scholarly journals Evaluation of Sub-Lethal Toxicity of Benzethonium Chloride in Cyprinus carpio Liver

2020 ◽  
Vol 10 (23) ◽  
pp. 8485
Author(s):  
Stefania Gheorghe ◽  
Daniel N. Mitroi ◽  
Miruna S. Stan ◽  
Cristina A. Staicu ◽  
Marius Cicirma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cyprinus Carpio ◽  
Morphological Changes ◽  
Normal Function ◽  
Hepatic Tissue ◽  
Glutathione S Transferase ◽  
Antioxidant Enzyme System ◽  
Lethal Toxicity ◽  
Benzethonium Chloride ◽  
Glucose 6 Phosphate Dehydrogenase

Benzenthonium chloride (BEC, Hyamine 1622) is a quaternary ammonium surfactant with cationic properties widely used in cleaning, sanitation, and medical products that can become harmful to humans and also to the environment. This study aimed to evaluate its acute effects on Cyprinus carpio fish in terms of oxidative stress and morphological changes on hepatic tissue in order to show the sub-lethal toxicity of BEC. Fish were exposed to 1 mg/L BEC for 24, 48, and 96 h, and the liver samples were collected. The most significant changes were noticed after 96 h of exposure when the entire antioxidant enzyme system was affected. The activities of catalase, glutathione peroxidase, glutathione reductase, and glutathione S-transferase decreased by 44%, 31%, 30%, and 45%, respectively, compared to control. Glucose-6-phosphate dehydrogenase activity decreased by 29% after 96 h of control, inducing a reduction of NADPH formation which decreased by half the level of reduced glutathione, the main non-enzymatic antioxidant. These effects correlated with the raised value of lipid peroxidation after 96 h and the morphology changes on hepatic tissue, such as cytoplasmic vacuolization and nuclear hypertrophy that could affect the normal function of the liver. All of these results showed acute toxicity of BEC on C. carpio after 96 h of exposure, causing oxidative stress response at the hepatic level.

Effect of diallyldisulphide on an antioxidant enzyme system in Candida species

2010 ◽  
Vol 56 (10) ◽  
pp. 816-821 ◽  
Author(s):  
Snowber Yousuf ◽  
Aijaz Ahmad ◽  
Amber Khan ◽  
Nikhat Manzoor ◽  
Luqman Ahmad Khan
Keyword(s):  
Oxidative Stress ◽  
Candida Species ◽  
Allium Sativum ◽  
Enzyme System ◽  
Antioxidant Systems ◽  
Glutathione S Transferase ◽  
Antioxidant Enzyme System ◽  
Antioxidant Metabolites ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Sublethal Concentrations

This study was carried out to show the effect of diallyldisulphide (DADS), an important organosulphur compound found in garlic ( Allium sativum ), on antioxidant systems in Candida species. Changes in antioxidant metabolites and antioxidant activity in the presence of DADS were found in Candida albicans and Candida tropicalis . Candida cells were treated with sublethal concentrations of DADS. DADS caused a decrease in the activity of all antioxidant enzymes except catalase, resulting in oxidative stress and damaged cells. The amount of oxidative stress generated by DADS was found to be a function of its concentration. A significant decrease in superoxide dismutase, glutathione-S-transferase, and glutathione peroxidase activities but an increase in catalase activity were observed. Increased levels of lipid peroxidation and decreased levels of glutathione were observed in treated cells. Activity of glucose-6-phosphate dehydrogenase decreased significantly following DADS treatment and could be correlated with a decrease in glutathione concentration in both Candida species. These results indicate that diallyl disulphide acts as a pro-oxidant to Candida species and hence may act as a potent antifungal in the management of candidiasis.

scholarly journals Effects of ibogaine per os treatment on redox homeostasis in rat kidney

2019 ◽  
Vol 71 (2) ◽  
pp. 245-252
Author(s):  
Teodora Vidonja-Uzelac ◽  
Nikola Tatalovic ◽  
Milica Mijovic ◽  
Aleksandra Nikolic-Kokic ◽  
Zorana Orescanin-Dusic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Kidney Function ◽  
Morphological Changes ◽  
Human Subjects ◽  
Rat Kidney ◽  
Redox Homeostasis ◽  
Glutathione S Transferase ◽  
Kidney Morphology ◽  
And Oxidative Stress

