Design of a Novel Bioflavonoid and Phytonutrient Enriched Formulation in Boosting Immune Competence and Sports Performance: A product Development Investigation

An increase in anaerobic (oxygen-deprived) pathogenesis significantly increases the generation of reactive oxygen species (ROS) inflicting damage on cell membranes and intracellular constituents. Generation of ROS and concomitant inflammatory response is the two hallmarks of cellular damage caused by cellular injury or invasion by pathogens. Oxygen deprivation, as opposed to oxygen deficiency, is a major contributor to oxidative stress and damage, cytokine production, and inflammation. When our cells are unable to efficiently and effectively utilize the oxygen to facilitate aerobic glycolysis and other cellular metabolic events, the oxygen instead oxidizes cell membranes, lipids, neurons, cross-links proteins, damages DNA, and initiates inflammation among other consequences. These anaerobic events are hallmarks of chronic degenerative diseases (CDD). Excessive demands to curtail oxidative damage can overburden endogenous antioxidative capabilities. A key treatment strategy to tackle the adverse effects of inflammation involves the augmentation of the structural integrity and functional competence of cellular materials, reducing the impact and consequences of tissue insult; the generation of ROS; and the cascade of subsequent pathological disorders. Moreover, restoration of cellular aerobic metabolic events, such as aerobic glycolysis and oxidative respiration, is an equally important collateral goal. A healthy diet and supplementation, providing an abundance of exogenous sources of antioxidants and a host of phytochemical dietary components, becomes even more important to restore aerobic metabolism; augment and assist in improving cellular structural integrity, and thereby reducing oxidative stress, damage, and inflammatory sequela. VMP35 MNC, a research-affirmed Prodosomed nutraceutical technology-based phytonutrient formulation, enriched in structurally diverse bioflavonoids, polyphenols, and phenolic saccharides, etc., have been shown to boost cellular structural integrity and physiological functions, and restore aerobic metabolic competence including for athletic performance as well as for general well-being. This review provides a strategic approach for the design of a novel Prodosomed VMP35 Multinutrient/phytoceutical complex and to evaluate its ability to reverse anaerobic pathologies, including inflammation, and restore healthy cellular aerobic glycolysis.

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The Impact of L-Carnitine and Coenzyme Q10 as Protection Against Busulfan-Oxidative Stress in the Liver of Adult Rats

The Natural Products Journal ◽

10.2174/2210315509666190723131511 ◽

2020 ◽

Vol 10 (5) ◽

pp. 578-586

Author(s):

Areeg M. Abdelrazek ◽

Shimaa A. Haredy

Keyword(s):

Oxidative Stress ◽

Coenzyme Q10 ◽

Protective Role ◽

Albino Rats ◽

Distilled Water ◽

Negative Effects ◽

Adult Rats ◽

Stress Damage ◽

The Impact ◽

Liver Tissues

Background: Busulfan (Bu) is an anticancer drug with a variety of adverse effects for cancer patients. Oxidative stress has been considered as a common pathological mechanism and it has a key role in the initiation and progression of liver injury by Bu. Aim: The study aimed to evaluate the antioxidant impact of L-Carnitine and Coenzyme Q10 and their protective role against oxidative stress damage in liver tissues. Methods and Material: Thirty-six albino rats were divided equally into six groups. G1 (con), received I.P. injection of DMSO plus 1 ml of distilled water daily by oral gavages; G2 (Bu), received I.P. injection of Bu plus 1 ml of the distilled water daily; G3 (L-Car), received 1 ml of L-Car orally; G4 (Bu + L-Car) received I.P. injection of Bu plus 1 ml of L-Car, G5 (CoQ10) 1 ml of CoQ10 daily; and G6 (Bu + CoQ10) received I.P. injection of Bu plus 1 ml of CoQ10 daily. Results: The recent data showed that Bu induced significant (P<0.05) elevation in serum ALT, AST, liver GSSG, NO, MDA and 8-OHDG, while showing significant (P<0.05) decrease in liver GSH and ATP. On the other hand, L-Carnitine and Coenzyme Q10 ameliorated the negative effects prompted by Bu. Immunohistochemical expression of caspase-3 in liver tissues reported pathological alterations in Bu group while also showed significant recovery in L-Car more than CoQ10. Conclusion: L-Car, as well as CoQ10, can enhance the hepatotoxic effects of Bu by promoting energy production in oxidative phosphorylation process and by scavenging the free radicals.

