scholarly journals Croton campestris A. St.-Hill Methanolic Fraction in a Chlorpyrifos-Induced Toxicity Model in Drosophila melanogaster: Protective Role of Gallic Acid

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Karen Kich Gomes ◽  
Giulianna Echeverria Macedo ◽  
Nathane Rosa Rodrigues ◽  
Cynthia Camila Ziech ◽  
Illana Kemmerich Martins ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Protective Effect ◽  
Gallic Acid ◽  
Native Species ◽  
Protective Role ◽  
Northeastern Brazil ◽  
Transferase Activity ◽  
Glutathione S Transferase ◽  
Promising Source

Croton campestris A. St-Hill popularly known as “velame do campo” is a native species of the savannah from northeastern Brazil, being used in folk medicine due to its beneficial effects in the treatment of many diseases, inflammation, detoxification, gastritis, and syphilis; however, its potential use as an antidote against organophosphorus compound poisoning has not yet been shown. Here, the protective effect of the methanolic fraction of C. campestris A. St.-Hill (MFCC) in Drosophila melanogaster exposed to chlorpyrifos (CP) was investigated. Flies were exposed to CP and MFCC during 48 h through the diet. Following the treatments, parameters such as mortality, locomotor behavior, and oxidative stress markers were evaluated. Exposure of flies to CP induced significant impairments in survival and locomotor performance. In parallel, increased reactive oxygen species and lipoperoxidation occurred. In addition, the activity of acetylcholinesterase was inhibited by CP, and superoxide dismutase and glutathione S-transferase activity was induced. Treatment with MFCC resulted in a blockage of all CP-induced effects, with the exception of glutathione S-transferase. Among the major compounds found in MFCC, only gallic acid (GA) showed a protective role against CP while quercetin and caffeic acid alone were ineffective. When in combination, these compounds avoided the toxicity of CP at the same level as GA. As far as we know, this is the first study reporting the protective effect of MFCC against organophosphate toxicity in vivo and highlights the biotechnological potential of this fraction attributing a major role in mediating the observed effects to GA. Therefore, MFCC may be considered a promising source for the development of new therapeutic agents for the treatment of organophosphate intoxications.

scholarly journals Antioxidants in erythrocytes in aging and dementia

2013 ◽  
Vol 59 (4) ◽  
pp. 443-451 ◽  
Author(s):  
E.A. Kosenko ◽  
L.A. Tikhonova ◽  
A.C. Poghosyan ◽  
Y.G. Kaminsky
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Glutathione Peroxidase ◽  
Antioxidant Status ◽  
Transferase Activity ◽  
Glutathione S Transferase ◽  
Age Related ◽  
Organic Hydroperoxides

Age of patients and brain oxidative stress may contribute to pathogenesis of Alzheimer's disease (AD). Erythrocytes (red blood cells, RBC) are considered as passive “reporter cells” for the oxidative status of the whole organism and are not well studied in AD. The aim of this work was to assess whether the antioxidant status of RBC changes in aging and AD. Blood was taken from AD and non-Alzheimer's dementia patients, aged-matched and younger controls. In vivo antioxidant status was assessed in each of the study subjects by measuring RBC levels of Н О , organic hydroperoxides, glutathione (GSH) and glutathione disulfide (GSSG), activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione S-transferase, and glucose-6-phosphate dehydrogenase. In both aging and dementia, oxidative stress in RBC was shown to increase and to be expressed in elevated concentrations of H O and organic hydroperoxides, decreased the GSH/GSSG ratio and glutathione S-transferase activity. Decreased glutathione peroxidase activity in RBC may be considered as a new peripheral marker for Alzheimer’s disease while alterations of other parameters of oxidative stress reflect age-related events.

scholarly journals Flavonoids Regulate Lipid Droplets Biogenesis in Drosophila melanogaster

2019 ◽  
Vol 14 (5) ◽  
pp. 1934578X1985243 ◽  
Author(s):  
Marianna Fantin ◽  
Francesca Garelli ◽  
Barbara Napoli ◽  
Alessia Forgiarini ◽  
Sentiljana Gumeni ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Lipid Metabolism ◽  
Lipid Droplets ◽  
Metabolic Diseases ◽  
Protective Role ◽  
Fat Storage ◽  
Fat Bodies ◽  
Obesity And Cancer ◽  
Neuronal Disorders

Lipid droplets (LDs), cytosolic fat storage organelles, are emerging as major regulators of lipid metabolism, trafficking, and signaling in various cells and tissues. LDs are altered in cardiovascular and neuronal disorders, inflammation, obesity, and cancer. Flavonoids comprise different classes of molecules, characterized by a well-known antioxidant activity and a beneficial effect in several diseases. However, the cellular mechanism by which different classes of flavonoids improve health is poorly understood, in particular as far as LDs biogenesis is concerned. Here we used Drosophila melanogaster as a model system to investigate the effects of a selected group of flavonoids on larval tissues by examining LDs biogenesis. In our study, fruit flies were grown in xanthohumol-, isoquercetin-, and genistein-enriched food and larval tissues were analyzed using a LD marker. Total mRNA expression of two main enzymes (minotaur and midway) responsible for triacylglycerides synthesis was evaluated after treatments. Among the flavonoids analyzed, xanthohumol and isoquercetin resulted to be potent regulators of LDs biogenesis in a tissue-specific manner, inducing fat storage decrease in fat bodies and accumulation of LDs in nerves. Since LDs have been suggested to play a protective role against intracellular stress in nonadipocyte cells, our data support the hypothesis that some phytochemicals could act as strong modulators of LDs biogenesis in vivo. The knowledge of how different flavonoids act on lipid metabolism in different tissues can help to manage the use of phytochemicals with the aim of selectively ameliorating specific neuronal and metabolic diseases’ manifestations.

