Hexavalent chromium induces reactive oxygen species and impairs the antioxidant power of human erythrocytes and lymphocytes: Decreased metal reducing and free radical quenching ability of the cells

2017 ◽  
Vol 33 (8) ◽  
pp. 623-635 ◽  
Author(s):  
Nazim Husain ◽  
Riaz Mahmood
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Free Radical ◽  
Hexavalent Chromium ◽  
Reactive Oxygen ◽  
Human Erythrocytes ◽  
Cellular Damage ◽  
Oxygen Species ◽  
Antioxidant Power

The toxicity of hexavalent chromium [Cr(VI)] in biological systems is thought to be closely associated with the generation of free radicals and reactive oxygen species. These species are produced when Cr(VI) is reduced to its trivalent form in the cell. This process results in oxidative stress due to an imbalance between the detoxifying ability of the cell and the production of free radicals. We have studied the effect of potassium dichromate (K2Cr2O7), a [Cr(VI)] compound, on the antioxidant power of human erythrocytes and lymphocytes under in vitro conditions. Incubation of erythrocytes and lymphocytes with different concentrations of K2Cr2O7 resulted in a marked dose-dependent decrease in reduced glutathione and an increase in oxidized glutathione and reactive oxygen species levels. The antioxidant power of the cells was decreased, as determined by metal reducing and free radical quenching assays. These results show that [Cr(VI)] upregulates the generation of reactive oxygen species and, as a consequence, the cellular antioxidant defences are compromised. The resulting oxidative stress may contribute to Cr(VI)-induced cellular damage.

scholarly journals The Free Radical Theory of Aging and Antioxidant Supplements

2012 ◽  
Vol 17 (3) ◽  
pp. 218-220
Author(s):  
Bruce A. Buehler
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Free Radical ◽  
Life Span ◽  
Reactive Oxygen ◽  
Cell Aging ◽  
Oxygen Species ◽  
Radical Theory ◽  
Antioxidant Supplements

Free radical excess occurs when cells are exposed to reactive oxygen species greater than the amount that can be neutralized by cellular produced antioxidants such as superoxide dismutase. This is termed oxidative stress, which can be caused by excessive energy intake or external pollutants. Excess free radicals are proposed to increase the rate of cell aging, injury, and mutations leading to a shortened cell life span. Vitamins A, C, and E and flavoproteins are supplements that function as free radical scavengers. Antioxidants are present in natural foods but added amounts beyond the diet may detoxify excess free radicals during “oxidative stress.” Antioxidant supplements decrease cellular damage from excess reactive oxygen species but they have not been proven to prolong life span.

scholarly journals Interaction of Oxidative Stress and Misfolded Proteins in the Mechanism of Neurodegeneration

Life ◽  
2020 ◽  
Vol 10 (7) ◽  
pp. 101 ◽  
Author(s):  
Andrey Y. Abramov ◽  
Elena V. Potapova ◽  
Viktor V. Dremin ◽  
Andrey V. Dunaev
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Neurodegenerative Disorders ◽  
Structural Changes ◽  
Wide Spectrum ◽  
Physiological Role ◽  
Reactive Oxygen ◽  
Misfolded Proteins ◽  
Oxygen Species

Aggregation of the misfolded proteins β-amyloid, tau, huntingtin, and α-synuclein is one of the most important steps in the pathology underlying a wide spectrum of neurodegenerative disorders, including the two most common ones—Alzheimer’s and Parkinson’s disease. Activity and toxicity of these proteins depends on the stage and form of aggregates. Excessive production of free radicals, including reactive oxygen species which lead to oxidative stress, is proven to be involved in the mechanism of pathology in most of neurodegenerative disorders. Both reactive oxygen species and misfolded proteins play a physiological role in the brain, and only deregulation in redox state and aggregation of the proteins leads to pathology. Here, we review the role of misfolded proteins in the activation of ROS production from various sources in neurons and glia. We discuss if free radicals can influence structural changes of the key toxic intermediates and describe the putative mechanisms by which oxidative stress and oligomers may cause neuronal death.