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Radical Response: Effects of Heat Stress-Induced Oxidative Stress on Lipid Metabolism in the Avian Liver

Antioxidants ◽

10.3390/antiox10010035 ◽

2020 ◽

Vol 10 (1) ◽

pp. 35

Author(s):

Nima K. Emami ◽

Usuk Jung ◽

Brynn Voy ◽

Sami Dridi

Keyword(s):

Oxidative Stress ◽

Heat Stress ◽

Lipid Metabolism ◽

Egg Production ◽

Well Being ◽

Enzymatic Reactions ◽

Poultry Production ◽

Hepatic Lipid Metabolism ◽

Hepatic Lipid ◽

The Impact

Lipid metabolism in avian species places unique demands on the liver in comparison to most mammals. The avian liver synthesizes the vast majority of fatty acids that provide energy and support cell membrane synthesis throughout the bird. Egg production intensifies demands to the liver as hepatic lipids are needed to create the yolk. The enzymatic reactions that underlie de novo lipogenesis are energetically demanding and require a precise balance of vitamins and cofactors to proceed efficiently. External stressors such as overnutrition or nutrient deficiency can disrupt this balance and compromise the liver’s ability to support metabolic needs. Heat stress is an increasingly prevalent environmental factor that impairs lipid metabolism in the avian liver. The effects of heat stress-induced oxidative stress on hepatic lipid metabolism are of particular concern in modern commercial chickens due to the threat to global poultry production. Chickens are highly vulnerable to heat stress because of their limited capacity to dissipate heat, high metabolic activity, high internal body temperature, and narrow zone of thermal tolerance. Modern lines of both broiler (meat-type) and layer (egg-type) chickens are especially sensitive to heat stress because of the high rates of mitochondrial metabolism. While this oxidative metabolism supports growth and egg production, it also yields oxidative stress that can damage mitochondria, cellular membranes and proteins, making the birds more vulnerable to other stressors in the environment. Studies to date indicate that oxidative and heat stress interact to disrupt hepatic lipid metabolism and compromise performance and well-being in both broilers and layers. The purpose of this review is to summarize the impact of heat stress-induced oxidative stress on lipid metabolism in the avian liver. Recent advances that shed light on molecular mechanisms and potential nutritional/managerial strategies to counteract the negative effects of heat stress-induced oxidative stress to the avian liver are also integrated.

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Oxidative stress and lipid peroxidation with exposure of emerging disinfection byproduct 2,6-dichlorobenzoquinone in mice

10.21203/rs.3.rs-672041/v1 ◽

2021 ◽

Author(s):

Shi-Wei Li ◽

Ming-Hui Chang ◽

Wen-Jun Zhao ◽

He-Lian Li ◽

Hong-Jie Sun ◽

...

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Oxidative Damage ◽

Heme Oxygenase 1 ◽

Quinone Oxidoreductase ◽

Disinfection Byproduct ◽

Adult Mice ◽

Stress Damage ◽

The Impact

Abstract 2,6-dichlorobenzoquinone (2,6-DCBQ) is an emerging disinfection byproduct frequently detected in drinking water. Previous studies have indicated that 2,6-DCBQ causes oxidative stress damage in some live systems, but this has yet to be tested in vivo in mammals. In the present study, adult mice were exposed to 2,6-DCBQ for 30 d via gavage at 0 ~ 100 mg kg− 1 with the responses of antioxidant enzymes (superoxide dismutase [SOD] and catalase [CAT]), key oxidative stress response genes (Heme oxygenase-1 [HO-1], NADPH quinone oxidoreductase 1 [NQO1] and glutamate-L-cysteine ligase catalytic subunit [GCLC]) in the Nrf2-keap1 pathway, and lipid peroxidation (malonaldehyde, MDA) as an indicator of oxidative damage being measured. Our results indicated that 2,6-DCBQ decreased the activities of SOD and CAT, repressed transcription of key genes in the Nrf2-keap1 pathway, and caused measurable oxidative damage. These results reveal the impact of 2,6-DCBQ in a model mammalian system and are key to understanding the potential impacts of 2,6-DCBQ in humans.

