scholarly journals The Protective Effects of an Adsorbent against Oxidative Stress in Quails Fed Aflatoxin-Contaminated Diet

2017 ◽  
Vol 45 (1) ◽  
pp. 7 ◽  
Author(s):  
Marcos José Migliorini ◽  
Aleksandro Schafer da Silva ◽  
Janio Morais Santurio ◽  
Nathieli Bianchi Bottari ◽  
Roger Rocha Gebert ◽  
...  

Background: Contamination of crops with aflatoxin is considered a serious global threat to food safety, since potent carcinogenic, teratogenic, mutagenic and immunosuppressive effects of aflatoxins are well recognized. Recently, the use of adsorbents has been linked with protective effects against oxidative stress in several diseases. Thus, the aim of this study was to assess the occurrence of oxidative stress in quails (Coturnix coturnix) fed with aflatoxin-contaminated diet, as well as the protective effect of an adsorbent.Materials, Methods & Results: Twenty-eight quails were divided into four groups (n = 7): diet without additives (control; the group A), diet and adsorbent containing aluminosilicates (the group B), aflatoxin-contaminated diet (200 ppb) (the group C), and aflatoxin-contaminated diet (200 ppb) and adsorbent containing aluminosilicates (the group D). The composition of the adsorbent containing aluminosilicates was 0.3% based on yeast cell wall, silymarin, and bentonite. The animals received feed and water ad libitum during 20 days. At the end of the experimental period, total blood was collected by cardiac puncture in tubes without anticoagulant to obtain serum (centrifuged at 3500 g during 10 min) for later determination of biochemical parameters. The liver was placed in a solution of Tris–HCl 10 mM, pH 7.4 for TBARS (Thiobarbituric acid reactive substances), ROS (Reactive oxygen species), SOD (Superoxide dismutase) and CAT (Catalase) analysis. The hepatic tissue was gently homogenized in a glass potter in specific buffer, homogenated, and centrifuged at 10.000 g at 4ºC for 10 min to yield a supernatant (S1) used for analyses. Homogenate aliquots were stored at -80°C until utilization. Fragments of liver and intestine (5 cm) were collected for histopathological analyses. Between days 15 to 20 of the experiment, group C quails showed clinical signs, such as apathy, creepy feathers and reduced feed intake. At day 20 of experiment, macroscopically, the liver of quails belonging to the group C showed greenish yellow color differently from the other groups. Microscopically, no alterations were observed in the liver of animals in groups A and B. Severe diffuse microvacuolar degeneration (hydropic) of hepatocytes and small foci of necrosis in the liver were observed in the group C, as observed in the group D, but in a more moderate degree to microvacuolar degeneration. Seric total protein, albumin, globulin and uric acid levels decreased in the group C and D. The levels of alanine aminotransferase (ALT) increased in the group C, and the treatment with adsorbent was able to avoid this increment. Seric and hepatic reactive oxygen species and TBARS increased in the group C, and the treatment with adsorbent reduced theses parameters in the group D. Catalase (CAT) activity decreased, while ALA-D increased in the group C. The treatment with adsorbent was able to prevent CAT activity decrease, but it did not prevent the increase in ALA-D activity.Discussion: Aflatoxins are considered one of the most important problems in poultry production causing high economic losses to producers. In this study, the use of adsorbent showed a protective effect to hepatic tissue, minimizing histopathological lesions, as well as by preventing lipid peroxidation and exacerbated production of free radicals. Based on this data, aflatoxin intoxication causes hepatic oxidative stress that contributes directly to disease pathogenesis, and the addition of an adsorbent containing 0.3% based on bentonite, yeast cell wall and silymarin may be considered a new approach to prevent cellular and hepatic damage caused by aflatoxins.

Author(s):  
Dumitriţa RUGINǍ ◽  
Adela PINTEA ◽  
Raluca PÂRLOG ◽  
Andreea VARGA

Oxidative stress causes biological changes responsible for carcinogenesis and aging in human cells. The retinal pigmented epithelium is continuously exposed to oxidative stress. Therefore reactive oxygen species (ROS) and products of lipid peroxidation accumulate in RPE. Neutralization of ROS occurs in retina by the action of antioxidant defence systems. In the present study, the protective effect of caffeic acid (3,4-dihydroxy cinnamic acid), a dietary phenolic compound, has been examined in normal and in oxidative stress conditions (500 µM peroxide oxygen) in cultures human epithelial pigment retinal cells (Nowak, M. et al.). The cell viability, the antioxidant enzymes activity (CAT, GPx, SOD) and the level of intracellular reactive oxygen species (ROS) were determined. Exposure to l00 µM caffeic acid for 24 h induced cellular changes indicating the protective effect of caffeic acid in RPE cells. Caffeic acid did not show any cytotoxic effect at concentrations lower than 200 μM in culture medium. Treatment of RPE cells with caffeic acid causes an increase of catalase, glutathione peroxidase and superoxide dismutase activity, especially in cells treated with hydrogen peroxide. Caffeic acid causes a decrease of ROS level in cells treated with hydrogen peroxide. This study proved that caffeic acid or food that contain high levels of this phenolic acid may have beneficial effects in prevention of retinal diseases associated with oxidative stress by improving antioxidant defence systems.


