A Major Human Arsenic Metabolite, Dimethylarsinic Acid, Requires Reduced Glutathione To Induce Apoptosis

2002 ◽  
Vol 15 (5) ◽  
pp. 629-637 ◽  
Author(s):  
Teruaki Sakurai ◽  
Wei Qu ◽  
Masumi H. Sakurai ◽  
Michael P. Waalkes
Keyword(s):  
Reduced Glutathione ◽  
Dimethylarsinic Acid ◽  
Arsenic Metabolite

Effect of streptozotocin on red-blood-cell-reduced glutathione: modification by glucose, nicotinamide, and epinephrine

Diabetes ◽  
1976 ◽  
Vol 25 (3) ◽  
pp. 216-222 ◽  
Author(s):  
A. E. Slonim ◽  
T. Fletcher ◽  
V. Burke ◽  
I. M. Burr
Keyword(s):  
Blood Cell ◽  
Red Blood Cell ◽  
Reduced Glutathione

Indicators of the antioxidant system in the long-term period after acute mercury nitrate poisoning in the experiment

2020 ◽  
pp. 36-41
Author(s):  
E. G. Batotsyrenova ◽  
O. A. Vakunenkova ◽  
E. A. Zolotoverkhaya ◽  
V. A. Kashuro ◽  
T. A. Kostrova ◽  
...  
Keyword(s):  
Antioxidant System ◽  
Antioxidant Defense ◽  
Reduced Glutathione ◽  
Antioxidant Defense System ◽  
Mercury Content ◽  
The State ◽  
Cytotoxic Effects ◽  
Entire Study ◽  
Mercury Nitrate

The article presents experimental data on the state of the antioxidant system in red blood cells of white outbred rats 1 and 3 months after acute mercury nitrate poisoning with a semilethal dose. It has been established that this form of intoxication is accompanied by pronounced changes in the state of the antioxidant defense system in erythrocytes of poisoned animals (a decrease in the concentration of reduced glutathione, a decrease in the activity of superoxide dismutase and glutathione peroxidase, and an increase in the concentration of lipid peroxidation products).It has been shown that the mercury content in the blood of experimental animals remains elevated during the entire study period.The results obtained indicate the importance of impaired functioning of the antioxidant system in the implementation of long-term consequences of acute mercury poisoning. The reasons for the occurrence of these biochemical shifts and their role in the development of the long-term cytotoxic effects of mercury nitrate are discussed.

Bergenin Exhibits Hepatoprotective Activity Against Ethanol-Induced Oxidative Stress in ICR Mice

2019 ◽  
Vol 18 (4) ◽  
pp. 297-302
Author(s):  
Sriset Yollada ◽  
Chatuphonprasert Waranya ◽  
Jarukamjorn Kanokwan
Keyword(s):  
Reactive Oxygen Species ◽  
Gallic Acid ◽  
Aspartate Aminotransferase ◽  
Alanine Aminotransferase ◽  
Hepatic Injury ◽  
Reduced Glutathione ◽  
Reactive Oxygen ◽  
Hepatoprotective Activity ◽  
Oxygen Species ◽  
Hepatic Glutathione

Bergenin is a C-glucoside derivative of gallic acid but its antioxidant and hepatoprotective effects have not previously been compared with gallic acid. Male ICR mice were administered bergenin (10, 50, and 250 mg/kg/day) or gallic acid (100 mg/kg/day) for 7 consecutive days before a single administration of ethanol (5 g/kg). Liver sections were histopathologically examined. Aspartate aminotransferase, alanine aminotransferase, reactive oxygen species, and malondialdehyde levels were determined in plasma. Total glutathione, reduced glutathione, and oxidized glutathione levels were determined in liver homogenates. Ethanol induced hepatic injury with prominent histopathological markers including nuclear pyknosis and necrotic areas and this accorded with increases in the plasma levels of aspartate aminotransferase, alanine aminotransferase, reactive oxygen species, and malondialdehyde. Moreover, ethanol disturbed hepatic glutathione homeostasis by reducing glutathione stores. Hepatic injury in the ethanol-induced mice was prevented with bergenin and gallic acid by significant decreases in plasma aspartate aminotransferase, alanine aminotransferase, reactive oxygen species, and malondialdehyde levels and restoration of the hepatic glutathione profile through an increase in the reduced glutathione/oxidized glutathione ratio. Bergenin at 10 mg/kg/day showed comparable hepatoprotective activity to gallic acid in an ethanol-induced mouse model of oxidative stress. Therefore, bergenin might be a promising candidate for further development as a novel hepatoprotective product.

