Folic Acid Deficiency Enhances the Tyr705 and Ser727 Phosphorylation of Mitochondrial STAT3 in In Vivo and In Vitro Models of Ischemic Stroke

2020 ◽  
Author(s):  
Zhiping Dong ◽  
Xiaoshan Liang ◽  
Qiang Zhang ◽  
Suhui Luo ◽  
Huan Liu ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Folic Acid ◽  
In Vitro Models ◽  
Folic Acid Deficiency ◽  
Acid Deficiency

scholarly journals Collagen metabolism in folic acid deficiency

1974 ◽  
Vol 32 (2) ◽  
pp. 457-469 ◽  
Author(s):  
J. G. A. J. Hautvast ◽  
M. J. Barnes
Keyword(s):  
Ascorbic Acid ◽  
Protein Synthesis ◽  
Folic Acid ◽  
Growth Characteristic ◽  
Male Rats ◽  
Folic Acid Deficiency ◽  
Collagen Formation ◽  
Acid Deficiency

1. The effect of folic acid deficiency on collagen formation, with respect to the level of collagen-protein synthesis and the extent of collagen-proline hydroxylation, has been studied. A folic acid-free diet containing 10 g sulphasuxidine/kg was used to induce folate deficiency in young male rats. Animals were judged folic acid-deficient on the grounds of retardation of growth, characteristic haematological changes and the urinary excretion of formimino-L-glutamic acid.2. From isotope incorporation studies it was found that folic acid deficiency caused a marked impairment in collagen synthesis. It was shown, however, from the use of pair-fed control animals, that this was due in part to a reduced food intake accompanying the vitamin deficiency. The further reduction in synthesis in addition to that attributable to inanition was considered to arise from an involvement of folic acid in general protein synthesis, since it was found that the synthesis of elastin and non-collagenous skin proteins was similarly impaired.3. Reduced synthesis of collagen was not considered attributable to lack of hydroxylation of peptidyl proline that may occur in ascorbic acid deficiency. Hydroxylation of collagen- and elastin-proline was only very slightly impaired in folic acid deficiency. It was concluded that, at least when ascorbic acid is present, folic acid is not directly essential for the hydroxylation, in vivo, of peptidyl proline. The results support the view that ascorbic acid participates direct, in vivo, in this hydroxylation rather than indirect by simply maintaining an adequate level of reduced folates. They do not, however, exclude the possibility, arising from the known ability of tetrahydrofolate to participate in the hydroxylation of collagen proline in vitro, that when both ascorbate and folate are present, the latter may, in some measure, share in the role of reducing agent in the hydroxylation of peptidyl proline in vivo.

Development of embryonic rat eyes in organ culture

Development ◽  
1968 ◽  
Vol 19 (3) ◽  
pp. 407-414
Author(s):  
R. Christy Armstrong ◽  
Joel J. Elias
Keyword(s):  
Organ Culture ◽  
Culture Medium ◽  
Folic Acid Deficiency ◽  
Experimental Conditions ◽  
Acid Deficiency ◽  
Series Of Experiments ◽  
Development In Vitro ◽  
Ocular System

Abnormalities of the ocular system which appear in organ culture in Waymouth's medium with freshly added glutamine (Armstrong & Elias, 1968) resemble those caused by transitory pteryolglutamic acid (PGA or folic acid) deficiency in vivo (Armstrong & Monie, 1966). The configurations of such malformations as lens herniations, retinal diverticula, and rosette-like formations of the retina are remarkably similar in both cases. The experiments reported in this paper were undertaken in an effort to understand the mechanisms involved in the production of similar abnormalities by two very different experimental conditions: the addition of glutamine in vitro and the transitory deficiency of PGA in vivo. One series of experiments involved the effects of manipulation of the PGA and glutamine content of the culture medium on eye development in vitro. Parallel studies on PGA-deficiency in vivo were undertaken in conjunction with organ-culture experiments in order to compare the effects on abnormal eye morphogenesis.

scholarly journals Metabolome Changes in Cerebral Ischemia

Cells ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 1630 ◽  
Author(s):  
Tae Hwan Shin ◽  
Da Yeon Lee ◽  
Shaherin Basith ◽  
Balachandran Manavalan ◽  
Man Jeong Paik ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Cerebral Ischemia ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
In Vitro Models ◽  
Experimental Models ◽  
Metabolic Changes ◽  
Metabolic Disturbances