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Exogenous proanthocyanidins improve tolerance of Cu-toxicity by amelioration of oxidative damage and re-programming of gene expression in Medicago sativa

PLoS ONE ◽

10.1371/journal.pone.0259100 ◽

2021 ◽

Vol 16 (10) ◽

pp. e0259100

Author(s):

Siyi Zhao ◽

Yanqiao Zhu ◽

Wenwen Liu ◽

Xiaoshan Wang ◽

Han Wang ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Wall ◽

Ascorbic Acid ◽

Plant Growth ◽

Medicago Sativa ◽

Agricultural Practices ◽

Cell Wall Synthesis ◽

Genes Encoding ◽

Stress Damage ◽

The Impact

Excess copper (Cu) in soil due to industrial and agricultural practices can result in reduced plant growth. Excess Cu resulted in severely retarded root growth with severe discoloration of Alfalfa (Medicago sativa) and Medicago truncatula. Growth in the presence of hydrogen peroxide resulted in similar symptoms that could be partially recovered by the addition of the reductant ascorbic acid revealing damage was likely due to oxidative stress. The addition of proanthocyanidins (PAs) in the presence of Cu prevented much of the damage, including plant growth and restoration of lignin synthesis which was inhibited in the presence of excess Cu. Transcriptome analyses of the impact of excess Cu and the amelioration after PAs treatment revealed that changes were enriched in functions associated with the cell wall and extracellular processes, indicating that inhibition of cell wall synthesis was likely the reason for retarded growth. Excess Cu appeared to induce a strong defense response, along with alterations in the expression of a number of genes encoding transcription factors, notably related to ethylene signaling. The addition of PAs greatly reduced this response, and also induced novel genes that likely help ameliorate the effects of excess Cu. These included induction of genes involved in the last step of ascorbic acid biosynthesis and of enzymes involved in cell wall synthesis. Combined, these results show that excess Cu causes severe oxidative stress damage and inhibition of cell wall synthesis, which can be relieved by the addition of PAs.

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Metabolic Therapy in hypertensive encephalopathy: emphasis on comorbidity of pathology

East European Journal of Neurology ◽

10.33444/2411-5797.2018.4(22).4-9 ◽

2018 ◽

pp. 4-9

Author(s):

N. Svyrydova

Keyword(s):

Energy Metabolism ◽

Aerobic Glycolysis ◽

Wide Spectrum ◽

Tricarboxylic Acid Cycle ◽

Oxygen Deficiency ◽

Cerebrovascular Diseases ◽

Hypertensive Encephalopathy ◽

Radical Oxidation ◽

Metabolic Therapy ◽

The Impact

The development of primary and repeated disorders of cerebral circulation, vascular dementia, transient ischemic attacks, which are a consequence of the development of acute pathology in patients with hypertensive encephalopathy, lead to a state of persistent disability and disability. Today, the emphasis of treatment is placed on the important role of oxygen deficiency, which leads to the restriction of aerobic energy production due to disturbances in the energy-synthesizing function of the mitochondrial respiratory chain, depletion of endogenous antioxidant stores and activation of lipid peroxidation of cell membranes, leading to death of brain cells. By 2018, a large evidence base for the effectiveness of the use of metabolic therapy in neurology, which takes into account an important factor of the impact of comorbidity of the pathology. The effectiveness of antioxidant therapy in acute and chronic cerebrovascular diseases is confirmed by the fact that the antioxidant improves energy metabolism in the cell, and as a metabolite of the tricarboxylic acid cycle (succinate, which provides pronounced antioxidant and antihypoxic properties) has a positive effect on the main links of pathogenesis of diseases associated with processes freely Radical oxidation. It is proved that the preparation of Mexicor reduces the manifestation of oxidative stress, inhibits free radical peroxide oxidation of lipids, improves cellular energy metabolism, activates the energy-synthesizing functions of mitochondria, enhances compensatory activation of aerobic glycolysis and reduces the degree of inhibition of oxidative processes in the Krebs cycle. The drug Mexocor has a wide spectrum of pharmacological action, which allows it to be used successfully in acute and chronic cerebrovascular diseases, accompanied by vascular comorbidity.

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Assessment of Eco-geomorphological potential of Mongolia

Proceedings of the Mongolian Academy of Sciences ◽

10.5564/pmas.v60i3.1418 ◽

2020 ◽

pp. 1-16

Author(s):

Bayanjargal Bumtsend ◽

Purevsuren Munkhtur ◽

Avirmed Erdenedalai

Keyword(s):

