Protective Effects of Sodium Selenite against Aflatoxin  B1-Induced Oxidative Stress and Apoptosis in Broiler Spleen

Aflatoxin B1 (AFB1), a threatening mycotoxin, usually provokes oxidative stress and causes hepatotoxicity in animals and humans. Luteolin (LUTN), well-known as an active phytochemical agent, acts as a strong antioxidant. This research was designed to investigate whether LUTN exerts protective effects against AFB1-induced hepatotoxicity and explore the possible molecular mechanism in mice. A total of forty-eight mice were randomly allocated following four treatment groups (n = 12): Group 1, physiological saline (CON). Group 2, treated with 0.75 mg/kg BW aflatoxin B1 (AFB1). Group 3, treated with 50 mg/kg BW luteolin (LUTN), and Group 4, treated with 0.75 mg/kg BW aflatoxin B1 + 50 mg/kg BW luteolin (AFB1 + LUTN). Our findings revealed that LUTN treatment significantly alleviated growth retardation and rescued liver injury by relieving the pathological and serum biochemical alterations (ALT, AST, ALP, and GGT) under AFB1 exposure. LUTN ameliorated AFB1-induced oxidative stress by scavenging ROS and MDA accumulation and boosting the capacity of the antioxidant enzyme (CAT, T-SOD, GSH-Px and T-AOC). Moreover, LUTN treatment considerably attenuates the AFB1-induced apoptosis in mouse liver, as demonstrated by declined apoptotic cells percentage, decreased Bax, Cyt-c, caspase-3 and caspase-9 transcription and protein with increased Bcl-2 expression. Notably, administration of LUTN up-regulated the Nrf2 and its associated downstream molecules (HO-1, NQO1, GCLC, SOD1) at mRNA and protein levels under AFB1 exposure. Our results indicated that LUTN effectively alleviated AFB1-induced liver injury, and the underlying mechanisms were associated with the activation of the Nrf2 signaling pathway. Taken together, LUTN may serve as a potential mitigator against AFB1-induced liver injury and could be helpful for the development of novel treatment to combat liver diseases in humans and/or animals.

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Effects of sodium selenite on c-Jun N-terminal kinase signalling pathway induced by oxidative stress in human chondrocytes and c-Jun N-terminal kinase expression in patients with Kashin–Beck disease, an endemic osteoarthritis

British Journal Of Nutrition ◽

10.1017/s0007114516000362 ◽

2016 ◽

Vol 115 (9) ◽

pp. 1547-1555 ◽

Cited By ~ 8

Author(s):

XiaoXia Dai ◽

YuanYuan Li ◽

RongQiang Zhang ◽

Yan Kou ◽

XiaoYan Mo ◽

...

Keyword(s):

Oxidative Stress ◽

Sodium Selenite ◽

Reactive Oxygen Species Generation ◽

Signalling Pathway ◽

Mitogen Activated Protein Kinase ◽

Human Chondrocytes ◽

Protective Effects ◽

Jnk Pathway ◽

Beck Disease

AbstractThe c-Jun N-terminal kinases (JNK) are members of the mitogen-activated protein kinase family and are activated by environmental stress. Se plays an important role in the biological pathways by forming selenoprotein. Selenoproteins have been shown to exhibit a variety of biological functions including antioxidant functions and maintaining cellular redox balance, and compromise of such important proteins would lead to oxidative stress and apoptosis. We examined the expression levels of JNK in Kashin–Beck disease (KBD) patients, tested the potential protective effects of sodium selenite on tert-butyl hydroperoxide (tBHP)-induced oxidative injury and apoptosis in human chondrocytes as well as its underlying mechanism in this study. We produced an oxidative damage model induced by tBHP in C28/I2 human chondrocytes to test the essential anti-apoptosis effects of Se in vitro. The results indicated that the expression level of phosphorylated JNK was significantly increased in KBD patients. Cell apoptosis was increased and molecule expressions of the JNK signalling pathway were activated in the tBHP-injured chondrocytes. Na2SeO3 protected against tBHP-induced oxidative stress and apoptosis in cells by increasing cell viability, reducing reactive oxygen species generation, increasing Glutathione peroxidase (GPx) activity and down-regulating the JNK pathway. These results demonstrate that apoptosis induced by tBHP in chondrocytes might be mediated via up-regulation of the JNK pathway; Na2SeO3 has an effect of anti-apoptosis by down-regulating the JNK signalling pathway.

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Aflatoxin B1 induces oxidative stress in rats: possible protective effects of onion juice (Allium cepa L.)

مجلة البحوث فی مجالات التربیة النوعیة ◽

10.21608/jedu.2019.73655 ◽

2019 ◽

Vol 2019 (22) ◽

pp. 79-109

Author(s):

Ragaa A Sadeek ◽

Ghada Mahmoud Elbassiony ◽

Yousif A Elhassaneen

Keyword(s):

Oxidative Stress ◽

Allium Cepa ◽

Aflatoxin B1 ◽

Protective Effects ◽

Allium Cepa L

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Effect of Selenium and Iodine on Oxidative Stress in the First Trimester Human Placenta Explants

Nutrients ◽

10.3390/nu13030800 ◽

2021 ◽

Vol 13 (3) ◽

pp. 800

Author(s):

Nahal Habibi ◽

Agatha Labrinidis ◽

Shalem Yiner-Lee Leemaqz ◽

Tanja Jankovic-Karasoulos ◽

Dylan McCullough ◽

...