Our previous results showed that a single oral dose (1 or 20 mg/kg body weight) of the anti-addiction agent ibogaine induced in rats 6 and 24 h after administration glycogenolytic activity in hepatocytes, followed by a mild oxidative stress. In this work, we examined the in vivo effect of the same doses of ibogaine on rat kidney morphology, antioxidant enzyme (superoxide dismutases (SOD1 and 2), catalase, glutathione peroxidase, glutathione reductase (GR) and glutathione- S-transferase) activities, and oxidative stress (TBARS) and redox (-SH groups) parameters. The dose of 1 mg/kg ibogaine induced an elevation in SOD1 activity and decreased GR activity after 6 and 24 h. GR activity was decreased at 6 and 24 h after 20 mg/kg ibogaine administration, suggesting changed redox homeostasis. After 24 h, we observed an increase in moderate morphological changes, without changes in urinalyses, indicating that kidney function was not measurably affected. Nevertheless, kidney-function monitoring during and following ibogaine use in human subjects is advisable.

scholarly journals Direct Determination of Glutathione S-transferase and Glucose-6-phosphate Dehydrogenase Activities in Cells Cultured in Microtitre Plates as Biomarkers for Oxidative Stress

1998 ◽  
Vol 26 (3) ◽  
pp. 321-330 ◽  
Author(s):  
Concepción García-Alfonso ◽  
Guillermo Repetto ◽  
Pilar Sanz ◽  
Manuel Repetto ◽  
Juan López-Barea
Keyword(s):  
Oxidative Stress ◽  
Direct Determination ◽  
Cell Number ◽  
Glutathione S Transferase ◽  
Enzymatic Assays ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Gst Activity ◽  
In Cells

The enzymes glutathione S-transferase (GST) and glucose-6-phosphate dehydrogenase (G-6PDH) are implicated in the defence against oxidative stress. GST is mainly involved in the conjugation of electrophilic compounds with glutathione (GSH), although some of its isoenzymes display peroxidase activity. G-6PDH and glutathione reductase regenerate NADPH and GSH, respectively, to restore the reduced intracellular redox status following oxidative stress. Enzymatic assays for GST and G-6PDH were adapted and optimised to permit the direct in vitro determination of the effects of toxicants which induce oxidative stress in cells on microtitre plates, thereby avoiding the need to prepare cell-free extracts. To optimise the conditions of the enzymatic assays, GST activity’ was measured at substrate concentrations of 1–3mM GSH and 1–3mM 1-chloro-2,4-dinitrobenzene, while G-6PDH activity was measured at 7.5–37.5mM glucose-6-phosphate and 55–275mM NADP. Both enzymatic activities were directly proportional to cell number up to a density of 1 x 105 cells/well. The effects on GST and G-6PDH activities of three toxicants which induce oxidative stress — paraquat, iron (II) chloride and iron (III) chloride — were compared in cultured Vero cells to validate the new assays. Specific GST activity increased to 145% and 171% compared to the controls in cells treated with 5mM paraquat and 5mM iron (II) chloride, respectively, but was inhibited after exposure to 25mM iron (III) chloride. Specific G-6PDH activity increased to 136% compared to the control after exposure to 5mM paraquat, but was inhibited in cells exposed to 5mM iron (II) chloride and 25mM iron (III) chloride.

Nephrotoxicity and its prevention by taurine in tamoxifen induced oxidative stress in mice

2007 ◽  
Vol 26 (6) ◽  
pp. 509-518 ◽  
Author(s):  
Heena Tabassum ◽  
Suhel Parvez ◽  
Hasibur Rehman ◽  
Basu Dev Banerjee ◽  
Detlef Siemen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Tissue Injury ◽  
Treated Group ◽  
Protein Carbonyl ◽  
Enzymatic Antioxidants ◽  
Glutathione S Transferase ◽  
Metabolizing Enzymes ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Phase I And Ii

Tamoxifen (TAM) is an anti-neoplastic drug used for the treatment of breast cancer. It decreases the hexose monophosphate shunt and thereby increasing the incidence of oxidative stress in cells leading to tissue injury. The present study was undertaken to investigate modulatory effects of taurine on the nephrotoxicity of TAM with special reference to protection against disruption of nonenzymatic and enzymatic antioxidants. Oxidative stress was measured by renal lipid peroxidation (LPO) level, protein carbonyl (PC) content, reduced glutathione (GSH), activities of phase I and II drug metabolizing and antioxidant enzymes. TAM treatment resulted in a significant ( P < 0.001) increase in LPO in kidney tissues as compared to control, while taurine pretreatment showed a significant decrease ( P < 0.01) in the LPO in kidneys when compared with the TAM-treated group. Taurine + TAM group animals showed restoration in the level of cytochrome P450 content, activities of glutathione metabolizing enzymes viz., glutathione-S-transferase, glutathione peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase. Pretreatment of animals with taurine markedly attenuated, PC content, restored the depleted nonenzymatic and enzymatic antioxidants. These results clearly demonstrate the role of oxidative stress, and suggest a protective effect of taurine on TAM-induced nephrotoxicity in mice. Human & Experimental Toxicology (2007) 26: 509—518