Cerebral ischemia is caused by perturbations in blood flow to the brain that trigger sequential and complex metabolic and cellular pathologies. This leads to brain tissue damage, including neuronal cell death and cerebral infarction, manifesting clinically as ischemic stroke, which is the cause of considerable morbidity and mortality worldwide. To analyze the underlying biological mechanisms and identify potential biomarkers of ischemic stroke, various in vitro and in vivo experimental models have been established investigating different molecular aspects, such as genes, microRNAs, and proteins. Yet, the metabolic and cellular pathologies of ischemic brain injury remain not fully elucidated, and the relationships among various pathological mechanisms are difficult to establish due to the heterogeneity and complexity of the disease. Metabolome-based techniques can provide clues about the cellular pathologic status of a condition as metabolic disturbances can represent an endpoint in biological phenomena. A number of investigations have analyzed metabolic changes in samples from cerebral ischemia patients and from various in vivo and in vitro models. We previously analyzed levels of amino acids and organic acids, as well as polyamine distribution in an in vivo rat model, and identified relationships between metabolic changes and cellular functions through bioinformatics tools. This review focuses on the metabolic and cellular changes in cerebral ischemia that offer a deeper understanding of the pathology underlying ischemic strokes and contribute to the development of new diagnostic and therapeutic approaches.

Choline and/or Folic Acid Deficiency is Associated with Genomic Damage and Cell Death in Human Lymphocytes In Vitro

2012 ◽  
Vol 64 (3) ◽  
pp. 481-487 ◽  
Author(s):  
Lin Lu ◽  
Juan Ni ◽  
Tao Zhou ◽  
Weijiang Xu ◽  
Michael Fenech ◽  
...  
Keyword(s):  
Cell Death ◽  
Folic Acid ◽  
Human Lymphocytes ◽  
Folic Acid Deficiency ◽  
Acid Deficiency ◽  
Genomic Damage

scholarly journals Hematologic Studies on Erythropoietic Porphyria: A New Case with Severe Hemolysis, Chronic Thrombocytopenia, and Folic Acid Deficiency

Blood ◽  
1964 ◽  
Vol 23 (6) ◽  
pp. 762-775 ◽  
Author(s):  
SAMUEL GROSS ◽  
Vicki Keefer
Keyword(s):  
Folic Acid ◽  
Plasma Glucose ◽  
Unusual Case ◽  
Extramedullary Hematopoiesis ◽  
Folic Acid Deficiency ◽  
Definite Evidence ◽  
Additional Information ◽  
Acid Deficiency ◽  
The Relationship

Abstract An unusual case of erythropoietic porphyria with a severe hemolytic component and thrombocytopenia has been presented. The relationship between the porphyria and the thrombocytopenia, although unclear, showed definite evidence of persistent megakaryocytic hypoplasia. Additional information emphasizing the severity and chronicity of the anemic process included elevated F and A2 hemoglobins, hyperferremia and extramedullary hematopoiesis. The nature of the hemolytic process appeared to be intracorpuscular and not correctible by normal plasma, glucose or ATP. The abnormal in vitro hemolysis, coupled with the appearance of the abnormal nucleated and mature red cells, are suggestive of the defect in heme synthesis seen in some of the hypochromic hypersideremic anemias. A description of therapeutic attempts as well as the appearance of a folate deficiency are included in the report.

scholarly journals THE ACTION OF PTEROYL GLUTAMIC ACID AND NATURAL SOURCES OF FOLIC ACID ON BLOOD DYSCRASIAS INDUCED BY SULFONAMIDE DRUGS

Blood ◽  
1947 ◽  
Vol 2 (5) ◽  
pp. 440-450 ◽  
Author(s):  
H. G. PETERING ◽  
R. A. DELOR ◽  
H. C. MURRAY
Keyword(s):  
Folic Acid ◽  
Yeast Extract ◽  
Liver Extract ◽  
Folic Acid Deficiency ◽  
Growth Depression ◽  
Large Measure ◽  
Acid Deficiency ◽  
Liver Powder ◽  
Effect On Growth