Chemosphere ◽  
2007 ◽  
Vol 68 (8) ◽  
pp. 1511-1518 ◽  
Author(s):  
P.V. Kiruthiga ◽  
R. Beema Shafreen ◽  
S. Karutha Pandian ◽  
S. Arun ◽  
S. Govindu ◽  
...  

Biomolecules ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 1266
Author(s):  
Noelia Carballeda Sangiao ◽  
Susana Chamorro ◽  
Sonia de Pascual-Teresa ◽  
Luis Goya

Cocoa is a rich source of polyphenols, especially flavanols and procyanidin oligomers, with antioxidant properties, providing protection against oxidation and nitration. Cocoa phenolic compounds are usually extracted with methanol/ethanol solvents in order to obtain most of their bioactive compounds; however, aqueous extraction seems more representative of the physiological conditions. In this study, an aqueous extract of cocoa powder has been prepared and chemically characterized, and its potential protective effect against chemically-induced oxidative stress has been tested in differentiated human neuroblastoma SH-SY5Y cells. Neuronal-like cultured cells were pretreated with realistic concentrations of cocoa extract and its major monomeric flavanol component, epicatechin, and then submitted to oxidative stress induced by a potent pro-oxidant. After one hour, production of reactive oxygen species was evaluated by two different methods, flow cytometry and in situ fluorescence by a microplate reader. Simultaneously, reduced glutathione and antioxidant defense enzymes glutathione peroxidase and glutathione reductase were determined and the results used for a comparative analysis of both ROS (reactive oxygen species) methods and to test the chemo-protective effect of the bioactive products on neuronal-like cells. The results of this approach, never tested before, validate both analysis of ROS and indicate that concentrations of an aqueous extract of cocoa phenolics and epicatechin within a physiological range confer a significant protection against oxidative insult to neuronal-like cells in culture.


Molecules ◽  
2020 ◽  
Vol 25 (6) ◽  
pp. 1264 ◽  
Author(s):  
Huifang Zhang ◽  
Rui Liu ◽  
Qun Lu

Phenolamines and flavonoids are two important components in bee pollen. There are many reports on the bioactivity of flavonoids in bee pollen, but few on phenolamines. This study aims to separate and characterize the flavonoids and phenolamines from rape bee pollen, and compare their antioxidant activities and protective effects against oxidative stress. The rape bee pollen was separated to obtain 35% and 50% fractions, which were characterized by HPLC-ESI-QTOF-MS/MS. The results showed that the compounds in 35% fraction were quercetin and kaempferol glycosides, while the compounds in 50% fraction were phenolamines, including di-p-coumaroyl spermidine, p-coumaroyl caffeoyl hydroxyferuloyl spermine, di-p-coumaroyl hydroxyferuloyl spermine, and tri-p-coumaroyl spermidine. The antioxidant activities of phenolamines and flavonoids were evaluated by 2,2-diphenyl-1-picrylhydrazyl (DPPH), 2,2’-azino-bis-3-ethylbenzothiazoline-6-sulphonic acid (ABTS), and ferric reducing antioxidant power (FRAP) assays. It was found that the antioxidant activity of phenolamines was significantly higher than that of flavonoids. Moreover, phenolamines showed better protective effects than flavonoids on HepG2 cells injured by AAPH. Furthermore, phenolamines could significantly reduce the reactive oxygen species (ROS), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, and increase the superoxide dismutase (SOD) and glutathione (GSH) levels. This study lays a foundation for the further understanding of phenolamines in rape bee pollen.


2020 ◽  
Vol 21 (14) ◽  
pp. 4962 ◽  
Author(s):  
Humna Bhagani ◽  
Suzanne A. Nasser ◽  
Ali Dakroub ◽  
Ahmed F. El-Yazbi ◽  
Assaad A. Eid ◽  
...  

Diabetic cardiomyopathy (DCM) is a constellation of symptoms consisting of ventricular dysfunction and cardiomyocyte disarray in the presence of diabetes. The exact cause of this type of cardiomyopathy is still unknown; however, several processes involving the mitochondria, such as lipid and glucose metabolism, reactive oxygen species (ROS) production, apoptosis, autophagy and mitochondrial biogenesis have been implicated. In addition, polyphenols have been shown to improve the progression of diabetes. In this review, we discuss some of the mechanisms by which polyphenols, particularly resveratrol, play a role in slowing the progression of DCM. The most important intermediates by which polyphenols exert their protective effect include Bcl-2, UCP2, SIRT-1, AMPK and JNK1. Bcl-2 acts to attenuate apoptosis, UCP2 decreases oxidative stress, SIRT-1 increases mitochondrial biogenesis and decreases oxidative stress, AMPK increases autophagy, and JNK1 decreases apoptosis and increases autophagy. Our dissection of these molecular players aims to provide potential therapeutic targets for the treatment of DCM.