scholarly journals In vivo Role of Cytochrome P450 2E1 and Glutathione-S-Transferase Activity for Acrylamide Toxicokinetics in Humans

2009 ◽  
Vol 18 (2) ◽  
pp. 433-443 ◽  
Author(s):  
Oxana Doroshyenko ◽  
Uwe Fuhr ◽  
Daria Kunz ◽  
Dorothee Frank ◽  
Martina Kinzig ◽  
...  
Keyword(s):  
Cytochrome P450 ◽  
Transferase Activity ◽  
Cytochrome P450 2E1 ◽  
Glutathione S Transferase

scholarly journals THE IN VIVO INTERACTION BETWEEN STAPHYLOCOCCUS BACTERIOPHAGE AND STAPHYLOCOCCUS AUREUS

1963 ◽  
Vol 118 (1) ◽  
pp. 13-26 ◽  
Author(s):  
P. F. Bartell ◽  
I. S. Thind ◽  
T. Orr ◽  
W. S. Blakemore
Keyword(s):  
Staphylococcus Aureus ◽  
Protective Effect ◽  
Host Defense ◽  
Defense Mechanisms ◽  
Protective Role ◽  
Protection Time ◽  
Determining Factors ◽  
Specific Bacteriophage ◽  
And Staphylococcus Aureus

Staphylococcus bacteriophage 81 is capable of in vivo interaction with Staphylococcus aureus, Type 80/81. This is immediately made evident by increased levels of bacteriophage and concomitant survival of 81 per cent infected mice. The reaction is dependent upon the use of active, type-specific bacteriophage. The maximal protective effect is observed at a bacteriophage to bacteria ratio of 1:2 and decreased quantities of bacteriophage result in decreased protection. Time and sequence of administration are also determining factors. It is evident that bacteriophage administered intravenously is capable of interaction with the infecting bacterial cell at the site of infection. In vivo produced bacteriophage is apparently eliminated or otherwise rendered nondetectable fairly rapidly, occurring within a period of 5 to 10 days. However, it appears that host defense mechanisms are stimulated in the process and actively play a protective role against subsequent challenge inocula administered up to 3 weeks later.

scholarly journals P0026METFORMIIN IMPROVES DYSFUNCTION OF MESENCHYMAL STEM CELLS ASSOCIATED WITH CHRONIC KIDNEY DISEASE VIA SENESCENCE INHIBITION

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Hyunjin Noh ◽  
Mi Ra Yu ◽  
Kyoungin Choi ◽  
Dohui Hwang
Keyword(s):  
Chronic Kidney Disease ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Kidney Disease ◽  
Cellular Senescence ◽  
Critical Factor ◽  
Protective Role ◽  
Metformin Treatment ◽  
Promising Source

Abstract Background and Aims Mesenchymal stem cells (MSC) are promising source of cell-based regenerative therapy; however, adequate cell functionality is a critical factor for the success of autotransplantation. Method We investigated the effects of metformin on chronic kidney disease (CKD)-associated cellular senescence using MSC isolated from sham operated and subtotal nephrectomized mice and further explored the protective role of metformin-treated CKD MSC in renal progression. Results When compared to normal MSC, MSC isolated from CKD mice displayed reduced proliferation and early senescence as determined by enlarged cell morphology, increased oxidative stress, accumulation of DNA damage response marker p53 binding protein 1 (53BP1), phospho p53, p16INK4a, and β-gal expression, and decreased cyclin-dependent kinase 4 (CDK4) and cyclin D. CKD MSC exhibited activation of NFκB resulting in expression of senescence-associated secretory phenotype (SASP) factors compared to normal MSC. All of these changes were significantly prevented by metformin treatment. In vivo, metformin-treated CKD MSC attenuated inflammation and fibrosis in UUO kidney as compared to CKD MSC. Co-culture of LPS or TGF-β1-treated HK2 cells with metformin-treated CKD MSC markedly decreased LPS or TGF-β-induced tubular expression of proinflammatory markers and fibrogenesis when compared to CKD MSC suggesting paracrine action of CKD MSC enhanced by metformin treatment. Conclusion Our data suggest that metformin inhibits cellular senescence of CKD MSC and improves their renoprotective effects.

