scholarly journals Effects of Fusarium Mycotoxin Exposure on Lipid Peroxidation and Glutathione Redox System in the Liver of Laying Hens

Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1313
Author(s):  
Szabina Kulcsár ◽  
Benjámin Kövesi ◽  
Krisztián Balogh ◽  
Erika Zándoki ◽  
Zsolt Ancsin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Laying Hens ◽  
Fumonisin B1 ◽  
Redox System ◽  
Fusarium Mycotoxins ◽  
Glutathione Redox System ◽  
Glutathione Redox ◽  
Gene Expression Levels

It has been proven by several studies that Fusarium mycotoxins induce oxidative stress in animals, consequently inducing lipid peroxidation, which the glutathione system can neutralize. A short-term (3-day) in vivo feeding trial was performed with laying hens using a double dose of the EU recommendation for mycotoxin contamination (T-2 toxin 0.5 mg/kg feed; deoxynivalenol (DON) 10 mg/kg feed; fumonisin B1 (FB1) 40 mg/kg feed). Some lipid peroxidation and glutathione redox system parameters and gene expression levels were measured in the liver. The results show that FB1 significantly decreased the reduced glutathione (GSH) content and the activity of glutathione peroxidase (GPx) compared to the control and the two other mycotoxin-treated groups on day 3. Lipid peroxidation was affected by all three mycotoxins. Significantly lower values were observed in the case of conjugated dienes for all of the three mycotoxins and malondialdehyde concentration as an effect of DON on day 3. T-2 toxin and DON upregulated the expression of the GPX4 gene. The results show that Fusarium mycotoxins had different effects at the end of the trial. The FB1 exposure caused a decrease in the glutathione redox markers, while DON decreased the formation of malondialdehyde. The results suggest that the Fusarium mycotoxins investigated individually differently activated the antioxidant defense and caused low-level oxidative stress at the dose applied.

scholarly journals Role of glutathione redox system on the susceptibility to deoxynivalenol of pheasant (Phasianus colchicus)

2019 ◽  
Vol 36 (2) ◽  
pp. 175-182 ◽  
Author(s):  
Csaba Fernye ◽  
Zsolt Ancsin ◽  
Márta Erdélyi ◽  
Miklós Mézes ◽  
Krisztián Balogh
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Blood Plasma ◽  
Reduced Glutathione ◽  
Redox System ◽  
Phasianus Colchicus ◽  
Glutathione Peroxidase Activity ◽  
Glutathione Redox System ◽  
Dose Dependent ◽  
Glutathione Redox

AbstractThere are only a few reports on the effects of mycotoxins on pheasant (Phasianus colchicus) and the susceptibility to deoxynivalenol of these birds have never been reported before. The present experiment focuses to investigate the effects of different dietary concentrations of deoxynivalenol on blood plasma protein content, some parameters of lipid peroxidation and glutathione redox system and on the performance of pheasant chicks. A total of 320 1-day-old female pheasants were randomly assigned to four treatment groups fed with a diet contaminated with deoxynivalenol (control, 5.11 mg/kg, 11.68 mg/kg and 16.89 mg/kg). Birds were sacrificed at early (12, 24 and 72 h) and late (1, 2 and 3 weeks) stages of the experiment to demonstrate the oxidative stress-inducing effect of deoxynivalenol. Feed refusal was dose dependent, especially in the last third of the trial, but only minor body weight gain decrease was found. Lipid-peroxidation parameters did not show dose-dependent effect, except in blood plasma during the early stage of the trial. The glutathione redox system, reduced glutathione content and glutathione peroxidase activity, was activated in the liver, but primarily in the blood plasma. Glutathione peroxidase activity has changed parallel with reduced glutathione concentration in all tissues. Comparing our results with literature data, pheasants seem to have the same or higher tolerance to deoxynivalenol than other avian species, and glutathione redox system might contribute in some extent to this tolerance, as effective antioxidant defence against oxidative stress.

scholarly journals Short-term effects of deoxynivalenol, T-2 toxin, fumonisin B1 or ochratoxin on lipid peroxidation and glutathione redox system and its regulatory genes in common carp (Cyprinus carpio L.) liver