Astaxanthin, the Natural Antioxidant, Reduces Reserpine Induced Depression in Mice

2020 ◽  
Vol 16 (9) ◽  
pp. 1319-1327
Author(s):  
Ferdous Khan ◽  
Syed A. Kuddus ◽  
Md. H. Shohag ◽  
Hasan M. Reza ◽  
Murad Hossain
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Reduced Glutathione ◽  
Forced Swim Test ◽  
Tail Suspension Test ◽  
Glutathione Depletion ◽  
Swim Test ◽  
Stress Markers ◽  
Immobility Time ◽  
Biochemical Level

Background: An imbalance between pro-oxidants and antioxidants determines the level of oxidative stress which is implicated in the etiopathogenesis of various neuropsychiatric disorders including depression. Therefore, treatment with antioxidants could potentially improve the balance between pro-oxidants and antioxidants. Objective: The objective of this study was to evaluate the ability of astaxanthin, a potential antioxidant, to reduce reserpine-induced depression in BALB/c mice (Mus musculus). Methods: On the behavioral level, antidepressant property of astaxanthin (50 mg/kg, orally) on reserpine (2 mg/kg, subcutaneously) induced depressed mice was evaluated by Forced Swim Test (FST) and Tail Suspension Test (TST). In the biochemical level, the ability of astaxanthin to mitigate reserpine-induced oxidative stress was evaluated by the measurement of Malondialdehyde (MDA) and nitric oxide (NO) in brain, liver and plasma samples. On the other hand, the efficiency of astaxanthin to replenish glutathione depletion and antioxidant enzyme activity augmentation in the same samples were also investigated. Results: Astaxanthin was able to lower reserpine induced immobility time significantly (p<0.05) in FST and TST. Mice treated with astaxanthin showed significantly (p<0.05) low level of oxidative stress markers such as Malondialdehyde (MDA), Nitric Oxide (NO). Consistently, the level of reduced Glutathione (GSH), and the activity of Superoxide Dismutase (SOD) and catalase were augmented due to the oral administration of astaxanthin. Conclusion: This study suggests that astaxanthin reduces reserpine-induced oxidative stress and therefore might be effective in treating oxidative stress associated depression.

Renal Cortical Slices: An In Vitro Model for Kidney Metabolism and Toxicity

1992 ◽  
Vol 20 (1) ◽  
pp. 71-76
Author(s):  
Andrea Trevisan ◽  
Stefano Maso ◽  
Paola Meneghetti
Keyword(s):  
Wistar Rats ◽  
Reduced Glutathione ◽  
Organic Anion ◽  
Cortical Slice ◽  
Lactate Dehydrogenase Release ◽  
Age Related ◽  
Renal Cortical Slice ◽  
Male Wistar Rats ◽  
Vitro Model

The in vitro renal cortical slice model was used to study: 1) the effects on the kidney of some haloalkanes and haloalkenes using 3-month-old male Wistar rats; 2) influence of age and sex on renal cortical slice indices in non-treated rats; and 3) effects of 1,2-dichloropropane on the slices after pretreatment of 3-month-old male Wistar rats with DL-butathionine-[S,R]-sulphoximine. The most nephrotoxic chemical used was 1,3-dichloropropene, which caused a total depletion in the levels of reduced glutathione, a high peroxidation of lipid (about three thousand-fold with respect to control), a significant release of tubular enzymes into the medium, and loss of organic anion ( p-aminohippurate) accumulation. All the chemicals affected the cytosol more than the brush border. The most remarkable age-related differences in the untreated slices were the progressive decrease of reduced glutathione (p<0.05 from three months of age), and an increase in lactate dehydrogenase release into the medium (p<0.05 from six months of age). By contrast, sex differences were slight. The ‘treatment with 1,2-dichloropropane of slices prepared from rats pretreated with DL-butathionine-[S,R]-sulphoximine significantly increased the depletion of glutathione content (p<0.05) and malondialdehyde release in the medium (p<0.001) caused by the solvent alone.

scholarly journals Mitigative effect of Momordica cymbalaria fruit extract against sodium fluoride induced hepatotoxicity in Wistar male albino rats

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Raghavendra Mitta ◽  
Sushmitha Duddu ◽  
Raghuveer Yadav Pulala ◽  
Pradeepkumar Bhupalam ◽  
Venkatakirankumar Mandlem ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Blood Serum ◽  
Sodium Fluoride ◽  
Total Protein ◽  
Reduced Glutathione ◽  
Serum Biomarkers ◽  
Albino Rats ◽  
Serum Total Protein ◽  
Treatment Groups ◽  
Group I