In silico investigation of Methyl parathion and Diazinon with different Metabolic protein in Drosophila melanogaster

2021 ◽  
pp. 3794-3798
Author(s):  
Suman Sahoo ◽  
Md. Lutfur Rahman ◽  
Sagarika Mitra ◽  
Rajiniraja M.
Keyword(s):  
Drosophila Melanogaster ◽  
Protein Function ◽  
Methyl Parathion ◽  
Function Analysis ◽  
Glutathione S Transferase ◽  
Agriculture Industry ◽  
Bimolecular Interactions ◽  
Metabolic Protein ◽  
Chemical Pollutant

Chemical pollutant such as insecticide, pesticide and drugs are mainly used for agriculture, industry and economic development, which are well known for environment pollutant due to its toxicity and persistence in the nature. It can accumulate into the environment and continuously contaminate the food chain which causes threat to the health of consumer including human. Based on all these studies our investigation deals with the effects of two insecticides viz. methyl parathion and diazinon to non target organism like Drosophila melanogaster. In this study we have performed molecular modeling, docking and protein function analysis of different metabolic and physiological enzyme of Drosophila melanogaster such as acetylcholinesterase (AchE), Glutathione S-transferase D1(GST) and Protein kinase C (PKC) with these insecticides of six combinations (AchE + Diazinon, AchE + methyl parathion, GST+Diazinon, GST+Methyl parathion, PKC+Diazinon, PKC+Methyl parathion). Molecular docking results showing best binding affinity for GST+ Methyl parathion with binding energy of -4.79 kcal/mol. Overall, methyl parathion produces efficient binding toward all target protein when compare to diazinon. However, more detailed analysis need to be carried out to have an in-depth understanding of in vivo significance of these bimolecular interactions.

Possible role of blood insulin levels on glutathione S-transferase activities from different tissues of male rats

1990 ◽  
Vol 68 (2) ◽  
pp. 170-173 ◽  
Author(s):  
Cristina E. Carnovale ◽  
Juan A. Monti ◽  
Viviana A. Catania ◽  
Maria C. Carrillo
Keyword(s):  
Diabetic Rats ◽  
Male Rats ◽  
Blood Levels ◽  
Transferase Activity ◽  
Glutathione S Transferase ◽  
Insulin Levels ◽  
Blood Insulin ◽  
Glucose Levels

The activity of in vitro glutathione S-transferase towards 1-chloro-2,4-dinitrobenzene was examined in liver, renal cortex, and small intestine (duodenum, jejunum, ileum) after the in vivo treatment of male Wistar rats with streptozotocin or alloxan. The studies were performed at 2, 10, 24, and 48 h and 7 and 15 days after streptozotocin treatment or 24 and 48 h after alloxan treatment. The results indicated that while the blood levels of insulin–glucose did not show variations, there were no alterations of the glutathione S-transferase activity in the tissues tested. On the other hand, when the treatments caused modifications on blood insulin–glucose levels, there were changes of glutathione S-transferase activity in all tissues (except in the ileum) in such a way that a direct relationship between plasma insulin levels and glutathione S-transferase activity could be demonstrated. These results were also confirmed through insulin administration to control and diabetic rats. The data demonstrate a possible regulation of glutathione S-transferase activity by blood insulin and (or) glucose levels in the tissues tested.Key words: insulin, glutathione S-transferase, streptozotocin, alloxan.

scholarly journals Comparison of renal and hepatic glutathione S-transferases in the rat

1976 ◽  
Vol 158 (2) ◽  
pp. 243-248 ◽  
Author(s):  
N Kaplowitz ◽  
G Clifton ◽  
J Kuhlenkamp ◽  
J D Wallin
Keyword(s):  
Organic Anion ◽  
Gel Filtration ◽  
Competitive Inhibitor ◽  
Transferase Activity ◽  
Close Correspondence ◽  
Glutathione S Transferase ◽  
Competitive Inhibitors ◽  
Liver And Kidney ◽  
Glutathione S Transferases

Renal and hepatic GSH (reduced glutathione) S-transferase were compared with respect to substrate and inhibitory kinetics and hormonal influences in vivo. An example of each of five classes of substrates (aryl, aralkyl, epoxide, alkyl and alkene) was used. In the gel filtration of renal or hepatic cytosol, an identical elution volume was found for all the transferase activities. Close correspondence in Km values was found for aryl, epoxide- and alkyl-transferase activities, with only the aralkyl activity significantly lower in kidney. Probenecid and p-aminohippurate were competitive inhibitors of renal aryl-, aralkyl-, epoxide- and alkyl-transferase activities and inhibited renal alkene activity. Close correspondence in Ki values for inhibition by probenecid of these activities in kidney and liver was found. In addition, furosemide was a potent competitive inhibitor of renal alkyl-transferase activity. Hypophysectomy resulted in significant increases in aryl-, araklyl-, and expoxide-transferase activities in liver and kidney. The hypophysectomy-induced increases in renal aryl- and aralkyl-transferase activities (approx. 100%) were more than twofold greater than increases in hepatic activities (approx. 40%). Administration of thyroxine prevented the hypophysectomy-induced increase in aryltransferase activity in both kidney and liver. The renal GSH S-transferases, in view of similarities to the hepatic activities, may play a role as cytoplasmic organic-anion receptors, as previously proposed for the hepatic enzymes.

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