scholarly journals Effect of High Glucose-Induced Oxidative Stress on Paraoxonase 2 Expression and Activity in Caco-2 Cells

Cells ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 1616 ◽  
Author(s):  
Camilla Morresi ◽  
Laura Cianfruglia ◽  
Davide Sartini ◽  
Monia Cecati ◽  
Stefania Fumarola ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Free Radical ◽  
High Glucose ◽  
Gastrointestinal Diseases ◽  
Intestinal Cells ◽  
Glycation End Products ◽  
Radical Generation ◽  
Apoptotic Pathways ◽  
Expression And Activity

(1) Background: Hyperglycemia leads to several biochemical and physiological consequences, such as the generation of advanced glycation end products (AGEs) and reactive oxygen species (ROS), which are involved in the development of several human diseases. Intestinal cells are continuously exposed to pro-oxidants and lipid peroxidation products from ingested foods, and also to glyco-oxidative damage. It has been reported that free radical generation may be linked to the development of inflammation-related gastrointestinal diseases. (2) Methods: The effects of high glucose (HG) treatment (50 mM) were assessed in terms of free radical production, lipid peroxidation, and AGEs formation. Furthermore, the expression and the antiapoptotic and antioxidant activity of the paraoxonase-2 (PON2) enzyme in intestinal cells has been investigated. (3) Results: Caco-2 cells treated with media supplied with high glucose (HG) (50 mM) showed, with respect to physiological glucose concentration (25 mM), an increase in ROS production, lipid peroxidation, and AGEs formation. Moreover, a lower PON2 expression and activity in HG-treated cells was related to activation of the apoptotic pathways. (4) Conclusions: Our results demonstrated that high glucose concentrations triggered glyco-oxidative stress in intestinal cells; the downregulation of PON2 could result in a higher oxidative stress and might contribute to intestinal dysfunction.

scholarly journals Oxidative stress in ageing

2017 ◽  
Vol 5 (11) ◽  
pp. 4826 ◽  
Author(s):  
Fasna K. A. ◽  
Geetha N. ◽  
Jean Maliekkal
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Free Radicals ◽  
Free Radical ◽  
Age Groups ◽  
The Body ◽  
Antioxidant Systems ◽  
Lipid Peroxidation Product ◽  
Free Radical Theory ◽  
Radical Theory

Background: Ageing is characterized by a gradual decline in body functions and decreased ability to maintain homeostasis. The free radical theory of ageing proposed by Harman D states that ageing is a result of cumulative damage incurred by free radical reactions. Free radicals are highly reactive molecular species with unpaired electrons; generated in the body by several physiological processes. Prime target to free radical attack are the polyunsaturated fatty acids of cell membranes causing lipid peroxidation. The free radicals are neutralized by the exogenous and endogenous antioxidant systems. Oxidative stress occurs when large number of free radicals are produced or the antioxidant activity is impaired. The present study is focused to find out the role of oxidative stress in ageing.Methods: A cross sectional observational study was undertaken to assess the oxidative stress in ageing; by determining the levels of lipid peroxidation product- malondialdehyde (MDA), the antioxidants- superoxide dismutase (SOD) and ceruloplasmin in various age groups. 150 healthy subjects were selected randomly and categorised into three different age groups of 20-30 years, 40-59 years and 60-90 years; with 50 subjects in each group. Results were expressed as mean ± standard deviation.Results: a significant elevation in serum MDA level and a decline in SOD were observed in 40-59 years and 60-90 years age groups. However, an elevated ceruloplasmin level was found in the above age groups.Conclusions: Aforementioned observations are suggestive of an association between oxidative stress and the progression of ageing process.

scholarly journals Has Oxidative Stress any Role on Mechanisms of Aminophylline – Induced Seizures? An Animal Study

