scholarly journals Vitamin C Attenuates Oxidative Stress and Behavioral Abnormalities Triggered by Fipronil and Pyriproxyfen Insecticide Chronic Exposure on Zebrafish Juvenile

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 944
Author(s):  
Madalina Andreea Robea ◽  
Roxana Jijie ◽  
Mircea Nicoara ◽  
Gabriel Plavan ◽  
Alin Stelian Ciobica ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Social Behavior ◽  
Vitamin C ◽  
Chronic Exposure ◽  
Protective Role ◽  
Autism Spectrum ◽  
Oxidative Stress Biomarkers ◽  
And Oxidative Stress ◽  
Vit C

Chronic exposure to synthetic insecticides in the early life of a child can lead to a series of disorders. Several causes as parental age, maternal smoking, birth complications, and exposure to toxins such as insecticides on childhood can lead to Autism spectrum disorder (ASD) occurrence. The aim of this study was to evaluate the potential protective role of vitamin C (Vit. C) from children’s supplements after 14 days chronic exposure to insecticide mixture fipronil (Fip) + pyriproxyfen (Pyr) on juvenile zebrafish for swimming performances, social behavior and oxidative stress associated with ASD model. Juvenile (14–17 mm) wild-type AB zebrafish (Danio rerio) (45 days) were exposed to relevant concentrations: vit. C (25 µg L−1), Fip (600 µg L−1/1.372 μM) + Pyr (600 µg L−1/1.89 μM), and [Fip (600 µg L−1/1.372 μM) + Pyr (600 µg L−1 /1.89 μM)] + vit. C (25 µg L−1). Our results showed that insecticides can disturb the social behavior of zebrafish during 14 days of the administration, decreased the swimming performances, and elevated the oxidative stress biomarkers of SOD (superoxide dismutase), GPx (glutathione peroxidase), and MDA (malondialdehyde). The vitamin C supplement significantly attenuated the neurotoxicity of insecticide mixture and oxidative stress. This study provides possible in vivo evidence to show that vitamin C supplements could attenuate oxidative stress and brain damage of fipronil and pyriproxyfen insecticide chronic exposure on zebrafish juvenile.

scholarly journals Vitamin C attenuates methotrexate-induced oxidative stress in kidney and liver of rats

2017 ◽  
Vol 104 (2) ◽  
pp. 139-149 ◽  
Author(s):  
M Savran ◽  
E Cicek ◽  
DK Doguc ◽  
H Asci ◽  
S Yesilot ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vitamin C ◽  
Histopathological Examination ◽  
Redox System ◽  
Protective Role ◽  
Hepatic Tissue ◽  
Control Group ◽  
Liver And Kidney ◽  
Vit C

Like several other anticancer drugs, methotrexate (MTX) causes side effects, such as neuropathic pain, hepatotoxicity, and nephrotoxicity. Abnormal production of reactive oxygen species has been suspected in the pathophysiology of MTX-induced hepatorenal toxicity. Therefore, the aim of this study was to investigate the probable protective role of vitamin C (Vit C) on oxidative stress induced by MTX in the liver and kidney tissues of rats. A total of 32 rats were randomly and equally divided into four groups. The first group served as the control group. The second group received a single dose of 20 mg/kg of MTX intraperitoneally. To demonstrate our hypothesis, the third and the fourth groups received 250 mg/kg of Vit C for 3 days by oral gavage, with or without MTX treatment. At the end of the study, the liver and kidney tissues of the rats were collected and examined using histology. Both the tissues were assayed for malondialdehyde concentration and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities. In hepatic and renal tissues, lipid peroxidation levels were increased, whereas SOD, CAT, and GSH-Px levels were decreased by MTX. All parameters, including CAT levels in hepatic tissue, were significantly restored after the administration of Vit C for 3 days. Similar to the biochemical findings, evidence of oxidative damage was examined in both types of tissues by histopathological examination. From the results of this study, we were able to observe that Vit C administration modulates the antioxidant redox system and reduces the renal and hepatic oxidative stress induced by MTX. Vit C can ameliorate the toxic effect of MTX in liver and kidney tissues of rat.

scholarly journals Low dietary intake of β-carotene, α-tocopherol and ascorbic acid is associated with increased inflammatory and oxidative stress status in a Swedish cohort

2008 ◽  
Vol 101 (12) ◽  
pp. 1775-1782 ◽  
Author(s):  
Johanna Helmersson ◽  
Johan Ärnlöv ◽  
Anders Larsson ◽  
Samar Basu
Keyword(s):  
Oxidative Stress ◽  
Ascorbic Acid ◽  
Dietary Intake ◽  
Vegetable Consumption ◽  
Dietary Intakes ◽  
Oxidative Stress Biomarkers ◽  
Negatively Associated ◽  
And Oxidative Stress ◽  
Β Carotene

Fruit and vegetable consumption has been associated with a reduced risk of several diseases including CVD. A part of these effects seen could be linked to anti-inflammatory and antioxidative effects, although this has not been thoroughly investigated. The present study was designed to investigate the effects of the dietary intake of β-carotene, α-tocopherol and ascorbic acid on in vivo biomarkers of inflammation (PGF2α, high-sensitive C-reactive protein (hsCRP) and IL-6 formation) and oxidative stress (F2-isoprostane formation), the two important factors associated with accelerated atherosclerosis. The dietary intake of 704 participants in the Uppsala Longitudinal Study of Adult Men (ULSAM) at age 70 years was registered and inflammatory and oxidative stress biomarkers were quantified 7 years later. The registered dietary intakes of ascorbic acid and α-tocopherol were negatively associated linearly and in quartiles with both PGF2α, hsCRP, IL-6 and F2-isoprostanes, where ascorbic acid intake generally was more strongly associated. Dietary intake of β-carotene was only significantly negatively associated with F2-isoprostanes. In conclusion, the present study is the first to suggest that the intake of food rich in antioxidants is associated with reduced cyclo-oxygenase- and cytokine-mediated inflammation and oxidative stress at 7 years of follow-up. These associations could be linked to the beneficial effects of fruit and vegetables observed on CVD.

