scholarly journals Sex affects the response of Wistar rats to polyvinyl pyrrolidone (PVP)-coated silver nanoparticles in an oral 28 days repeated dose toxicity study

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Marija Ćurlin ◽  
Rinea Barbir ◽  
Sanja Dabelić ◽  
Marija Ljubojević ◽  
Walter Goessler ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Silver Nanoparticles ◽  
Stress Responses ◽  
Wistar Rats ◽  
Scientific Information ◽  
Female Rats ◽  
Repeated Dose ◽  
Low Doses

Abstract Background Silver nanoparticles (AgNPs) are widely used in biomedicine due to their strong antimicrobial, antifungal, and antiviral activities. Concerns about their possible negative impacts on human and environmental health directed many researchers towards the assessment of the safety and toxicity of AgNPs in both in vitro and in vivo settings. A growing body of scientific information confirms that the biodistribution of AgNPs and their toxic effects vary depending on the particle size, coating, and dose as well as on the route of administration and duration of exposure. This study aimed to clarify the sex-related differences in the outcomes of oral 28 days repeated dose exposure to AgNPs. Methods Wistar rats of both sexes were gavaged daily using low doses (0.1 and 1 mg Ag/kg b.w.) of polyvinylpyrrolidone (PVP)-coated small-sized (10 nm) AgNPs. After exposure, blood and organs of all rats were analysed through biodistribution and accumulation of Ag, whereas the state of the liver and kidneys was evaluated by the levels of reactive oxygen species (ROS) and glutathione (GSH), catalase (CAT) activity, superoxide dismutase (SOD) and glutathione peroxidase (GPx), expression of metallothionein (Mt) genes and levels of Mt proteins. Results In all animals, changes in oxidative stress markers and blood parameters were observed indicating the toxicity of AgNPs applied orally even at low doses. Sex-related differences were noticed in all assessed parameters. While female rats eliminated AgNPs from the liver and kidneys more efficiently than males when treated with low doses, the opposite was observed for animals treated with higher doses of AgNPs. Female Wistar rats exposed to 1 mg PVP-coated AgNPs/kg b.w. accumulated two to three times more silver in the blood, liver, kidney and hearth than males, while the accumulation in most organs of digestive tract was more than ten times higher compared to males. Oxidative stress responses in the organs of males, except the liver of males treated with high doses, were less intense than in the organs of females. However, both Mt genes and Mt protein expression were significantly reduced after treatment in the liver and kidneys of males, while they remained unchanged in females. Conclusions Observed toxicity effects of AgNPs in Wistar rats revealed sex-related differences in response to an oral 28 days repeated exposure.

scholarly journals Protective Effect of Coconut Oil Meal Phenolic Antioxidants against Macromolecular Damage: In Vitro and In Vivo Study

2020 ◽  
Vol 2020 ◽  
pp. 1-8 ◽  
Author(s):  
A. N. Karunasiri ◽  
C. M. Senanayake ◽  
H. Hapugaswatta ◽  
N. Jayathilaka ◽  
K. N. Seneviratne
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Stress Responses ◽  
Coconut Oil ◽  
Oral Feeding ◽  
Phenolic Antioxidants ◽  
Significant Difference ◽  
Macromolecular Damage

Coconut oil meal, a cheap by-product of coconut oil production, is a rich source of phenolic antioxidants. Many age-related diseases are caused by reactive oxygen species- (ROS-) induced damage to macromolecules such as lipids, proteins, and DNA. In the present study, the protective effect of the phenolic extract of coconut oil meal (CMPE) against macromolecular oxidative damage was evaluated using in vitro and in vivo models. Sunflower oil, bovine serum albumin (BSA), and plasmid DNA were used in the in vitro study, and thiobarbituric acid reactive substances (TBARS), protein carbonyl, and nicked DNA were evaluated as oxidation products. The inhibitory effect of CMPE against H2O2-induced macromolecular damage was evaluated using cultured HEp-2 cells. The results indicate that CMPE inhibits macromolecular damage both in vitro and in vivo. In addition, CMPE regulates redox status of HEp-2 cells under oxidative stress conditions by maintaining higher reduced glutathione levels. There was no significant difference in the expression of glutathione peroxidase in stressed and unstressed cells suggesting that CMPE regulates the cellular oxidative stress responses without affecting the expression of oxidative stress response genes. Oral feeding of Wistar rats with CMPE improves the serum and plasma antioxidant status without causing any toxic effects.

