Alteration of activation energy of reaction in the catalase of human erythrocyte by cimetidine, an in vitro thermokinetics study

2020 ◽  
Vol 09 ◽  
Author(s):  
Dariush Minai-Tehrani
Keyword(s):  
Activation Energy ◽  
Human Erythrocyte ◽  
Cell Injury ◽  
Gastrointestinal Diseases ◽  
Maximum Activity ◽  
The Body ◽  
Effect Of Temperature ◽  
Histamine H2 Receptor ◽  
In Cells

Background: Hydrogen peroxide is normally formed during the metabolic pathway of the body. It is a toxic compound for vital cells, which can oxidize many macromolecules and cause damage in cells. Catalase can degrade H2O2 in cells and prevent cell injury. Cimetidine is a histamine H2 receptor blocker which decreases the release of stomach acid and is used for gastrointestinal diseases. Cimetidine inhibited catalase by mixed inhibition. Objective: In this study, effect of temperature on the binding of cimetidine to human erythrocyte catalase was investigated and kinetic factors of the binding were determined. Results: Dixon plot confirmed the mixed type of inhibition and determined the Ki of the drug. Maximum activity of the enzyme was observed at 30oC. Arrhenius plot demonstrated that the activation energy of the enzyme reaction in the absence and presence of cimetidine was about 4.7 and 8.13 kJ/mol, respectively. Temperature coefficient (Q30-40) was determined as about 1.11 and 1.09 in the absence and presence of cimetidine. Conclusion: Cimetidine was able to increase the activation energy of the reaction of catalase, which confirmed the inhibition of the enzyme based on the kinetic results.

scholarly journals Anti-adipogenic and anti-obesity activities of purpurin in 3T3-L1 preadipocyte cells and in mice fed a high-fat diet

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Woo Nam ◽  
Seok Hyun Nam ◽  
Sung Phil Kim ◽  
Carol Levin ◽  
Mendel Friedman
Keyword(s):  
Weight Gain ◽  
High Fat Diet ◽  
Biological Activities ◽  
The Body ◽  
High Fat ◽  
In Vivo Models ◽  
Triglyceride Accumulation ◽  
In Cells

Abstract Background The body responds to overnutrition by converting stem cells to adipocytes. In vitro and in vivo studies have shown polyphenols and other natural compounds to be anti-adipogenic, presumably due in part to their antioxidant properties. Purpurin is a highly antioxidative anthraquinone and previous studies on anthraquinones have reported numerous biological activities in cells and animals. Anthraquinones have also been used to stimulate osteoblast differentiation, an inversely-related process to that of adipocyte differentiation. We propose that due to its high antioxidative properties, purpurin administration might attenuate adipogenesis in cells and in mice. Methods Our study will test the effect purpurin has on adipogenesis using both in vitro and in vivo models. The in vitro model consists of tracking with various biomarkers, the differentiation of pre-adipocyte to adipocytes in cell culture. The compound will then be tested in mice fed a high-fat diet. Murine 3T3-L1 preadipocyte cells were stimulated to differentiate in the presence or absence of purpurin. The following cellular parameters were measured: intracellular reactive oxygen species (ROS), membrane potential of the mitochondria, ATP production, activation of AMPK (adenosine 5′-monophosphate-activated protein kinase), insulin-induced lipid accumulation, triglyceride accumulation, and expression of PPARγ (peroxisome proliferator activated receptor-γ) and C/EBPα (CCAAT enhancer binding protein α). In vivo, mice were fed high fat diets supplemented with various levels of purpurin. Data collected from the animals included anthropometric data, glucose tolerance test results, and postmortem plasma glucose, lipid levels, and organ examinations. Results The administration of purpurin at 50 and 100 μM in 3T3-L1 cells, and at 40 and 80 mg/kg in mice proved to be a sensitive range: the lower concentrations affected several measured parameters, whereas at the higher doses purpurin consistently mitigated biomarkers associated with adipogenesis, and weight gain in mice. Purpurin appears to be an effective antiadipogenic compound. Conclusion The anthraquinone purpurin has potent in vitro anti-adipogenic effects in cells and in vivo anti-obesity effects in mice consuming a high-fat diet. Differentiation of 3T3-L1 cells was dose-dependently inhibited by purpurin, apparently by AMPK activation. Mice on a high-fat diet experienced a dose-dependent reduction in induced weight gain of up to 55%.