2021 ◽  
pp. 096032712110361
Author(s):  
Marzieh Farahani-Zangaraki ◽  
Azade Taheri ◽  
Mahmoud Etebari

Introduction: Hyperinsulinemia occurs in type 2 diabetic patients with insulin resistance. This increase in insulin levels in the blood increases reactive oxygen species production and oxidative stress, resulting in DNA damage. Carvedilol (CRV) is a non-selective beta-blocker, and research has shown that this compound and its metabolites have anti-oxidative properties. Carvedilol can, directly and indirectly, reduce reactive oxygen species (ROS) and has a protective effect on DNA damage from oxidative stress. Given the insolubility of CRV in water, finding new methods to increase its solubility can be an essential step in research. This study aimed to determine whether carvedilol could have a protective effect on insulin-induced genomic damage. Methods: We treated cells with insulin alone, amorphous-CRV alone, and amorphous-CRV and niosomal-CRV with insulin and DNA damage were investigated using the comet method to achieve this goal. Results: Our results showed that insulin in the studied concentration has a significant genotoxic effect and non-cytotoxic at higher concentrations. CRV, both in amorphous and niosome form, reduced insulin-induced DNA damage by reducing ROS production. The comet assay results demonstrate that treating HUVEC cells in pretreatment condition with amorphous-CRV and niosome-CRV significantly reduces DNA damage of insulin.


2021 ◽  
Vol 2021 ◽  
pp. 1-14
Author(s):  
Xing Chang ◽  
Tian Zhang ◽  
Qingyan Meng ◽  
ShiyuanWang ◽  
Peizheng Yan ◽  
...  

Cardiomyocyte apoptosis is an important pathological mechanism underlying cardiovascular diseases and is commonly caused by hypoxia. Moreover, hypoxic injury occurs not only in common cardiovascular diseases but also following various treatments of heart-related conditions. One of the major mechanisms underlying hypoxic injury is oxidative stress. Quercetin has been shown to exert antioxidant stress and vascular protective effects, making it a promising candidate for treating cardiovascular diseases. Therefore, we examined the protective effect of quercetin on human cardiomyocytes subjected to hypoxia-induced oxidative stress damage and its underlying mechanism. Human cardiomyocytes were subjected to hypoxia/reoxygenation (H/R) in vitro with or without quercetin pretreatment; thereafter, flow cytometry, Cell Counting Kit-8 assay, laser scanning confocal microscopy, quantitative PCR, western blotting, and enzyme-linked immunosorbent assay were performed to analyze the effects of quercetin on cardiomyocytes. We found that H/R induced reactive oxygen species overproduction and endoplasmic reticulum stress, as well as inhibited the function of the mitochondria/endoplasmic reticulum and mitophagy, eventually leading to apoptosis and decreasing the viability of human cardiomyocytes. Quercetin pretreatment inhibited H/R-mediated overproduction of reactive oxygen species and damage caused by oxidative stress, increased mitophagy, regulated mRNA and protein expression of transmembrane BAX inhibitor-1 motif-containing 6 (TMBIM6), regulated endoplasmic reticulum stress, and improved the vulnerability of human cardiomyocytes to H/R. Furthermore, transfection with short interfering RNA against silent information regulator protein 1 (SIRT1) counteracted the protective effects of quercetin on cardiomyocytes. Thus, quercetin was predicted to regulate mitophagy and endoplasmic reticulum stress through SIRT1/TMBIM6 and inhibit H/R-induced oxidative stress damage. These findings may be useful for developing treatments for hypoxic injury-induced cardiovascular diseases and further highlight the potential of quercetin for regulating mitochondrial quality control and endoplasmic reticulum function.


2020 ◽  
Vol 3 (2) ◽  
pp. 184-192
Author(s):  
Ji Eun Park ◽  
◽  
Young Mi Kim

Ultraviolet (UV) irradiation generates reactive oxygen species (ROS) in cells, which induces sunburn cell formation, melanoma, photoaging, and skin cancer. This study examines the anti-photodamage effects of kudzu root vinegar and adenosine in UVB-exposed human keratinocytes (HaCaT cells). UVB significantly decreased HaCaT cell viability, whereas kudzu root vinegar and adenosine did not exhibit cytotoxic effects and increased the viability of HaCaT cells. To investigate the protective effects of kudzu root vinegar and adenosine on UVB-induced oxidative stress in HaCaT cells, ROS, matrix metalloproteinases (MMPs), and mitogen-activated protein kinase (MAPK) were analyzed. UVB-induced treatment reduced the activity of antioxidant enzymes; however, kudzu root vinegar and adenosine increased their activity. These results indicated that kudzu root vinegar and adenosine exert cytoprotective activity against UVB-induced oxidative stress in HaCaT cells. Moreover, they suppressed the UVB-induced downregulation of MMPs and inhibited the phosphorylation of MAPK induced by UVB-irradiation. Therefore, kudzu root vinegar and adenosine offer anti-oxidative effects, via lowering ROS production, suppressing JNK activation, and downregulating expression of MMPs. Our findings suggest that kudzu root vinegar and adenosine have potential application in preventing skin damage owing to UVB exposure. Keywords: reactive oxygen species (ROS), HaCaT cell, UVB, skin damage, anti-aging


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