scholarly journals Mechanism of Oxidative Stress in Neurodegeneration

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Sonia Gandhi ◽  
Andrey Y. Abramov
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Neurodegenerative Disease ◽  
Reactive Oxygen ◽  
Biological Tissues ◽  
Antioxidant Systems ◽  
Oxygen Species

Biological tissues require oxygen to meet their energetic demands. However, the consumption of oxygen also results in the generation of free radicals that may have damaging effects on cells. The brain is particularly vulnerable to the effects of reactive oxygen species due to its high demand for oxygen, and its abundance of highly peroxidisable substrates. Oxidative stress is caused by an imbalance in the redox state of the cell, either by overproduction of reactive oxygen species, or by dysfunction of the antioxidant systems. Oxidative stress has been detected in a range of neurodegenerative disease, and emerging evidence from in vitro and in vivo disease models suggests that oxidative stress may play a role in disease pathogenesis. However, the promise of antioxidants as novel therapies for neurodegenerative diseases has not been borne out in clinical studies. In this review, we critically assess the hypothesis that oxidative stress is a crucial player in common neurodegenerative disease and discuss the source of free radicals in such diseases. Furthermore, we examine the issues surrounding the failure to translate this hypothesis into an effective clinical treatment.

scholarly journals Reactive Oxygen Species and the Cardiovascular System

2013 ◽  
Vol 2013 ◽  
pp. 1-15 ◽  
Author(s):  
Yannick J. H. J. Taverne ◽  
Ad J. J. C. Bogers ◽  
Dirk J. Duncker ◽  
Daphne Merkus
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Oxygen Consumption ◽  
Free Radicals ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Cellular Homeostasis ◽  
Cardiovascular Pathology ◽  
Pathological Conditions ◽  
By Products

Ever since the discovery of free radicals, many hypotheses on the deleterious actions of reactive oxygen species (ROS) have been proposed. However, increasing evidence advocates the necessity of ROS for cellular homeostasis. ROS are generated as inherent by-products of aerobic metabolism and are tightly controlled by antioxidants. Conversely, when produced in excess or when antioxidants are depleted, ROS can inflict damage to lipids, proteins, and DNA. Such a state of oxidative stress is associated with many pathological conditions and closely correlated to oxygen consumption. Although the deleterious effects of ROS can potentially be reduced by restoring the imbalance between production and clearance of ROS through administration of antioxidants (AOs), the dosage and type of AOs should be tailored to the location and nature of oxidative stress. This paper describes several pathways of ROS signaling in cellular homeostasis. Further, we review the function of ROS in cardiovascular pathology and the effects of AOs on cardiovascular outcomes with emphasis on the so-called oxidative paradox.

Association of Oxidative Stress with Neurological Disorders

2021 ◽  
Vol 19 ◽  
Author(s):  
Waseem Hassan ◽  
Hamsa Noreen ◽  
Shakila Rehman ◽  
Mohammad Amjad Kamal ◽  
Joao Batista Teixeira da Rocha
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Neurodegenerative Diseases ◽  
Neurological Disorders ◽  
Biological Effects ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Neuronal Membranes

Background: Oxidative stress is one of the main contributing factors involved in cerebral biochemical impairment. The higher susceptibility of the central nervous system to reactive oxygen species mediated damage could be attributed to several factors. For example, neurons use a greater quantity of oxygen, many parts of the brain have higher concentraton of iron, and neuronal mitochondria produce huge content of hydrogen peroxide. In addition, neuronal membranes have polyunsaturated fatty acids, which are predominantly vulnerable to oxidative stress (OS). OS is the imbalance between reactive oxygen species generation and cellular antioxidant potential. This may lead to various pathological conditions and diseases, especially neurodegenerative diseases such as, Parkinson’s, Alzheimer’s, and Huntington’s diseases. Objectives: In this study, we explored the involvement of OS in neurodegenerative diseases. Methods: We used different search terms like “oxidative stress and neurological disorders” “free radicals and neurodegenerative disorders” “oxidative stress, free radicals, and neurological disorders” and “association of oxidative stress with the name of disorders taken from the list of neurological disorders. We tried to summarize the source, biological effects, and physiologic functions of ROS. Results: Finally, it was noted that more than 190 neurological disorders are associated with oxidative stress.