The effect of temperature, age and density of gametocytes, and changes in gas composition on exflagellation of Leucocytozoon simondi

1973 ◽  
Vol 51 (6) ◽  
pp. 577-587 ◽  
Author(s):  
N. R. Roller ◽  
S. S. Desser
Keyword(s):  
Inverse Relationship ◽  
The Body ◽  
Effect Of Temperature ◽  
Gas Composition ◽  
Fresh Blood ◽  
Infected Blood ◽  
Per Se ◽  
Time Required ◽  
Made In

The rate of initiation of exflagellation of microgametocytes of Leucocytozoon simondi was studied in relation to temperature, age and density of gametocytes, and changes in gas composition. Observations were made in vitro through examination of fresh blood, and thin blood films were prepared at appropriate intervals. An inverse relationship between temperature and the time required for initiation of ex-flagellation was demonstrated. There was a decrease in the time required for initiation of exflagellation as the temperature increased from 15 to 26C. Between 26 and 40C exflagellation usually occurred in 1–1½ min. Exflagellation at 40C, which approximates the body temperature of the host, indicates that a drop in temperature per se is not necessary for the initiation of exflagellation. Gametocytes appear to be capable of exflagellation for about 5 days postmaturity. Differences in density of parasitemia do not affect the time for initiation of exflagellation. The presence of O2 and a decrease in CO2 are important stimuli for exflagellation. The effect of the above factors on the initiation of exflagellation is discussed in relation to the uptake of infected blood by the simuliid vector of the parasite, and compared with the situation in related Haemosporina

Histamine at low concentrations aggravates rat liver BRL-3A cell injury induced by hypoxia/reoxygenation through histamine H2 receptor in vitro

2013 ◽  
Vol 27 (1) ◽  
pp. 378-386 ◽  
Author(s):  
Tiansheng Wu ◽  
Xiaoliang Gan ◽  
Shaoli Zhou ◽  
Mian Ge ◽  
Zheng Zhang ◽  
...  
Keyword(s):  
Rat Liver ◽  
Cell Injury ◽  
Histamine H2 Receptor ◽  
H2 Receptor ◽  
Low Concentrations ◽  
Hypoxia Reoxygenation

Temperature dependence of in vitro androgen production in testes from hibernating ground squirrels, Spermophilus lateralis

1987 ◽  
Vol 65 (12) ◽  
pp. 3020-3023 ◽  
Author(s):  
Brian M. Barnes ◽  
Paul Licht ◽  
Irving Zucker
Keyword(s):  
Ground Squirrel ◽  
Temperature Compensation ◽  
Laboratory Mouse ◽  
Ground Squirrels ◽  
The Body ◽  
Effect Of Temperature ◽  
Dependent Manner ◽  
Spermophilus Lateralis ◽  
Dose Dependent

The effect of temperature on the in vitro androgen secretion of testes from hibernating ground squirrels was measured in response to stimulation by luteinizing hormone (LH). We wished to determine whether hibernating ground squirrels can maintain responsiveness of gonads while at the low body temperatures of torpor. In gonads incubated at 32 °C, secretion of testosterone increased in a dose-dependent manner in response to ovine-LH or ground squirrel pituitary homogenate. This responsiveness was reduced at 20 and 9 °C and absent at 5 °C, the temperature that most closely approximates the body temperature of torpid ground squirrels. This temperature sensitivity was similar to that in the nonhibernating laboratory mouse. Superfusion of ground squirrel testes revealed a lag of testosterone secretion in response to LH and, additionally, an ability of testes to secrete testosterone after being only briefly exposed to ovine-LH while at 5 °C. These results provide evidence against a hypothesis of temperature compensation that would allow continued testis function during torpor, and support a previous study which indicated that gonadal growth is restricted to intervals of normothermy during and after the hibernation season.

scholarly journals Inulin and oligofructose as prebiotics in the prevention of intestinal infections and diseases

2006 ◽  
Vol 19 (2) ◽  
pp. 216-226 ◽  
Author(s):  
D. Bosscher ◽  
J. Van Loo ◽  
A. Franck
Keyword(s):  
Barrier Function ◽  
Bacterial Flora ◽  
Gastrointestinal Diseases ◽  
The Body ◽  
Intestinal Infections ◽  
Progression Of Disease ◽  
Acid Producing Bacteria ◽  
Intervention Trials ◽  
Epithelial Layers