Oxygen Deficiency ◽

Well Being ◽

Human Society ◽

Strong Wind ◽

Economic Activities ◽

Economic Implications ◽

Mountainous Landscapes ◽

The Impact ◽

Geomorphological Analysis ◽

Specific Impact

The eco-geomorphological analysis includes the impact assessment of relief under various ecosystem conditions in as much relief has various ecological roles, both direct and indirect. Rising elevation above sea level is mostly influenced by climate indirectly leading to reduced air pressure, oxygen deficiency, reduction of air temperature, excessive solar radiation, and creation of strong wind. The depth of relief dissection of the bumpy surface of mountainous areas created by floods and mudflows, and the depth of the bumpy surface increases energy consumption and poses risks during mountain climbing, and also has negative economic implications if economic activities are undertaken in such terrain. On the other hand, mountainous landscapes have a specific impact on human well-being and also have considerable potential for promoting tourism. Although, in the steppe environment, relief dissection increases the unique features of the landscape and increases the potential of tourism in other respects, however, it is assessed negatively to a large extent. The nature of corelationship between and the interdependence of the terrestrial surface and population, terrestrial surface and livestock, terrestrial surface and agriculture, which are significant in the study into the inter-relationship between environment and human society, was assessed and determined , and the relevant conclusion was drawn.

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Oxidative Stress and Reproductive Function in the Aging Male

Biology ◽

10.3390/biology9090282 ◽

2020 ◽

Vol 9 (9) ◽

pp. 282

Author(s):

Paulina Nguyen-Powanda ◽

Bernard Robaire

Keyword(s):

Oxidative Stress ◽

Antioxidant Defense ◽

Structural Integrity ◽

Germ Line ◽

Reproductive Function ◽

Antioxidant Defense System ◽

Male Reproduction ◽

Paternal Age ◽

Theories Of Aging ◽

The Impact

With the delay of parenthood becoming more common, the age at which men father children is on the rise. While the effects of advanced maternal age have been well documented, only recently have studies started to focus on the impact of advanced paternal age (APA) in the context of male reproduction. As men age, the antioxidant defense system gradually becomes less efficient and elevated levels of reactive oxygen species (ROS) accumulate in spermatozoa; this can impair their functional and structural integrity. In this review, we present an overview of how oxidative stress is implicated in male reproductive aging by providing a summary of the sources and roles of ROS, the theories of aging, and the current animal and human studies that demonstrate the impacts of APA on the male germ line, the health of progeny and fertility, and how treatment with antioxidants may reverse these effects.

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N-Acetylcysteine Prevents Hypertension via Regulation of the ADMA-DDAH Pathway in Young Spontaneously Hypertensive Rats

BioMed Research International ◽

10.1155/2013/696317 ◽

2013 ◽

Vol 2013 ◽

pp. 1-9 ◽

Cited By ~ 19

Author(s):

Nai-Chia Fan ◽

Chih-Min Tsai ◽

Chien-Ning Hsu ◽

Li-Tung Huang ◽

You-Lin Tain

Keyword(s):

Oxidative Stress ◽

Spontaneously Hypertensive Rats ◽

Asymmetric Dimethylarginine ◽

Hypertensive Rats ◽

Dimethylarginine Dimethylaminohydrolase ◽

Spontaneously Hypertensive ◽

Plasma Adma ◽

Wistar Kyoto ◽

Stress Damage ◽

The Impact

Asymmetric dimethylarginine (ADMA) reduces nitric oxide (NO), thus causing hypertension. ADMA is metabolized by dimethylarginine dimethylaminohydrolase (DDAH), which can be inhibited by oxidative stress. N-Acetylcysteine (NAC), an antioxidant, can facilitate glutathione (GSH) synthesis. We aimed to determine whether NAC can prevent hypertension by regulating the ADMA-DDAH pathway in spontaneously hypertensive rats (SHR). Rats aged 4 weeks were assigned into 3 groups (n=8/group): control Wistar Kyoto rats (WKY), SHR, and SHR receiving 2% NAC in drinking water. All rats were sacrificed at 12 weeks of age. SHR had higher blood pressure than WKY, whereas NAC-treated animals did not. SHR had elevated plasma ADMA levels, which was prevented by NAC therapy. SHR had lower renal DDAH activity than WKY, whereas NAC-treated animals did not. Renal superoxide production was higher in SHR than in WKY, whereas NAC therapy prevented it. NAC therapy was also associated with higher GSH-to-oxidized GSH ratio in SHR kidneys. Moreover, NAC reduced oxidative stress damage in SHR. The observed antihypertensive effects of NAC in young SHR might be due to restoration of DDAH activity to reduce ADMA, leading to attenuation of oxidative stress. Our findings highlight the impact of NAC on the development of hypertension by regulating ADMA-DDAH pathway.

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