2020 ◽  
Vol 46 (6) ◽  
pp. 1921-1932
Author(s):  
Benjámin Kövesi ◽  
Szabina Kulcsár ◽  
Erika Zándoki ◽  
Judit Szabó-Fodor ◽  
Miklós Mézes ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Glutathione Peroxidase ◽  
Common Carp ◽  
Fumonisin B1 ◽  
Redox System ◽  
Short Term ◽  
Initiation Phase ◽  
Glutathione Redox System ◽  
Antioxidant Defence System ◽  
Glutathione Redox

Abstract The effects of a single oral dose of 1.82 mg kg−1 bw of T-2 and HT-2 toxin (T-2), 1.75 mg kg−1 bw deoxynivalenol (DON) and 15-acetyl DON, 1.96 mg kg−1 bw fumonisin B1 (FB1) or 1.85 mg kg−1 bw ochratoxin A (OTA) were investigated in common carp juveniles on lipid peroxidation, the parameters of the glutathione redox system including the expression of their encoding genes in a short-term (24 h) experiment. Markers of the initiation phase of lipid peroxidation, conjugated dienes, and trienes, were slightly affected by DON and OTA treatment at 16-h sampling. The termination marker, malondialdehyde, concentration increased only as an effect of FB1. Glutathione content and glutathione peroxidase activity showed significantly higher levels in the T-2 and FB1 groups at 8 h, and in the DON and FB1 groups at 16 h. The expression of glutathione peroxidase genes (gpx4a, gpx4b) showed a dual response. Downregulation of gpxa was observed at 8 h, as the effect of DON, FB1, and OTA, but an upregulation in the T-2 group. At 16 h gpx4a upregulated as an effect of DON, T-2, and FB1, and at 24 h in the DON and T-2 groups. Expression of gpx4b downregulated at 8 h, except in the T-2 group, and upregulation observed as an effect of T-2 at 24 h. The lack of an increase in the expression of nrf2, except as the effect of DON at 8 h, and a decrease in the keap1 expression suggests that the antioxidant defence system was activated at gene and protein levels through Keap1–Nrf2 independent pathways.

scholarly journals Arsenic Trioxide Inhibits Hepatitis C Virus RNA Replication through Modulation of the Glutathione Redox System and Oxidative Stress

2008 ◽  
Vol 83 (5) ◽  
pp. 2338-2348 ◽  
Author(s):  
Misao Kuroki ◽  
Yasuo Ariumi ◽  
Masanori Ikeda ◽  
Hiromichi Dansako ◽  
Takaji Wakita ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Arsenic Trioxide ◽  
Redox System ◽  
Rna Replication ◽  
Hcv Rna ◽  
Glutathione Redox System ◽  
And Oxidative Stress ◽  
Glutathione Redox

ABSTRACT Arsenic trioxide (ATO), a therapeutic reagent used for the treatment of acute promyelocytic leukemia, has recently been reported to increase human immunodeficiency virus type 1 infectivity. However, in this study, we have demonstrated that replication of genome-length hepatitis C virus (HCV) RNA (O strain of genotype 1b) was notably inhibited by ATO at submicromolar concentrations without cell toxicity. RNA replication of HCV-JFH1 (genotype 2a) and the release of core protein into the culture supernatants were also inhibited by ATO after the HCV infection. To clarify the mechanism of the anti-HCV activity of ATO, we examined whether or not PML is associated with this anti-HCV activity, since PML is known to be a target of ATO. Interestingly, we observed the cytoplasmic translocation of PML after treatment with ATO. However, ATO still inhibited the HCV RNA replication even in the PML knockdown cells, suggesting that PML is dispensable for the anti-HCV activity of ATO. In contrast, we found that N-acetyl-cysteine, an antioxidant and glutathione precursor, completely and partially eliminated the anti-HCV activity of ATO after 24 h and 72 h of treatment, respectively. In this context, it is worth noting that we found an elevation of intracellular superoxide anion radical, but not hydrogen peroxide, and the depletion of intracellular glutathione in the ATO-treated cells. Taken together, these findings suggest that ATO inhibits the HCV RNA replication through modulation of the glutathione redox system and oxidative stress.

