scholarly journals Effects of Dental Methacrylates on Oxygen Consumption and Redox Status of Human Pulp Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Giuseppina Nocca ◽  
Cinzia Callà ◽  
Giuseppe Ettore Martorana ◽  
Loredana Cicillini ◽  
Sandro Rengo ◽  
...  

Several studies have already demonstrated that the incomplete polymerization of resin-based dental materials causes the release of monomers which might affect cell metabolism. The aim of this study was to investigate the effects of triethylene glycol dimethacrylate, 1,4-butanediol dimethacrylate, urethane dimethacrylate, and 2-hydroxyethyl methacrylate on (1) cellular energy metabolism, evaluating oxygen consumption rate, glucose consumption, glucose 6-phosphate dehydrogenase activity, and lactate production, and (2) cellular redox status, through the evaluation of glutathione concentration and of the activities of enzymes regulating glutathione metabolism.Methods. Human pulp cells were used and oxygen consumption was measured by means of a Clark electrode. Moreover, reactive oxygen species production was quantified. Enzymatic activity and glucose and lactate concentrations were determined through a specific kit.Results. Triethylene glycol dimethacrylate, 1,4-butanediol dimethacrylate, and 2-hydroxyethyl methacrylate induced a decrease in oxygen consumption rate, an enhancement of glucose consumption, and lactate production, whilst glucose 6-phosphate dehydrogenase and glutathione reductase activity were not significantly modified. Moreover, the monomers induced an increase of reactive oxygen species production with a consequent increase of superoxide dismutase and catalase enzymatic activities. A depletion of both reduced and total glutathione was also observed.Conclusion. The obtained results indicate that dental monomers might alter energy metabolism and glutathione redox balance in human pulp cells.

1960 ◽  
Vol XXXV (IV) ◽  
pp. 575-584 ◽  
Author(s):  
C. Borel ◽  
J. Frei ◽  
A. Vannotti

ABSTRACT Enzymatic studies, on leucocytes of pregnant women, show an increase of the alkaline phosphatase activity and a decrease of the glucose consumption and lactate production, as well as of proteolysis. The oxygen consumption, with succinate as substrate, does not vary.


Polymers ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 699
Author(s):  
Bálint Viktor Lovász ◽  
Gergely Berta ◽  
Edina Lempel ◽  
György Sétáló ◽  
Mónika Vecsernyés ◽  
...  

Monomers leached from resin-based composites (RBCs) may reach intrapulpal concentrations of the millimolar (mM) range, which could contribute to inflammation. The aim of this investigation was to assess the cytotoxicity of triethylene glycol dimethacrylate (TEGDMA) monomers on pulp cells as well as to identify molecular mechanisms leading to apoptosis. Pulp cells were harvested from molars extracted for orthodontic reasons and cultured through an explant method. To assess cytotoxicity, cells underwent a 5-day exposure to 0.75, 1.5, and 3 mM TEGDMA and were subject to cell counting and WST-1 staining. Based on the findings, cells were subsequently exposed to 0.1, 0.2, 0.75, 1.5, and 3 mM TEGDMA for 24 h to uncover the details of apoptosis. Changes in the production or cleavage of the apoptosis-specific proteins caspase-8, caspase-9, caspase-3, caspase-12, and Apoptosis-Inducing Factor (AIF) were measured by Western blot. The 5-day study showed concentration- and time-dependent cytotoxicity. Significant cell death was detected after 24 h with TEGDMA concentrations of 1.5 and 3 mM. One-day exposure to TEGDMA led to the activation of caspase-8, -9, -3, and -12 and an increased AIF production. Results suggest that relevant concentrations of TEGDMA monomers, leached from RBCs, induce apoptosis in pulp cells through both caspase-dependent as well as caspase-independent mechanisms. Endoplasmic reticulum stress and the activation of caspase-independent apoptotic pathways may be further mechanisms by which monomers induce apoptosis in pulp cells.


2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Wei Li ◽  
Zhen-Fu Hu ◽  
Bin Chen ◽  
Guo-Xin Ni

Background. Oxygen and glucose are two important nutrients for mammalian cell function. In this study, the effect of glucose and oxygen concentrations on C2C12 cellular metabolism was characterized with an emphasis on detecting whether cells show oxygen conformance (OC) in response to hypoxia.Methods. After C2C12 cells being cultured in the levels of glucose at 0.6 mM (LG), 5.6 mM (MG), or 23.3 mM(HG) under normoxic or hypoxic (1% oxygen) condition, cellular oxygen consumption, glucose consumption, lactate production, and metabolic status were determined. Short-term oxygen consumption was measured with a novel oxygen biosensor technique. Longer-term measurements were performed with standard glucose, lactate, and cell metabolism assays.Results. It was found that oxygen depletion in normoxia is dependent on the glucose concentration in the medium. Cellular glucose uptake and lactate production increased significantly in hypoxia than those in normoxia. In hypoxia the cellular response to the level of glucose was different to that in normoxia. The metabolic activities decreased while glucose concentration increased in normoxia, while in hypoxia, metabolic activity was reduced in LG and MG, but unchanged in HG condition. The OC phenomenon was not observed in the present study.Conclusions. Our findings suggested that a combination of low oxygen and low glucose damages the viability of C2C12 cells more seriously than low oxygen alone. In addition, when there is sufficient glucose, C2C12 cells will respond to hypoxia by upregulating anaerobic respiration, as shown by lactate production.