Melatonin synthesis enzymes interact with ascorbate peroxidase to protect against oxidative stress in cassava

2020 ◽  
Vol 71 (18) ◽  
pp. 5645-5655 ◽  
Author(s):  
Yujing Bai ◽  
Jingru Guo ◽  
Russel J Reiter ◽  
Yunxie Wei ◽  
Haitao Shi
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Capacity ◽  
Stress Tolerance ◽  
Ascorbate Peroxidase ◽  
Stress Responses ◽  
Direct Interaction ◽  
Ros Scavenging ◽  
Melatonin Synthesis

Abstract Melatonin is an important indole amine hormone in animals and plants. The enzymes that catalyse melatonin synthesis positively regulate plant stress responses through modulation of the accumulation of reactive oxygen species (ROS). However, the relationship between melatonin biosynthetic enzymes and ROS-scavenging enzymes has not been characterized. In this study, we demonstrate that two enzymes of the melatonin synthesis pathway in Manihot esculenta (MeTDC2 and MeASMT2) directly interact with ascorbate peroxidase (MeAPX2) in both in vitro and in vivo experiments. Notably, in the presence of MeTDC2 and MeASMT2, MeAPX2 showed significantly higher activity and antioxidant capacity than the purified MeAPX2 protein alone. These findings indicate that MeTDC2–MeAPX2 and MeASMT2–MeAPX2 interactions both activate APX activity and increase antioxidant capacity. In addition, the combination of MeTDC2, MeASMT2, and MeAPX2 conferred improved resistance to hydrogen peroxide in Escherichia coli. Moreover, this combination also positively regulates oxidative stress tolerance in cassava. Taken together, these findings not only reveal a direct interaction between MeTDC2, MeASMT2, and MeAPX2, but also highlight the importance of this interaction in regulating redox homoeostasis and stress tolerance in cassava.

scholarly journals Dextromethorphan Reduces Oxidative Stress and Inhibits Uremic Artery Calcification

2021 ◽  
Vol 22 (22) ◽  
pp. 12277
Author(s):  
En-Shao Liu ◽  
Nai-Ching Chen ◽  
Tzu-Ming Jao ◽  
Chien-Liang Chen
Keyword(s):  
Oxidative Stress ◽  
Nadph Oxidase ◽  
Vascular Calcification ◽  
Wistar Rats ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Oxidase Inhibitor ◽  
In Vivo Studies ◽  
Ros Production

Medial vascular calcification has emerged as a key factor contributing to cardiovascular mortality in patients with chronic kidney disease (CKD). Vascular smooth muscle cells (VSMCs) with osteogenic transdifferentiation play a role in vascular calcification. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitors reduce reactive oxygen species (ROS) production and calcified-medium–induced calcification of VSMCs. This study investigates the effects of dextromethorphan (DXM), an NADPH oxidase inhibitor, on vascular calcification. We used in vitro and in vivo studies to evaluate the effect of DXM on artery changes in the presence of hyperphosphatemia. The anti-vascular calcification effect of DXM was tested in adenine-fed Wistar rats. High-phosphate medium induced ROS production and calcification of VSMCs. DXM significantly attenuated the increase in ROS production, the decrease in ATP, and mitochondria membrane potential during the calcified-medium–induced VSMC calcification process (p < 0.05). The protective effect of DXM in calcified-medium–induced VSMC calcification was not further increased by NADPH oxidase inhibitors, indicating that NADPH oxidase mediates the effect of DXM. Furthermore, DXM decreased aortic calcification in Wistar rats with CKD. Our results suggest that treatment with DXM can attenuate vascular oxidative stress and ameliorate vascular calcification.

scholarly journals OsnR is an autoregulatory negative transcription factor controlling redox-dependent stress responses in Corynebacterium glutamicum

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Haeri Jeong ◽  
Younhee Kim ◽  
Heung-Shick Lee
Keyword(s):  
Oxidative Stress ◽  
Corynebacterium Glutamicum ◽  
Stress Responses ◽  
Promoter Region ◽  
Underlying Mechanism ◽  
In Vitro Assays ◽  
Expression Of Genes

Abstract Background Corynebacterium glutamicum is used in the industrial production of amino acids and nucleotides. During the course of fermentation, C. glutamicum cells face various stresses and employ multiple regulatory genes to cope with the oxidative stress. The osnR gene plays a negative regulatory role in redox-dependent oxidative-stress responses, but the underlying mechanism is not known yet. Results Overexpression of the osnR gene in C. glutamicum affected the expression of genes involved in the mycothiol metabolism. ChIP-seq analysis revealed that OsnR binds to the promoter region of multiple genes, including osnR and cg0026, which seems to function in the membrane-associated redox metabolism. Studies on the role of the osnR gene involving in vitro assays employing purified OsnR proteins and in vivo physiological analyses have identified that OsnR inhibits the transcription of its own gene. Further, oxidant diamide stimulates OsnR-binding to the promoter region of the osnR gene. The genes affected by the overexpression of osnR have been found to be under the control of σH. In the osnR-overexpressing strain, the transcription of sigH is significantly decreased and the stimulation of sigH transcription by external stress is lost, suggesting that osnR and sigH form an intimate regulatory network. Conclusions Our study suggests that OsnR not only functions as a transcriptional repressor of its own gene and of those involved in redox-dependent stress responses but also participates in the global transcriptional regulation by controlling the transcription of other master regulators, such as sigH.