Ovariectomy and its Antioxidative Effect on Bone

2010 ◽  
Author(s):  
Durg V. Rai ◽  
Harcharan Singh Ranu
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Bone Loss ◽  
Wistar Rats ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Female Wistar Rats ◽  
The Impact

Ovarian hormone deficiency increases the generation of reactive oxygen species. Oxidative stress due to reactive oxygen species (ROS) can cause oxidative damage to cells. Cells have a number of defense mechanisms to protect themselves from the toxicity of ROS. There is increasing evidence of the role of free radicals in bone resorption and bone loss. Ovariectomised female wistar rats had been used as the animal model for the study of osteoporosis. Even though, there are studies portraying the role of free radicals in bone loss, the defense mechanism adapted by bone in ovariectomised animals remains obscure. So, the impact of ovariectomy on the bone antioxidant system in rats was investigated. Twenty female wistar rats were taken and divided into two groups: ovariectomised and control. It had been found that a significant (p<0.001) decrease in the activity of various enzymes like CAT (catalase), SOD (superoxide dismutase) (p<0.001), GST (glutathione-s-transferase). However, an increase in the malondialdehyde levels was found to be 30% in the ovariectomised rats as compared to the controls. Thus the study elucidates the oxidative stress in bone under ovariectomy.

Oxidative Stress, Antioxidant Status, and the Contracting Diaphragm

1998 ◽  
Vol 23 (1) ◽  
pp. 23-55 ◽  
Author(s):  
John M. Lawler ◽  
Scott K. Powers
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Membrane Lipids ◽  
Reactive Oxygen ◽  
Respiratory Muscles ◽  
Strenuous Exercise ◽  
Antioxidant Enzyme Activities ◽  
Key Words Aging ◽  
Oxygen Species

Reactive oxygen species, including free radicals, are produced through a number of biochemical reactions, often as a consequence of aerobic metabolism. A system of antioxidant enzymes and scavenger substrates provides protection of membrane lipids, proteins, and DNA. An imbalance between production of reactive oxygen species and antioxidant protection results in "oxidative stress." Oxidative stress is believed to contribute to numerous pathological conditions including atherosclerosis, obstructive lung disease, aging, and fatigue of skeletal muscles including the diaphragm. Strenuous exercise, inflammation, infection, obstructive lung diseases, etc. increase exposure of the diaphragm to reactive oxygen species. Emerging data indicate that reactive oxygen species alter diaphragm contractions primarily in response to low-frequency stimulation. The response of the diaphragm is profoundly influenced by the degree of oxidative stress, fatigue state, glutathione status, and age. Exercise training results in an upregulation of antioxidant enzyme activities in the diaphragm and thus could provide additional protection against oxidative stress. Key words: aging, excitation-contraction coupling, exercise, fatigue, free radicals, glutathione peroxidase, oxidation/reduction, reactive oxygen species, respiratory muscles, skeletal muscle, superoxide dismutase

scholarly journals Implication of Oxidative Stress in Small Intestine Disorders, Constipation and Diarrhea: A Mini Review

2017 ◽  
Vol 03 ◽  
pp. 66 ◽  
Author(s):  
Ka�s Rtibi ◽  
Mohamed Amri ◽  
Hichem Sebai ◽  
Lamjed Marzouki ◽  
◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Small Intestine ◽  
Free Radicals ◽  
Antioxidant System ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Absorption Process ◽  
Gi Tract ◽  
Intestinal Peristalsis

Diarrhea pathophysiology and constipation are multifactorial gastrointestinal (GI) disorders characterized by intestinal peristalsis disruption of and an irregularity in secretion/absorption process. Oxidative stress, as an imbalance in prooxidants/antioxidants, has recently been recognized as a significant player in these GI disturbances. In this respect, numerous studies were performed and have shown that the deleterious effects on GI tract were accompanied by accumulation of oxidants and depletion of antioxidant system. Antioxidant remedy is necessary in scavenging free radicals and reactive oxygen species preventing oxidative stress-induced GI interruptions.

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