Lactose and Casein Cause Changes on Biomarkers of Oxidative Damage and Dysbiosis in an Experimental Model of Multiple Sclerosis

2021 ◽  
Vol 20 ◽  
Author(s):  
Begoña M. Escribano ◽  
Ana Muñoz-Jurado ◽  
Evelio Luque ◽  
Cristina Conde ◽  
Montse Feijóo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Multiple Sclerosis ◽  
Oxidative Damage ◽  
Clinical Status ◽  
Lipid Peroxides ◽  
Redox System ◽  
Dark Agouti ◽  
Glutathione Redox System ◽  
And Oxidative Stress ◽  
Glutathione Redox

Background and Objectives: Experimental autoimmune encephalomyelitis (EAE) in rats closely reproduces multiple sclerosis (MS), a disease characterized by neuroinflammation and oxidative stress, that also appears to extend to other organ compartments. The origin of MS is a matter for discussion, but it would seem that altering certain bacterial populations present in the gut may lead to a proinflammatory condition due to the bacterial lipopolysaccharides (LPS) in the so-called brain-gut axis. The casein and lactose in milk confer anti-inflammatory properties and immunomodulatory effects. The objectives of this study were: to evaluate the effects of administration of casein and lactose on the oxidative damage and the clinical status caused by EAE, and to verify whether both, casein and lactose, had any effect on the LPS and its transport protein -LBP-. Methods: Twenty male dark Agouti rats were divided into: control rats (control), EAE rats and EAE rats to which casein and lactose, EAE+casein and EAE+lactose, respectively, were administered. Fifty-one days after casein and lactose administration, the rats were sacrificed and different organs were studied (brain, spinal cord, blood, heart, liver, kidney, small and large intestine). In the latter, products derived from oxidative stress were studied (lipid peroxides and carbonylated proteins) as well as the glutathione redox system, various inflammation factors (total nitrite, Nuclear Factor-kappa B p065, the Rat Tumour Necrosis Factor-α) and the LPS and LBP values. Results and Conclusion: Casein and lactose administration improved the clinical aspect of the disease at the same time as reducing inflammation and oxidative stress, exerting its action on the glutathione redox system or increasing GPx levels.

scholarly journals Lack of Dose- and Time-Dependent Effects of Aflatoxin B1 on Gene Expression and Enzymes Associated with Lipid Peroxidation and the Glutathione Redox System in Chicken

Toxins ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 84 ◽  
Author(s):  
Benjámin Kövesi ◽  
Mátyás Cserháti ◽  
Márta Erdélyi ◽  
Erika Zándoki ◽  
Miklós Mézes ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Aflatoxin B1 ◽  
Control Diet ◽  
Dose Range ◽  
Thiobarbituric Acid ◽  
Redox System ◽  
Time Dependent ◽  
Treatment Groups ◽  
Glutathione Redox System ◽  
Glutathione Redox

Effects of aflatoxin B1 (AFB1) on lipid peroxidation and glutathione system were investigated in chicken liver. In a three-week feeding trial, different doses (<1.0 μg/kg (control diet), 17.0 µg (diet A1), 92.0 µg (diet A2), and 182.0 µg (diet A3) AFB1 kg/feed) were used. Markers of lipid peroxidation, conjugated dienes and trienes showed higher values in A3, while amounts of thiobarbituric acid reactive substances were increased in the A1 group at day 21. Glutathione content was lower at day 14 in Group A2. Glutathione peroxidase 4 activity was increased at days 7 and 21 in the A3 group but reduced in the A2 and A3 groups at day 14. The GPX4 gene was downregulated at day 7 in the A2 group, but overregulated at days 14 and 21, and at day 14 in the A3 group. GSS was downregulated at day 14 in the A1 group but overregulated at day 21 in A1 and A2 groups. GSR was downregulated at days 7 and 21 in all treatment groups, but on day 14, induction was observed in the A3 group. The results indicated that AFB1 did not induce dose- or time-dependent effects on the glutathione redox system and its encoding genes at the dose range used, which means that oxidative stress is not the primary effect of AFB1 toxicity.

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