Extract of the plant Cotinus coggygria Scop. attenuates pyrogallol-induced hepatic oxidative stress in Wistar rats

2011 ◽  
Vol 89 (6) ◽  
pp. 401-411 ◽  
Author(s):  
Sanja Matić ◽  
Snežana Stanić ◽  
Desanka Bogojević ◽  
Melita Vidaković ◽  
Nevena Grdović ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Phase ◽  
Wistar Rats ◽  
Thiobarbituric Acid ◽  
Hepatoprotective Activity ◽  
Acute Phase Reactants ◽  
Markers Of Oxidative Stress ◽  
Cotinus Coggygria

To examine the protective potential of the Cotinus coggygria Scop. methanol extract, Wistar rats were treated with the hepatotoxic compound pyrogallol, which possesses a potent ability to generate free radicals and induce oxidative stress. The ability of the extract to counteract the oxidative stress was examined in rats that were injected with the extract intraperitoneally (500 mg·(kg body weight)–1) either 2 or 12 h before the pyrogallol treatment. The extract possesses a reducing activity in vitro and an ability to chelate the ferrous ion both in vivo and in vitro. Application of the extract prior to pyrogallol treatment led to a decrease in the levels of thiobarbituric acid-reactive substances, aspartate aminotransferase, and alanine aminotransferase, increased activities of antioxidant enzymes and attenuation of DNA damage, as well as increased Akt activity and inhibition of NF-κB protein expression. Treatment with the extract 12 h prior to pyrogallol administration was more effective in suppressing pyrogallol-induced oxidative damage than the 2 h pretreatment. Extract administration promoted an increase in acute phase reactants haptoglobin and α2-macroglobulin that was short of a full-fledged acute phase response. Administration of the extract considerably improved the markers of oxidative stress, thus revealing a potential hepatoprotective activity. Our results suggest that Akt activation, NF-κB inhibition, and induction of the acute phase play important roles in mediating hepatic protection by the extract. The greater effectiveness of the 12 h pretreatment with extract points to the important role that preconditioning assumes in improving resistance to subsequent exposure to oxidative stress.

scholarly journals A Toxicological Assessment of Creatyl-l-Leucine

2018 ◽  
Vol 37 (2) ◽  
pp. 171-187 ◽  
Author(s):  
Robin A. Reddeman ◽  
Róbert Glávits ◽  
John R. Endres ◽  
Timothy S. Murbach ◽  
Gábor Hirka ◽  
...  
Keyword(s):  
Micronucleus Test ◽  
Female Rats ◽  
Repeated Dose ◽  
Oral Toxicity ◽  
Synthetic Compound ◽  
Male And Female Rats ◽  
Toxicological Studies ◽  
Dose Oral

A battery of toxicological studies was conducted to investigate the genotoxicity and repeated-dose oral toxicity of creatyl-l-leucine, a synthetic compound, in rats in accordance with internationally accepted guidelines. There was no evidence of mutagenicity in a bacterial reverse mutation test and in an in vitro mammalian chromosomal aberration test. There was no genotoxic activity observed in an in vivo mammalian micronucleus test at concentrations up to the limit dose of 2,000 mg/kg bw/d. Creatyl-l-leucine did not cause mortality or toxic effects in Hsd.Han Wistar rats in a 90-day repeated-dose oral (gavage) toxicity study at doses of 1,250, 2,500, and 5,000 mg/kg bw/d. The no observed adverse effect level from the 90-day study was determined to be 5,000 mg/kg bw/d, the highest dose tested, for both male and female rats.

scholarly journals Antioxidant activity of novel selena-diazole derivative against oxidative stress induced by dipyrone in female rats

2020 ◽  
Vol 24 (3) ◽  
pp. 202-210
Author(s):  
Nadheerah Neamah ◽  
◽  
Abdul-Razzak Naaeem Khudair ◽  
Shaker A.N Al-Jadaan ◽  
◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Female Rats ◽  
Good Effect ◽  
Antitumor Activities ◽  
Elisa Kit ◽  
Peroxidase Enzyme ◽  
Anti Oxidant

Introduction: Selena-diazole has antioxidant, and antitumor activities. Also selena-diazol exhibited promising antifungal, antibacterial, viral infection and neurodegenerative disease. The aim of the study is to evaluate the antioxidant activity of a novel -(4,5,6,7-tetrahydro- [1,2,3-] selenadiazolo [4,5 e] pyridine-4,6-diyl) bis(benzene-1,3-diol) (T) against dipyrone (Di) induced oxidative stress. Methods: In vitro antioxidant using DPPH, concentrations of T and ascorbic acid (AA) at 10, 20, 30, 40 and 50μg was measured. In vivo study conducted using four groups, received 50mg/kg of T or/and Di and DW for 30 days. Antioxidant estimated in vivo by serum superoxide dismutase activity (SOD); Glutathione Peroxidase enzyme GPx measured by using Rat SOD1 kit and Rat GPX1 ELISA Kit respectively. Furthermore, Malondialdehyde (MDA) is reliable biomarkers to predict oxidative stress. Results: The results indicate IC50 rate using DPPH of T compound 48.888μg/ml. GPx of T and T&Di groups were significantly increased. SOD of T was significantly increased than other groups. MDA results presented essential reduction in T group value than Di group. Conclusion: The study concluded that synthesized novel selena-diazole derivative T has a good effect as an anti-oxidant.

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