AbstractObjectivesThe main objective of the present study is to evaluate the mitigative effect of hydroalcoholic extract of Momordica cymbalaria fruits against sodium fluoride (NaF) induced hepatotoxicity.MethodsIn this study, Wistar male albino rats were randomly divided into five groups of six rats each. Group I and II served as normal and toxic controls. Group III as plant control received extract at a dose of 400 mg/kg b. wt, p.o and Groups IV and V as treatment groups received extract at a dose 200 and 400 mg/kg b. wt, p.o for 30 days. All groups except Groups I and III received 100 ppm of NaF through drinking water. After completion of the study, blood collected for the estimation of liver blood serum biomarkers such as aspartate aminotransferases (AST), alanine aminotransferases (ALT), alkaline Phosphatase (ALP), direct and total bilirubin, total protein and albumin. The liver tissue homogenate was for estimation of lipid peroxidation, catalase, and reduced glutathione levels.ResultsThe results showed that NaF intoxication caused elevation of liver blood serum levels and lipid peroxidation; decreased levels of serum total protein, albumin and liver reduced glutathione, and catalase observed. The treatment groups showed decreased elevated serum biomarkers (ALT, AST, and ALP), liver lipid peroxidation and increased serum total protein and albumin, liver reduced glutathione and catalase levels in a dose-dependent manner. Histopathological studies also further strongly supported for mitigative effects of the plant.ConclusionsIn conclusion, our findings of the study indicated that M. cymbalaria fruits were a potential drug candidate in the treatment of NaF induced hepatotoxicity.

scholarly journals Dietary Black Seed Effects on Growth Performance, Proximate Composition, Antioxidant and Histo-Biochemical Parameters of a Culturable Fish, Rohu (Labeo rohita)

Animals ◽  
2020 ◽  
Vol 11 (1) ◽  
pp. 48
Author(s):  
Maria Latif ◽  
Mehwish Faheem ◽  
Asmatullah ◽  
Seyed Hossein Hoseinifar ◽  
Hien Van Doan
Keyword(s):  
Growth Performance ◽  
Proximate Composition ◽  
Biochemical Parameters ◽  
Reduced Glutathione ◽  
Labeo Rohita ◽  
Nigella Sativa ◽  
Growth Promoter ◽  
Feeding Trial ◽  
Glutathione S Transferase ◽  
Black Seed

This feeding trial was conducted to investigate the effects of dietary black seed (Nigella sativa) supplementation on the growth performance, muscles proximate composition, antioxidant and histo-biochemical parameters of rohu (Labeo rohita). Fingerlings (8.503 ± 0.009 g) were fed on 0.0%, 1% and 2.5% black seed supplemented diets for 28 days. Fish sampling was done on the 7th, 14th, 21st and 28th day of experiment. The results of the present study indicated that black seed supplementation significantly increased growth performance and muscles protein contents of rohu over un-supplemented ones. Lipid peroxidation levels significantly decreased in all the studied tissues (liver, gills, kidney and brain) of black seed fed rohu, whereas the antioxidant enzymes (catalase, glutathione-S-transferase, glutathione peroxidase and reduced glutathione) activities were increased in all the studied tissues of black seed supplemented rohu at each sampling day. The hepatic-nephric marker enzymes levels were decreased for black seed fed rohu. The present study showed that tested black seed levels are safe for rohu. Black seed is cheaply available in local markets of Pakistan; therefore, based on the results of the present study, it is suggested that black seed has potential to be used as natural growth promoter and antioxidant in the diet of rohu.

scholarly journals Oxidative Stress in Non-Dialysis-Dependent Chronic Kidney Disease Patients

2021 ◽  
Vol 18 (15) ◽  
pp. 7806
Author(s):  
Patricia Tomás-Simó ◽  
Luis D’Marco ◽  
María Romero-Parra ◽  
Mari Carmen Tormos-Muñoz ◽  
Guillermo Sáez ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Reduced Glutathione ◽  
Genetic Material ◽  
Future Research ◽  
Control Group ◽  
Dialysis Patients ◽  
Early Stages ◽  
Molecular Lines