2015 ◽  
Vol 12 (4) ◽  
pp. 269-274 ◽  
Author(s):  
UK Roy ◽  
M Pal ◽  
S Datta ◽  
S Harlalka
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Free Radical ◽  
Molecular Mechanisms ◽  
Clinical History ◽  
Antioxidant Vitamin ◽  
Dependent Manner ◽  
Free Radical Generation ◽  
Radical Generation ◽  
Pre Treatment

Background Aminophylline can trigger seizures in patients without known underlying epilepsy or added risk factor for seizure exacerbation in epilepsy. Most of these seizures are difficult to control and are underappreciated compared to other drug toxicities. Despite a long clinical history of aminophylline-induced seizures, relatively little is known about the underlying molecular mechanisms that contribute to methylxanthine-induced seizure generation.Objective The present study evaluated the possible involvement of free radicals in aminophylline induced seizures in rat.Method The rats were divided into two groups. The first group graded single doses of aminophylline from 100 to 300 mg/kg were administered intraperitoneally. On the basis of the results Aminophylline, a dose (300 mg/kg) producing tonic-clonic seizures and mortality in 100% animals was selected as control in the study. The second group were subjected to single antioxidant (Vitamin E or Vitamin C) or in combination for 45 days then single doses of aminophylline 300 mg/kg administered intraperitoneally to rats.Result Aminophylline induced convulsions in rats in a dose-dependent manner, and both incidence of seizure and mortality were maximum at 300 mg/kg and there was significant increase of free radical generation. But though pre-treatment with antioxidants showed differential attenuating effects on aminophylline induced free radical generation as we all known but they were very much ineffective in antagonizing aminophylline induced seizures and post-seizure mortality by any appreciable extent.Conclusion Though Aminophylline induces oxidative stress the results are suggestive that at least free radicals is not only cause of convulsiogenic effects and post-seizure mortality of aminophylline.Kathmandu University Medical Journal Vol.12(4) 2014; 269-274

Mechanism of Antihepatotoxic Activity of Glycyrrhizin, I: Effect on Free Radical Generation and Lipid Peroxidation

Planta Medica ◽  
1984 ◽  
Vol 50 (04) ◽  
pp. 298-302 ◽  
Author(s):  
Yoshinobu Kiso ◽  
Masahiro Tohkin ◽  
Hiroshi Hikino ◽  
Masao Hattori ◽  
Tatsuya Sakamoto ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Free Radical ◽  
Free Radical Generation ◽  
Radical Generation ◽  
Antihepatotoxic Activity

scholarly journals Effect of thioltransferase on oxidative stress induced by high glucose and advanced glycation end products in human lens epithelial cells

2021 ◽  
Vol 14 (7) ◽  
pp. 965-972
Author(s):  
Qing Liu ◽  
◽  
Hong Yan ◽  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Advanced Glycation End Products ◽  
High Glucose ◽  
Human Lens ◽  
Lens Epithelial Cells ◽  
Advanced Glycation ◽  
Human Lens Epithelial Cells ◽  
Glycation End Products ◽  
End Products

AIM: To study the effect of thioltransferase (TTase) on oxidative stress in human lens epithelial cells (HLECs) induced by high glucose and advanced glycation end products (AGEs). METHODS: HLECs were treated with 35.5 mmol/L glucose or 1.5 mg/mL AGEs modified bovine serum albumin (AGEs-BSA) as the experimental groups, respectively. Cells were collected at the time point of 1, 2, 3, and 4d. The TTase activity were measured accordingly. TTase mRNA levels were detected by quantitative reverse transcription polymerase chain response (qRT-RCR) and its protein level was detected by Western blot. The siRNA was used to knock down the expression of TTase. The activity of catalase (CAT) and superoxide dismutase (SOD), the content of reactive oxygen species (ROS) and the ratio of oxidized glutathione/total glutathione (GSSG/T-GSH) were assessed in different groups, respectively. RESULTS: The level of TTase mRNA gradually increased and reached the top at 2d, then it decreased to the normal level at 4d, and the TTase activity increased from 2 to 3d in both high glucose and AGEs-BSA groups. The TTase expression elevated from 2d in high glucose group, and it began to rise from 3d in AGEs-BSA group. The activity of CAT and SOD showed a decrease and the content of ROS and the ratio of GSSG/T-GSH showed an increase in high glucose and AGEs-BSA group. These biochemical alterations were more prominent in the groups with TTase siRNA. CONCLUSION: High glucose and AGEs can increase ROS content in HLECs; therefore, it induces oxidative stress. This may result in the decreased GSH and increased GSSG content, impaired activity of SOD and CAT. The up-regulated TTase likely provides oxidation damage repair induced by high glucose and AGEs in the early stage.