Health and wellbeing are challenged constantly by pathogens. A number of defence mechanisms exist to protect the body from pathogen colonisation and invasion, with an important role to play for the natural intestinal bacterial flora (mainly by bifidobacteria and lactobacilli). The present paper reviews the evidence on the effects of inulin and oligofructose on colonisation and translocation of pathogens and the prevention of intestinal diseases. In vitro experiments have shown that lactic acid-producing bacteria have antagonistic (antibacterial) activity against pathogens partly because of the production of organic acids which are the endproducts of inulin and oligofructose fermentation. In addition, studies with epithelial layers have shown that inulin and oligofructose inhibit pathogen colonisation and that endproducts of their fermentation have the ability to support barrier function. Furthermore, studies in various animal models have shown that inulin and oligofructose accelerate the recovery of beneficial bacteria, slow down pathogen growth, decreasing pathogen colonisation and systemic translocation. Finally, data from human intervention trials either in patients with intestinal disorders or disease, or prone to critical illness, found that inulin and oligofructose restore the balance when the gut microbial community is altered, inhibit the progression of disease or prevent it from relapsing and/or developing. To conclude, the dietary use of inulin and oligofructose offers a promising approach to restore microbial communities and to support barrier function of the epithelia by their prebiotic action. This may offer the host protection against invasion and translocation of pathogens (endogenous and/or exogenous) and in the prevention of gastrointestinal diseases.

scholarly journals Active Fragment ofVeronica ciliataFisch. Attenuates t-BHP-Induced Oxidative Stress Injury in HepG2 Cells through Antioxidant and Antiapoptosis Activities

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Yiran Sun ◽  
Qiuxia Lu ◽  
Libo He ◽  
Yueyue Shu ◽  
Shiyan Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepg2 Cells ◽  
Cell Injury ◽  
Hepatoprotective Activity ◽  
The Body ◽  
Protein Carbonyls ◽  
Stress Injury ◽  
Oxidative Stress Injury ◽  
Active Fragment

Excessive amounts of reactive oxygen species (ROS) in the body are a key factor in the development of hepatopathies such as hepatitis. The aim of this study was to assess the antioxidation effect in vitro and hepatoprotective activity of the active fragment ofVeronica ciliataFisch. (VCAF). Antioxidant assays (DPPH, superoxide, and hydroxyl radicals scavenging) were conducted, and hepatoprotective effects through the application oftert-butyl hydroperoxide- (t-BHP-) induced oxidative stress injury in HepG2 cells were evaluated. VCAF had high phenolic and flavonoid contents and strong antioxidant activity. From the perspective of hepatoprotection, VCAF exhibited a significant protective effect on t-BHP-induced HepG2 cell injury, as indicated by reductions in cytotoxicity and the levels of ROS, 8-hydroxydeoxyguanosine (8-OHdG), and protein carbonyls. Further study demonstrated that VCAF attenuated the apoptosis of t-BHP-treated HepG2 cells by suppressing the activation of caspase-3 and caspase-8. Moreover, it significantly decreased the levels of ALT and AST, increased the activities of acetyl cholinesterase (AChE), glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT), and increased total antioxidative capability (T-AOC). Collectively, we concluded that VCAF may be a considerable candidate for protecting against liver injury owing to its excellent antioxidant and antiapoptosis properties.

Acute toxicity of polychlorinated naphthalenes and their effect on cytochrome P450

2006 ◽  
Vol 25 (2) ◽  
pp. 85-92 ◽  
Author(s):  
A Galoch ◽  
A Sapota ◽  
M Skrzypinska-Gawrysiak ◽  
A Kilanowicz
Keyword(s):  
Body Weight Loss ◽  
Fold Increase ◽  
Maximum Activity ◽  
The Body ◽  
Control Group ◽  
Polychlorinated Naphthalenes ◽  
Order Of Magnitude ◽  
Cytochrome P 450

Polychlorinated naphthalenes (PCNs) are able to induce cytochrome P-450-dependent microsomal monooxygenase activities in vivo and in vitro. The aim of this study was to investigate the toxicity of a PCN mixture, and its effect on the levels of cytochrome P-450 in rats. The animals were intragastrically administered a mixture of PCNs in single doses of 250, 500 and 1000 mg/kg b.w. Dissection of animals was performed 24, 72 and 240 hours after administration. After PCN administration (all doses) the body weight loss (up to 30% in comparison with the control group, 240 hours after administration) and an increase of relative liver mass (about 126 - 153% of controls, 72 hours after administration) were observed. The exposure to PCN evoked an increase in the level of total cytochrome P-450 as well as the activity of CYP 1A (mediated 7-ethoxyresorufin O-deethylation) at all time points. The maximum activity of CYP 1A (about 12-to 15-fold increase in comparison with the control group) was observed 72 hours after dosing. Malondialdehyde (MDA), determined in the liver, showed a high increase and 240 hours after administration, the level of MDA was about one order of magnitude greater in comparison with control.

scholarly journals A Simple Method for Evaluation of Superoxide Radical Production in Neural Cells under Various Culture Conditions: Application to Hypoxia