Background: Cardiovascular complications are the leading cause of morbidity and mortality at any stage of chronic kidney disease (CKD). Moreover, the high rate of cardiovascular mortality observed in these patients is associated with an accelerated atherosclerosis process that likely starts at the early stages of CKD. Thus, traditional and non-traditional or uremic-related factors represent a link between CKD and cardiovascular risk. Among non-conventional risk factors, particular focus has been placed on anaemia, mineral and bone disorders, inflammation, malnutrition and oxidative stress and, in this regard, connections have been reported between oxidative stress and cardiovascular disease in dialysis patients. Methods: We evaluated the oxidation process in different molecular lines (proteins, lipids and genetic material) in 155 non-dialysis patients at different stages of CKD and 45 healthy controls. To assess oxidative stress status, we analyzed oxidized glutathione (GSSG), reduced glutathione (GSH) and the oxidized/reduced glutathione ratio (GSSG/GSH) and other oxidation indicators, including malondialdehyde (MDA) and 8-oxo-2’-deoxyguanosine (8-oxo-dG). Results: An active grade of oxidative stress was found from the early stages of CKD onwards, which affected all of the molecular lines studied. We observed a heightened oxidative state (indicated by a higher level of oxidized molecules together with decreased levels of antioxidant molecules) as kidney function declined. Furthermore, oxidative stress-related alterations were significantly greater in CKD patients than in the control group. Conclusions: CKD patients exhibit significantly higher oxidative stress than healthy individuals, and these alterations intensify as eGFR declines, showing significant differences between CKD stages. Thus, future research is warranted to provide clearer results in this area.

scholarly journals Importance of monitoring arsenic methylation metabolism in acute promyelocytic leukemia patients receiving the treatment of arsenic trioxide

2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Yu Zheng ◽  
Yuan-Fei Mao ◽  
Hui-Jin Zhao ◽  
Li Chen ◽  
Li-Ning Wang ◽  
...  
Keyword(s):  
Arsenic Trioxide ◽  
Acute Promyelocytic Leukemia ◽  
Arsenic Speciation ◽  
Promyelocytic Leukemia ◽  
Chronic Liver ◽  
Dimethylarsinic Acid ◽  
Metabolic Pattern ◽  
Methylation Index ◽  
Arsenic Methylation

Abstract Background Arsenic trioxide [ATO, inorganic arsenite (iAsIII) in solution] plays an important role in the treatment of acute promyelocytic leukemia (APL). However, the long-term adverse effects (AEs) and the retention of arsenic among APL patients are rarely reported. In this study, we focused on arsenic methylation metabolism and its relationship with chronic hepatic toxicity, as we previously reported, among APL patients who had finished the treatment of ATO. Methods A total of 112 de novo APL patients who had completed the ATO-containing treatment were enrolled in the study. Arsenic species [iAsIII, inorganic arsenate (iAsV), and their organic metabolites, monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA)] in patients’ plasma, urine, hair and nails were detected by high-performance liquid chromatography combined with inductively coupled plasma mass spectrometry (HPLC-ICP-MS). Eighteen single nucleotide polymorphisms (SNPs) of the arsenic (+ 3 oxidative state) methylation transferase (AS3MT) gene, which was known as the main catalyzer for arsenic methylation, were tested with the polymerase chain reaction method. Results The study showed the metabolic pattern of arsenic in APL patients undergoing and after the treatment of ATO, in terms of total arsenic (TAs) and four species of arsenic. TAs decreased to normal after 6 months since cessation of ATO. But the arsenic speciation demonstrated significantly higher portion of iAsIII in patient’s urine (40.08% vs. 1.94%, P < 0.001), hair (29.25% vs. 13.29%, P = 0.002) and nails (30.21% vs. 13.64%, P = 0.003) than the healthy controls’, indicating a decreased capacity of arsenic methylation metabolism after the treatment of ATO. Urine primary methylation index (PMI) was significantly lower in patients with both chronic liver dysfunction (0.14 vs. 0.28, P = 0.047) and hepatic steatosis (0.19 vs. 0.3, P = 0.027), suggesting that insufficient methylation of arsenic might be related to chronic liver disorders. Two SNPs (A9749G and A27215G) of the AS3MT gene were associated with impaired urine secondary methylation index (SMI). Conclusions The long-term follow-up of arsenic speciation indicated a decreased arsenic methylation metabolism and a probable relationship with chronic hepatic disorders among APL patients after the cessation of ATO. Urine PMI could be a monitoring index for chronic AEs of ATO, and the SNPs of AS3MT gene should be considered when determining the dosage of ATO.

Sign in / Sign up

Export Citation Format

Share Document