scholarly journals Water deficit-induced membrane injury and oxidative stress in two barley genotypes

2014 ◽  
Vol 71 (1) ◽  
pp. 17-21 ◽  
Author(s):  
Hanna Bandurska ◽  
Jolanta Floryszak-Wieczorek
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Water Stress ◽  
Water Deficit ◽  
Superoxide Radical ◽  
Membrane Injury ◽  
Induced Membrane ◽  
Radical Generation ◽  
And Oxidative Stress ◽  
Barley Genotypes

The purpose of this paper was to examine the effect of water deficit on membrane injuries, superoxide radical generation and lipid peroxidation in the leaves of two barley genotypes. Six-day-old seedlings of the cv. Aramir and line R567 were used in the experiments. According to our earlier work these genotypes significantly differ in the level of membrane injuries under water deficit conditions. Water stress was applied directly to leaves or to roots. The stress caused considerable membrane injuries in the leaves of all genotypes investigated.The percentage membrane injury was higher in the line R567 than in the cv. Aramir. Water stress imposed on leaves caused higher membrane injuries than water stress imposed on roots. The water stress treatment followed by an oxidative stress in the leaves. Line R567 having noticeably larger membrane injuries also exhibited a higher level of superoxide radical generation than the cv. Aramir. The level of lipid peroxidation increased in the both genotypes under the conditions of water stress imposed on leaves, but not on roots.

Abstract 444: Differential Contribution of Oxygenases in Glycerol-Induced Acute Renal Failure in the Rats

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Mohammad Newaz
Keyword(s):  
Oxidative Stress ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Free Radical ◽  
Disease Model ◽  
Oxidase Inhibitor ◽  
Sprague Dawley ◽  
Free Radical Generation ◽  
Sprague Dawley Rats ◽  
Radical Generation

Oxidative stress has long been identified as one if the mechanism in glycerol-induced acute renal failure (ARF), a disease model of human rhabdomyolysis. Besides NAD(P)H Oxidase, cyclooxygenase (COX) and xanthine oxidase (XO) are important oxygenase system that contributes in free radical generation in the biological system. In this study we explore involvement of these oxygenase system as the source of free radical in ARF and investigate the relationship between NAD(P)H oxidase, COX and XO in this process. Renal failure was induced in male Sprague Dawley rats by injecting glycerol (8 ml / kg; 50% v/v; i.m) with or without pretreatment of apocynin (Apo: mg/kg in drinking water, 7 days) a NAD(P)H Oxidase inhibitor. Rats were sacrificed 24 hrs after inducing ARF and kidney tissues were analyzed for biochemical assays. Glycerol increased free radical production by 39% as evident by elevated 8-isoprostane. Inhibition of NAD(P)H oxidase by apocynin reduced free radicals by 46%. In ARF rats, NAD(P)H oxidase, COX and XO activities were elevated by 106%, 70%, and 208%, respectively. Apocynin prevented this attenuation of NAD(P)H oxidase (54%; p<0.05) and COX (62%; p<0.05) but did not alter XO activity. These data suggests that NAD(P)H oxidase, COX, and XO are involved in generating oxidative stress in ARF. We also propose that COX-mediated free radical generation requires a functional NAD(P)H oxidase.

Sign in / Sign up

Export Citation Format

Share Document