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Potassium Iodide ◽

Human Placenta ◽

Sodium Selenite ◽

First Trimester ◽

Antioxidant Systems ◽

Protective Effects ◽

High Concentration ◽

Icp Ms

Imbalanced maternal micronutrient status, poor placentation, and oxidative stress are associated with greater risk of pregnancy complications, which impact mother and offspring health. As selenium, iodine, and copper are essential micronutrients with key roles in antioxidant systems, this study investigated their potential protective effects on placenta against oxidative stress. First trimester human placenta explants were treated with different concentrations of selenium (sodium selenite), iodine (potassium iodide), their combination or copper (copper (II) sulfate). The concentrations represented deficient, physiological, or super physiological levels. Oxidative stress was induced by menadione or antimycin. Placenta explants were collected, fixed, processed, and embedded for laser ablation inductively coupled plasma-mass spectrometry (LA ICP-MS) element imaging or immunohistochemical labelling. LA ICP-MS showed that placenta could uptake selenium and copper from the media. Sodium selenite and potassium iodide reduced DNA damage and apoptosis (p < 0.05). Following oxidative stress induction, a higher concentration of sodium selenite (1.6 µM) was needed to reduce DNA damage and apoptosis while both concentrations of potassium iodide (0.5 and 1 µM) were protective (p < 0.05). A high concentration of copper (40 µM) increased apoptosis and DNA damage but this effect was no longer significant after induction of oxidative stress. Micronutrients supplementation can increase their content within the placenta and an optimal maternal micronutrient level is essential for placenta health.

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Evaluation of Neuroprotective Effects of Quercetin against Aflatoxin B1-Intoxicated Mice

Animals ◽

10.3390/ani10050898 ◽

2020 ◽

Vol 10 (5) ◽

pp. 898 ◽

Cited By ~ 3

Author(s):

Enrico Gugliandolo ◽

Alessio Filippo Peritore ◽

Ramona D’Amico ◽

Patrizia Licata ◽

Rosalia Crupi

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Aflatoxin B1 ◽

Protective Effects ◽

Behavioral Alterations ◽

Sod Activity ◽

Neuroprotective Effects ◽

Oxidative Stress Pathway ◽

Ameliorative Effect ◽

The Brain

Aflatoxin B1 (AFB1) is a mycotoxin commonly present in feed, characterized by several toxic effects. AFB1 seems to have a neurotoxical effect that leads to memory impairment behavior. AFB1 toxicity involves the induction of the oxidative stress pathway, rising lipid peroxidation, and it decreases antioxidant enzyme levels. Hence, in our research, we wanted to evaluate the potential protective effects of quercetin 30 mg/kg in AFB1-mediated toxicity in the brain and the ameliorative effect on behavioral alterations. Oral supplementation with quercetin increased glutathione peroxidase (GSH) levels, superoxidedismutase (SOD) activity and catalase (CAT) in the brain, and it reduced lipid peroxidation in AFB1-treated mice. This antioxidant effect of quercetin in the brains of AFB1-intoxicated mice is reflected in better cognitive and spatial memory capacity, as well as a better profile of anxiety and lethargy disorders. In conclusion, our study suggests that quercetin exerts a preventive role against oxidative stress by promoting antioxidative defense systems and limiting lipid peroxidation.

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Dietary Resveratrol Alleviates AFB1-Induced Ileum Damage in Ducks via the Nrf2 and NF-κB/NLRP3 Signaling Pathways and CYP1A1/2 Expressions

Agriculture ◽

10.3390/agriculture12010054 ◽

2022 ◽

Vol 12 (1) ◽

pp. 54

Author(s):

Hao Yang ◽

Yingjie Wang ◽

Chunting Yu ◽

Yihan Jiao ◽

Ruoshi Zhang ◽

...

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Signaling Pathways ◽

Dna Adducts ◽

Aflatoxin B1 ◽

Mrna Level ◽

Basal Diet ◽

Protective Effects ◽

Expression Of Genes ◽

And Oxidative Stress

The aim of this study was to explore the mechanism underlying the protective effects of resveratrol against Aflatoxin B1-induced ileum injury in ducks. A corn–soybean meal-basal diet and two test diets (500 mg/kg resveratrol +0.2 mg Aflatoxin B1/kg, 0.2 mg AFB1/kg) were used in a 10-wk design trial (n = 15 ducks/group). These results showed that the toxicity of Aflatoxin B1 significantly reduced the antioxidant capacity of duck ileum and induced inflammation, oxidative stress, mitochondrial dysfunction and DNA damage in ducks. The expression of genes, including CYP1A2, CYP2A6, and CYP3A4, at the mRNA level was significantly upregulated (p < 0.05) by AFB1. The level of Nrf2 was suppressed (p < 0.05) and the mRNA and protein level of NF-κB was activated (p < 0.05) in the AFB1 group. However, supplementation with 500 mg/kg dietary resveratrol in Aflatoxin B1-induced ducks significantly ameliorated these alterations and decreased the mRNA expression of CYP1A1 and CYP1A2 (p < 0.05) and the production of AFB1-DNA adducts (p < 0.05). The results proved that resveratrol alleviated ileum injury induced by AFB1, decreased the production of AFB1-DNA adducts by downregulating the expression of CYP1A1 and CYP1A2, and reduced DNA damage and oxidative stress via the Nrf2/ Keap1 and NF-κB/NLRP3 signaling pathways.

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