1995 ◽  
Vol 15 (1) ◽  
pp. 71-77 ◽  
Author(s):  
Jean-Luc Daval ◽  
Jean-François Ghersi-Egea ◽  
Jean Oillet ◽  
Violette Koziel
Keyword(s):  
Cytochrome C ◽  
Superoxide Radical ◽  
Cell Injury ◽  
Acute Hypoxia ◽  
Culture Conditions ◽  
Superoxide Radicals ◽  
Extracellular Medium ◽  
Simple Method ◽  
In Cells

To evaluate the potential deleterious influence of oxygen-derived free radicals following hypoxia in a model of primary culture of neurons obtained from the fetal rat brain, superoxide radicals were measured as a function of time in the extracellular medium. Neuronal cells were grown for 8 days in the presence or absence of serum, then incubated in a buffered Krebs–Ringer solution containing 60 μ M acetyl-cytochrome c. The rate of superoxide radical formation was quantified spectrophotometrically by measuring the specific reduction of acetyl-cytochrome c. Under normoxic conditions (95% air-5% CO2), basal production of superoxide that increased with time was recorded. It was significantly more pronounced in cells grown in serum-free medium. Under both culture conditions, acute hypoxia (95% N2–5% CO2) for 6 h increased superoxide radical amounts in the extracellular medium, and they were still enhanced 3 h after reoxygenation. The addition of superoxide dismutase to the incubating medium abolished the detection of superoxide radicals. The present study describes a new reliable method for superoxide radical measurement in cells in vitro and demonstrates hypoxia/reoxygenation-induced overproduction of superoxide in cultured neurons that may account for cell injury.

The Effect of Temperature on the Survival In Vitro of Rabbit Spermatozoa Obtained from the Vas Deferens

1930 ◽  
Vol 7 (2) ◽  
pp. 201-219
Author(s):  
ARTHUR WALTON
Keyword(s):  
Body Temperature ◽  
Sex Ratio ◽  
Vas Deferens ◽  
Liquid Paraffin ◽  
The Body ◽  
Effect Of Temperature ◽  
Gaseous Exchange ◽  
Optimum Temperature ◽  
Rabbit Spermatozoa

1. A technique is described for the investigation of in vitro problems with spermatozoa removed from the vas deferens of the rabbit. The method involves the protection of the spermatozoa by means of liquid paraffin from evaporation of rapid gaseous exchange. 2. The survival of functional integrity (fertilizing capacity) has been shown to be a function of temperature and the effect of temperature has been studied over the range from 45° C. to 0° C. Above body temperature the spermatozoa are rapidly destroyed. At body temperature (40° C.) maximal survival is about 13 hours. As the temperature is lowered survival becomes increasingly prolonged until a maximum of 7 days is reached at 15°C. The curve over the range from 15° C. to 40° C. is only approximately exponential and it is doubtful whether an analogy can be drawn between the effect of temperature on the velocity with which the spermatozoa are destroyed, and the effect of temperature on the velocity of many biological reactions which follow approximately the van't Hoff and Arrhenius questions. Below the optimum temperature (10°-15°C.) the velocity of destruction is acclerated by fall of temperature. 3. The sex-ratio of the resulting offspring is not significantly altered by keeping the spermatozoa outside the body.

The Role of Polyphenols in the Modulation of Plasma Non-Enzymatic Antioxidant Capacity (NEAC)

2012 ◽  
Vol 82 (3) ◽  
pp. 228-232 ◽  
Author(s):  
Mauro Serafini ◽  
Giuseppa Morabito
Keyword(s):  
Antioxidant Capacity ◽  
Dietary Intervention ◽  
Ex Vivo ◽  
The Body ◽  
Dietary Polyphenols ◽  
Enzymatic Antioxidant ◽  
Endogenous Antioxidant

Dietary polyphenols have been shown to scavenge free radicals, modulating cellular redox transcription factors in different in vitro and ex vivo models. Dietary intervention studies have shown that consumption of plant foods modulates plasma Non-Enzymatic Antioxidant Capacity (NEAC), a biomarker of the endogenous antioxidant network, in human subjects. However, the identification of the molecules responsible for this effect are yet to be obtained and evidences of an antioxidant in vivo action of polyphenols are conflicting. There is a clear discrepancy between polyphenols (PP) concentration in body fluids and the extent of increase of plasma NEAC. The low degree of absorption and the extensive metabolism of PP within the body have raised questions about their contribution to the endogenous antioxidant network. This work will discuss the role of polyphenols from galenic preparation, food extracts, and selected dietary sources as modulators of plasma NEAC in humans.

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