Nickel and Oxidative Stress: Cell Signaling Mechanisms and Protective Role of Vitamin C

2020 ◽  
Vol 20 (7) ◽  
pp. 1024-1031
Author(s):  
Swastika Das ◽  
Rachamalla C. Reddy ◽  
Kailash S. Chadchan ◽  
Arun J. Patil ◽  
Mallanagouda S. Biradar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Ascorbic Acid ◽  
Vitamin C ◽  
Hypoxia Inducible Factor ◽  
Protective Role ◽  
Leukotriene B4 ◽  
Low Oxygen ◽  
Gene Expressions

Background: Nickel activates the signaling pathways through the oxygen sensing mechanism and the signaling cascades that control hypoxia-inducible transcriptional gene expressions through oxidative stress. This review emphasizes on the recent updates of nickel toxicities on oxidant and antioxidant balance, molecular interaction of nickel and its signal transduction through low oxygen microenvironment in the in-vivo physiological system. Discussion: ickel alters intracellular chemical microenvironment by increasing ionized calcium concentration, lipid peroxidation, cyclooxygenase, constitutive nitric oxide synthase, leukotriene B4, prostaglandin E2, interleukins, tumor necrosis factor-α, caspases, complement activation, heat shock protein 70 kDa and hypoxia-inducible factor-1α. The oxidative stress induced by nickel is responsible for the progression of metastasis. It has been observed that nickel exposure induces the generation of reactive oxygen species which leads to the increased expression of p53, NF-kβ, AP-1, and MAPK. Ascorbic acid (vitamin C) prevents lipid peroxidation, oxidation of low-density lipoproteins and advanced oxidation protein products. The mechanism involves that vitamin C is capable of reducing ferric iron to ferrous iron in the duodenum, thus the availability of divalent ferrous ion increases which competes with nickel (a divalent cation itself) and reduces its intestinal absorption and nickel toxicities. Conclusion: Reports suggested the capability of ascorbic acid as a regulatory factor to influence gene expression, apoptosis and other cellular functions of the living system exposed to heavy metals, including nickel.

scholarly journals Antia, a Natural Antioxidant Product, Attenuates Cognitive Dysfunction in Streptozotocin-Induced Mouse Model of Sporadic Alzheimer’s Disease by Targeting the Amyloidogenic, Inflammatory, Autophagy, and Oxidative Stress Pathways

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Nesrine S. El Sayed ◽  
Mamdooh H. Ghoneum
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurodegenerative Diseases ◽  
Protective Effect ◽  
Cognitive Dysfunction ◽  
Protective Role ◽  
Sporadic Alzheimer’S Disease ◽  
Stat3 Pathway ◽  
And Oxidative Stress

Background. Many neurodegenerative diseases such as Alzheimer’s disease are associated with oxidative stress. Therefore, antioxidant therapy has been suggested for the prevention and treatment of neurodegenerative diseases. Objective. We investigated the ability of the antioxidant Antia to exert a protective effect against sporadic Alzheimer’s disease (SAD) induced in mice. Antia is a natural product that is extracted from the edible yamabushitake mushroom, the gotsukora and kothala himbutu plants, diosgenin (an extract from wild yam tubers), and amla (Indian gooseberry) after treatment with MRN-100. Methods. Single intracerebroventricular (ICV) injection of streptozotocin (STZ) (3 mg/kg) was used for induction of SAD in mice. Antia was injected intraperitoneally (i.p.) in 3 doses (25, 50, and 100 mg/kg/day) for 21 days. Neurobehavioral tests were conducted within 24 h after the last day of injection. Afterwards, mice were sacrificed and their hippocampi were rapidly excised, weighed, and homogenized to be used for measuring biochemical parameters. Results. Treatment with Antia significantly improved mice performance in the Morris water maze. In addition, biochemical analysis showed that Antia exerted a protective effect for several compounds, including GSH, MDA, NF-κB, IL-6, TNF-α, and amyloid β. Further studies with western blot showed the protective effect of Antia for the JAK2/STAT3 pathway. Conclusions. Antia exerts a significant protection against cognitive dysfunction induced by ICV-STZ injection. This effect is achieved through targeting of the amyloidogenic, inflammatory, and oxidative stress pathways. The JAK2/STAT3 pathway plays a protective role for neuroinflammatory and neurodegenerative diseases such as SAD.

scholarly journals Canthin-6-one ameliorates TNBS-induced colitis in rats by modulating inflammation and oxidative stress. An in vivo and in silico approach

2021 ◽  
Vol 186 ◽  
pp. 114490
Author(s):  
Karuppusamy Arunachalam ◽  
Amilcar Sabino Damazo ◽  
Antonio Macho ◽  
Monica Steffi Matchado ◽  
Eduarda Pavan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
In Silico ◽  
And Oxidative Stress
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