Effects of Some Boron Compounds on Peripheral Human Blood

2007 ◽  
Vol 62 (11-12) ◽  
pp. 889-896 ◽  
Author(s):  
Hasan Türkez ◽  
Fatime Geyikoǧlu ◽  
Abdulgani Tatar ◽  
Sait Keleş ◽  
Asuman Özkan
Keyword(s):  
Oxidative Stress ◽  
Human Blood ◽  
Blood Cultures ◽  
Antioxidant Enzyme Activities ◽  
Glutathione S Transferase ◽  
Boron Compounds ◽  
Total Antioxidant ◽  
Tissue Damages ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Human Blood Cultures

Peripheral blood cultures were exposed to various doses (5 to 500 mg/L) of boron compounds. Sister-chromatid exchange, micronucleus and chromosomal aberration tests were applied to estimate the DNA damage, and biochemical parameters (superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase, glucose-6-phosphate dehydrogenase, total glutathione, malondialdehyde and total antioxidant capacity) were examined to determine oxidative stress. According to our findings, various boron compounds at low doses were useful in supporting antioxidant enzyme activities in human blood cultures. It was found that the boron compounds do not have genotoxic effects even in the highest concentrations, though in increasing doses they constitute oxidative stress. It is concluded that the tested boron compounds can be used safely, but it is necessary to consider the tissue damages which are likely to appear depending on the oxidative stress.

scholarly journals Polyploidy Analysis and Attenuation of Oxidative Stress in Hepatic Tissue of STZ-Induced Diabetic Rats Treated with an Aqueous Extract ofVochysia rufa

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Izabela Barbosa Moraes ◽  
Camilla Manzan-Martins ◽  
Neire Moura de Gouveia ◽  
Luciana Karen Calábria ◽  
Karen Renata Nakamura Hiraki ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Aqueous Extract ◽  
Morphological Changes ◽  
Liver Homogenate ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Hepatic Tissue ◽  
Polyploid Cell ◽  
Sod Activity ◽  
Rat Livers

Diabetes mellitus (DM) is characterized by hyperglycemia and alterations in the metabolism of lipids, carbohydrates, and proteins. Due to its hypoglycemic effectVochysia rufais frequently used in Uberlandia, Brazil, to treat DM. Despite its popularity, there is little information about its effect on hepatic tissue. Therefore, we evaluated the histoarchitecture, oxidative stress parameters, and polyploidy of liver tissue from streptozotocin- (STZ-) induced diabetic rats treated with aqueous extract ofVochysia rufa(AEV). Histology was determined by fixing the livers, processing, and staining with HE. Oxidative stress was determined by evaluating CAT, GPx, and SOD activity in liver homogenates and hepatic mitochondria fraction and by measuring GST, GSH levels and lipid peroxidation (MDA). Polyploidy was determined by subjecting isolated hepatocyte nuclei to flow cytometry. In the diabetic group, GST activity and GSH rates decreased whereas liver homogenate analysis showed that GPx, SOD activity and MDA increased. AEV treatment restored all parameters to normal levels. The oxidative stress analysis of hepatic mitochondria fraction showed similar results. Lower polyploid cell populations were found in the diabetic rat livers, even after glibenclamide treatment. Thus, AEV treatment efficiently reduced hepatic oxidative stress caused by STZ-induced diabetes and produced no morphological changes in the histological analysis.