Abstract Sulfanilamide, sulfathiazole, and sulfadiazine have been fed at 1 per cent levels in highly purified diets and their effect on growth, mortality, and blood dyscrasias compared with that of sulfasuxidine. The soluble drugs produce conditions which are similar to those produced by sulfasuxidine. The growth depression is alleviated in large measure in the case of sulfanilamide and to a lesser extent for sulfathiazole and sulfadiazine by folic acid. liver extract powder, and dried yeast extract as well as by para-aminobenzoic acid, The blood dyscrasias due to sulfanilamide, sulfathiazole, and sulfadiazine are severe leukopenia, granulocytopenia, and mild-to-severe anemia. These are uniformly prevented or the severity greatly curtailed by feeding folic acid, liver extract powder, or dried yeast extract. PABA has a lesser effect in the amounts fed. Liver extract powder seems to have a beneficial effect on growth and mortality which is not shown by the other supplements. Both free and conjugated folic acid (as yeast extract and in liver extract powder 1:20) are active in combating the dyscrasias. Evidence from in vitro experiments with Str. haemolyticus (B Lancefield) indicates that neither folic acid, liver extract powder, nor dried yeast extract in ratios to sulfonamide which are effective in preventing the blood dyscrasias will inhibit or block the bacteriostatic action of the sulfonamide drugs in vitro. It is suggested that the action of folic acid, liver powder, and yeast extract is not wholly explained by alleviating a folic acid deficiency caused by intestinal bacteriostasis due to the drugs, but by an increased demand of the animals for folic acid in the presence of certain sulfonamides.

Modulation of Matrix Metalloproteinases by Plant-Derived Products

2020 ◽  
Vol 20 ◽  
Author(s):  
Nur Najmi Mohamad Anuar ◽  
Nurul Iman Natasya Zulkafali ◽  
Azizah Ugusman
Keyword(s):  
Clinical Trials ◽  
Natural Products ◽  
Matrix Metalloproteinases ◽  
Animal Studies ◽  
Current Knowledge ◽  
In Vitro Models ◽  
In Vivo Studies ◽  
Extracellular Matrix Components

: Matrix metalloproteinases (MMPs) are a group of zinc-dependent metallo-endopeptidase that are responsible towards the degradation, repair and remodelling of extracellular matrix components. MMPs play an important role in maintaining a normal physiological function and preventing diseases such as cancer and cardiovascular diseases. Natural products derived from plants have been used as traditional medicine for centuries. Its active compounds, such as catechin, resveratrol and quercetin, are suggested to play an important role as MMPs inhibitors, thereby opening new insights into their applications in many fields, such as pharmaceutical, cosmetic and food industries. This review summarises the current knowledge on plant-derived natural products with MMP-modulating activities. Most of the reviewed plant-derived products exhibit an inhibitory activity on MMPs. Amongst MMPs, MMP-2 and MMP-9 are the most studied. The expression of MMPs is inhibited through respective signalling pathways, such as MAPK, NF-κB and PI3 kinase pathways, which contribute to the reduction in cancer cell behaviours, such as proliferation and migration. Most studies have employed in vitro models, but a limited number of animal studies and clinical trials have been conducted. Even though plant-derived products show promising results in modulating MMPs, more in vivo studies and clinical trials are needed to support their therapeutic applications in the future.

scholarly journals Human Saliva-Mediated Hydrolysis of Eugenyl-β-D-Glucoside and Fluorescein-di-β-D-Glucoside in In Vivo and In Vitro Models

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 172
Author(s):  
Mariusz Dziadas ◽  
Adam Junka ◽  
Henryk Jeleń
Keyword(s):  
Oral Cavity ◽  
Control Sample ◽  
Rapid Test ◽  
Human Saliva ◽  
In Vitro Models ◽  
Microbial Hydrolysis ◽  
Amoxicillin Trihydrate ◽  
Potassium Clavulanate

Eugenyl-β-D-glucopyranoside, also referred to as Citrusin C, is a natural glucoside found among others in cloves, basil and cinnamon plants. Eugenol in a form of free aglycone is used in perfumeries, flavourings, essential oils and in medicinal products. Synthetic Citrusin C was incubated with human saliva in several in vitro models together with substrate-specific enzyme and antibiotics (clindamycin, ciprofloxacin, amoxicillin trihydrate and potassium clavulanate). Citrusin C was detected using liquid chromatography with tandem mass spectrometry (LC-MS/MS). Citrusin C was completely degraded only when incubated with substrate-specific A. niger glucosidase E.C 3.2.1.21 (control sample) and when incubated with human saliva (tested sample). The addition of antibiotics to the above-described experimental setting, stopped Citrusin C degradation, indicating microbiologic origin of hydrolysis observed. Our results demonstrate that Citrusin C is subjected to complete degradation by salivary/oral cavity microorganisms. Extrapolation of our results allows to state that in the human oral cavity, virtually all β-D-glucosides would follow this type of hydrolysis. Additionally, a new method was developed for an in vivo rapid test of glucosidase activity in the human mouth on the tongue using fluorescein-di-β-D-glucoside as substrate. The results presented in this study serve as a proof of concept for the hypothesis that microbial hydrolysis path of β-D-glucosides begins immediately in the human mouth and releases the aglycone directly into the gastrointestinal tract.

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