1999 ◽  
Vol 277 (4) ◽  
pp. R947-R958 ◽  
Author(s):  
Peter W. Aldoretta ◽  
William W. Hay

To test the hypothesis that glucose supply to the uteroplacenta (UP) regulates UP glucose metabolism into oxidative and nonoxidative pathways, we studied eight late-gestation pregnant sheep at low (LG) and high (HG) maternal glucose concentrations (GM), using Fick principle and tracer glucose methodology. UP glucose consumption (UPGC) correlated directly with GM( r = 0.75, P = 0.0006), and UP glucose decarboxylation ( r = 0.80, P = 0.0001), and lactate production ( r = 0.90, P = 0.0001) rates were directly correlated with UPGC. The combined fractional production rate for lactate, fructose, and CO2 from UPGC was the same in LG and HG periods. The fraction of UP oxygen consumption used for glucose oxidation increased by about 50% from LG to HG conditions; however, there was no change in UP oxygen consumption. Nearly half of UPGC was not accounted for by lactate, fructose, and CO2 production, and about two-thirds of UP oxygen consumption was not accounted for by immediate oxidation of glucose carbon just taken up by the UP. These results indicate that glucose supply directly regulates UP glucose oxidative metabolism and that there is a reciprocal relationship between UP glucose oxidation and the oxidation of other substrates.


2018 ◽  
Vol 26 (6) ◽  
pp. 734-744 ◽  
Author(s):  
Hsiu-Chi Lee ◽  
Shih-Chieh Lin ◽  
Meng-Hsing Wu ◽  
Shaw-Jenq Tsai

Endometriosis is a common gynecological disease, which is defined as the growth of endometrial tissues outside the uterine cavity. It often causes dysmenorrhea, dyspareunia, chronic pelvic pain, and infertility in reproductive-age women. However, the pathogenesis of endometriosis remains largely unclear. Since our previous study revealed that ectopic endometriotic stromal cells experience greater hypoxic stress than their eutopic counterparts, we aim to investigate whether the metabolic properties are changed in the ectopic endometriotic stromal cell when compared to its eutopic counterpart. Here, we found the expression of pyruvate dehydrogenase kinase 1 (PDK1), a critical enzyme in regulating glucose metabolism, was increased in ectopic stromal cells. Molecular characterization reveals that overexpression of PDK1 is induced by hypoxia through transcriptional regulation. Upregulation of PDK1 in ectopic endometriotic stromal cells was accompanied by increases in lactate production and oxygen consumption rate when compared to eutopic endometrial stromal cells. Furthermore, our data showed that inhibition of PDK1 activity by treatment with dichloroacetate inhibits the lactate production and oxygen consumption rate of ectopic stromal cells. In addition, hypoxia-induced PDK1 expression prevented cells from H2O2- and low nutrient-induced cell death. These data indicate that ectopic endometriotic cells may adapt to hypoxic microenvironment via upregulating PDK1 and reprogramming metabolism, which provides a survival advantage in the hostile peritoneal microenvironment.


1978 ◽  
Vol 87 (1) ◽  
pp. 114-124 ◽  
Author(s):  
C. van Hardeveld ◽  
A. A. H. Kassenaar

ABSTRACT Hind-limb perfusion was used to study the effect of thyroidectomy on some metabolic parameters in the skeletal muscle of the rat. A week after thyroidectomy obtained by one dose of 3/4 mCi 131I, neither T4 nor T3 was detected in the blood. Lactate production and glycerol production were already decreased a week after the treatment and reached a base level at two weeks. At that time, the oxygen consumption was significantly lower (70 % of initial level) than in the control animals and decreased further in the third week to nearly 50 % of the control level. Glucose consumption and alanine release were decreased three weeks after thyroidectomy. One dose of T3 (10 μg/100 g b. w.), administered to animals two weeks after the injection of 131I, restored the oxygen consumption, lactate production, and glycerol production to normal levels in 24 h. After 48 h, the glucose consumption was normal. Glycerol production was already significantly increased 6 h after T3 injection in animals one week after thyroidectomy, and in another group of animals two weeks after thyroidectomy. Apparently the diminished oxygen consumption in the latter group does not retard the lipolytic response to T3. No direct relationship could be found between the activity of lipolytic process and the thyroid hormone controlled oxygen consumption.


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