Oxidative Stress, Ocular Disease and Diabetes Retinopathy

2019 ◽  
Vol 24 (40) ◽  
pp. 4726-4741 ◽  
Author(s):  
Orathai Tangvarasittichai ◽  
Surapon Tangvarasittichai
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Cell Death ◽  
Protein Modification ◽  
Morphological Changes ◽  
Corneal Dystrophy ◽  
Age Related Macular Degeneration ◽  
Ocular Diseases ◽  
Retinal Light Damage ◽  
Age Related

Background: Oxidative stress is caused by free radicals or oxidant productions, including lipid peroxidation, protein modification, DNA damage and apoptosis or cell death and results in cellular degeneration and neurodegeneration from damage to macromolecules. Results: Accumulation of the DNA damage (8HOdG) products and the end products of LPO (including aldehyde, diene, triene conjugates and Schiff’s bases) were noted in the research studies. Significantly higher levels of these products in comparison with the controls were observed. Oxidative stress induced changes to ocular cells and tissues. Typical changes include ECM accumulation, cell dysfunction, cell death, advanced senescence, disarrangement or rearrangement of the cytoskeleton and released inflammatory cytokines. It is involved in ocular diseases, including keratoconus, Fuchs endothelial corneal dystrophy, and granular corneal dystrophy type 2, cataract, age-related macular degeneration, primary open-angle glaucoma, retinal light damage, and retinopathy of prematurity. These ocular diseases are the cause of irreversible blindness worldwide. Conclusions: Oxidative stress, inflammation and autophagy are implicated in biochemical and morphological changes in these ocular tissues. The development of therapy is a major target for the management care of these ocular diseases.

Chemoprotective Effects of Propolis on Aflatoxin B1-Induced Hepatotoxicity in Rats: Oxidative Damage and Hepatotoxicity by Modulating TP53, Oxidative Stress

2020 ◽  
Vol 17 (3) ◽  
pp. 191-199
Author(s):  
Seval Yilmaz ◽  
Fatih Mehmet Kandemir ◽  
Emre Kaya ◽  
Mustafa Ozkaraca
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Oxidative Damage ◽  
Aflatoxin B1 ◽  
Tp53 Gene ◽  
Control Group ◽  
Glutathione S Transferase ◽  
Gene Expressions ◽  
Cat Gene ◽  
Gst Activity

Objective: This study aimed to detect hepatic oxidative damage caused by aflatoxin B1 (AFB1), as well as to examine how propolis protects against hepatotoxic effects of AFB1. Method: Rats were split into four groups as control group, AFB1 group, propolis group, AFB1+ propolis group. Results: There was significant increase in malondialdehyde (MDA) level and tumor suppressor protein (TP53) gene expression, Glutathione (GSH) level, Catalase (CAT) activity, CAT gene expression decreased in AFB1 group in blood. MDA level and Glutathione-S-Transferase (GST) activity, GST and TP53 gene expressions increased in AFB1 group, whereas GSH level and CAT activity alongside CAT gene expression decreased in liver. AFB1+propolis group showed significant decrease in MDA level, GST activity, TP53 and GST gene expressions, GSH level and CAT activity and CAT gene expression increased in liver compared to AFB1 group. Conclusion: These results suggest that propolis may potentially be natural agent that prevents AFB1- induced oxidative stress and hepatotoxicity.

scholarly journals The Pah-R261Q mouse reveals oxidative stress associated with amyloid-like hepatic aggregation of mutant phenylalanine hydroxylase

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Oscar Aubi ◽  
Karina S. Prestegård ◽  
Kunwar Jung-KC ◽  
Tie-Jun Sten Shi ◽  
Ming Ying ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Misfolding ◽  
Phenylalanine Hydroxylase ◽  
Hepatic Tissue ◽  
Loss Of Function ◽  
Advantageous Position ◽  
Protein Misfolding And Aggregation ◽  
Activity Decrease ◽  
Systemic Accumulation ◽  
Altered Lipid

AbstractPhenylketonuria (PKU) is caused by autosomal recessive variants in phenylalanine hydroxylase (PAH), leading to systemic accumulation of L-phenylalanine (L-Phe) that may reach neurotoxic levels. A homozygous Pah-R261Q mouse, with a highly prevalent misfolding variant in humans, reveals the expected hepatic PAH activity decrease, systemic L-Phe increase, L-tyrosine and L-tryptophan decrease, and tetrahydrobiopterin-responsive hyperphenylalaninemia. Pah-R261Q mice also present unexpected traits, including altered lipid metabolism, reduction of liver tetrahydrobiopterin content, and a metabolic profile indicative of oxidative stress. Pah-R261Q hepatic tissue exhibits large ubiquitin-positive, amyloid-like oligomeric aggregates of mutant PAH that colocalize with selective autophagy markers. Together, these findings reveal that PKU, customarily considered a loss-of-function disorder, can also have toxic gain-of-function contribution from protein misfolding and aggregation. The proteostasis defect and concomitant oxidative stress may explain the prevalence of comorbid conditions in adult PKU patients, placing this mouse model in an advantageous position for the discovery of mutation-specific biomarkers and therapies.

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