel mitocan agents compared to their prototype natural triterpenic acids.

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Mitochondrial Management of Reactive Oxygen Species

Antioxidants ◽

10.3390/antiox10111824 ◽

2021 ◽

Vol 10 (11) ◽

pp. 1824

Author(s):

Gaetana Napolitano ◽

Gianluca Fasciolo ◽

Paola Venditti

Keyword(s):

Reactive Oxygen Species ◽

Antioxidant System ◽

Energy Production ◽

Krebs Cycle ◽

Reactive Oxygen ◽

Biological Molecules ◽

Oxygen Species ◽

Primary Target ◽

Cellular Compartments ◽

Harmful Species

Mitochondria in aerobic eukaryotic cells are both the site of energy production and the formation of harmful species, such as radicals and other reactive oxygen species, known as ROS. They contain an efficient antioxidant system, including low-molecular-mass molecules and enzymes that specialize in removing various types of ROS or repairing the oxidative damage of biological molecules. Under normal conditions, ROS production is low, and mitochondria, which are their primary target, are slightly damaged in a similar way to other cellular compartments, since the ROS released by the mitochondria into the cytosol are negligible. As the mitochondrial generation of ROS increases, they can deactivate components of the respiratory chain and enzymes of the Krebs cycle, and mitochondria release a high amount of ROS that damage cellular structures. More recently, the feature of the mitochondrial antioxidant system, which does not specifically deal with intramitochondrial ROS, was discovered. Indeed, the mitochondrial antioxidant system detoxifies exogenous ROS species at the expense of reducing the equivalents generated in mitochondria. Thus, mitochondria are also a sink of ROS. These observations highlight the importance of the mitochondrial antioxidant system, which should be considered in our understanding of ROS-regulated processes. These processes include cell signaling and the progression of metabolic and neurodegenerative disease.

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Lineage-Selective Disturbance of Early Human Hematopoietic Progenitor Cell Differentiation by the Commonly Used Plasticizer Di-2-ethylhexyl Phthalate via Reactive Oxygen Species: Fatty Acid Oxidation Makes the Difference

Cells ◽

10.3390/cells10102703 ◽

2021 ◽

Vol 10 (10) ◽

pp. 2703

Author(s):

Lars Kaiser ◽

Isabel Quint ◽

René Csuk ◽

Manfred Jung ◽

Hans-Peter Deigner

Keyword(s):

Reactive Oxygen Species ◽

Fatty Acid ◽

Fatty Acid Oxidation ◽

Energy Production ◽

Hematopoietic Cells ◽

Reactive Oxygen ◽

Health Concern ◽

Acid Oxidation ◽

Oxygen Species ◽

Ethylhexyl Phthalate

Exposure to ubiquitous endocrine-disrupting chemicals (EDCs) is a major public health concern. We analyzed the physiological impact of the EDC, di-2-ethylhexyl phthalate (DEHP), and found that its metabolite, mono-2-ethylhexyl phthalate (MEHP), had significant adverse effects on myeloid hematopoiesis at environmentally relevant concentrations. An analysis of the underlying mechanism revealed that MEHP promotes increases in reactive oxygen species (ROS) by reducing the activity of superoxide dismutase in all lineages, possibly via its actions at the aryl hydrocarbon receptor. This leads to a metabolic shift away from glycolysis toward the pentose phosphate pathway and ultimately results in the death of hematopoietic cells that rely on glycolysis for energy production. By contrast, cells that utilize fatty acid oxidation for energy production are not susceptible to this outcome due to their capacity to uncouple ATP production. These responses were also detected in non-hematopoietic cells exposed to alternate inducers of ROS.

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The Role of Oxidative Stress in Metals Toxicity; Mitochondrial Dysfunction as a Key Player

Galen Medical Journal ◽

10.31661/gmj.v3i1.100 ◽

2014 ◽

Vol 3 (1) ◽

pp. 2-13

Author(s):

Akram Ranjbar ◽

Hassan Ghasemi ◽

Farshad Rostampour‎

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Energy Production ◽

Reactive Oxygen ◽

Atp Synthesis ◽

Ros Generation ◽

Oxygen Species ◽

Cellular Oxygen ◽

A Site

Metals can cause oxidative stress by increasing the formation of reactive oxygen species (ROS), which make antioxidants incapable of defiance against growing amounts of free radicals. Metal toxicity is related to their oxidative state and reactivity with other compounds. However, several reports about metals have been published in the recent years. Mitochondria, as a site of cellular oxygen consumption and energy production, can be a target for metals toxicity. Dysfunction of Mitochondrial oxidative phosphorylation led to the production of some metals toxicities metals through alteration in the activities of I, II, III, IV and V complexes and disruption of mitochondrial membrane. Reductions of adenosine triphosphate (ATP) synthesis or induction of its hydrolysis can impair the cellular energy production. In the present review study, the researchers have criticized reviews and some evidence about the oxidative stress as a mechanism of toxicity of metals. The metals disrupt cellular and antioxidant defense, reactive oxygen species (ROS) generation, and promote oxidative damage. The oxidative injuries induced by metals can be restored by use of antioxidants such as chelators, vitamin E and C, herbal medicine, and through increasing the antioxidants level. However, to elucidate many aspect of mechanism toxicity of metals, further studies are yet to be carried out.

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Mitochondria as a source of reactive oxygen species

Biochemical Journal ◽

10.1042/bj20090056 ◽

2009 ◽

pp. c3 ◽

Cited By ~ 1

Author(s):

Helena M. Cochemé ◽

Michael P. Murphy

Keyword(s):

Reactive Oxygen Species ◽

Reactive Oxygen ◽

Oxygen Species

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Clinical aspects of reactive oxygen and nitrogen species

Biochemical Society Symposium ◽

10.1042/bss0710121 ◽

2004 ◽

Vol 71 ◽

pp. 121-133 ◽

Cited By ~ 25

Author(s):

Ascan Warnholtz ◽

Maria Wendt ◽

Michael August ◽

Thomas Münzel

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Risk Factor ◽

Endothelial Dysfunction ◽

Vascular Tissue ◽

Rapid Development ◽

Reactive Oxygen ◽

Clinical Aspects ◽

No Production ◽

Oxygen Species

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.

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