Protective Effects of Gold Nanoparticles Against Malathion-Induced Cytotoxicity in Caco-2 Cells

Malathion is an organophosphorus insecticide widely used in agriculture, residential area, and public health programs with a known mechanism of toxicity of inhibition of acetylcholinesterase and induction of oxidative stress. Gold nanoparticles (AuNPs) represent stable and easily synthesized nanoparticles with extensive use in consumer products and medicine. Due to the antioxidant property of AuNPs, it is possible that AuNPs may prevent malathion-induced oxidative damage. In this study, the cytotoxicity of malathion and AuNPs (10 and 20 nm) were measured separately in Caco-2 cells. Then the protective effects of AuNPs were evaluated by measuring the oxidative stress (lipid peroxidation level and glutathione content) and acetylcholinesterase activity. The calculated IC50s values at 48 hr were 326.8±0.32, 43.09±0.65, and 41.46±0.24 µg/ml for malathion, AuNPs 10 and 20 nm, respectively. Then, the lowest concentration of AuNPs (1 µg/ml) and IC50 concentration of malathion (326.8 µg/ml) were selected to evaluate the effects of pretreatment of Caco-2 cells with AuNPs before exposure to malathion were evaluated. Interestingly, the results showed remarkably significant protective effects of AuNPs by attenuation the different parameters of oxidative stress and cytotoxicity induced by malathion in cells (P<0.001). It is the first report showing the protective effects of AuNPs against malathion-induced cytotoxicity in the Caco-2 cell line.

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Gold nanoparticles reduce inflammation in cerebral microvessels of mice with sepsis

Journal of Nanobiotechnology ◽

10.1186/s12951-021-00796-6 ◽

2021 ◽

Vol 19 (1) ◽

Author(s):

Davide Di Bella ◽

João P. S. Ferreira ◽

Renee de Nazare O. Silva ◽

Cinthya Echem ◽

Aline Milan ◽

...

Keyword(s):

Oxidative Stress ◽

Gold Nanoparticles ◽

Blood Vessels ◽

Platelet Adhesion ◽

Potential Candidate ◽

Cerebral Blood Vessels ◽

Cerebral Microvessels ◽

Antibiotic Effect ◽

Anti Inflammatory ◽

20 Nm

Abstract Background Sepsis is an emergency medical condition that can lead to death and it is defined as a life-threatening organ dysfunction caused by immune dysregulation in response to an infection. It is considered the main killer in intensive care units. Sepsis associated-encephalopathy (SAE) is mostly caused by a sepsis-induced systemic inflammatory response. Studies report SAE in 14–63% of septic patients. Main SAE symptoms are not specific and usually include acute impairment of consciousness, delirium and/or coma, along with electroencephalogram (EEG) changes. For those who recover from sepsis and SAE, impaired cognitive function, mobility and quality of life are often observed months to years after hospital discharge, and there is no treatment available today to prevent that. Inflammation and oxidative stress are key players for the SAE pathophysiology. Gold nanoparticles have been demonstrated to own important anti-inflammatory properties. It was also reported 20 nm citrate-covered gold nanoparticles (cit-AuNP) reduce oxidative stress. In this context, we tested whether 20 nm cit-AuNP could alleviate the acute changes caused by sepsis in brain of mice, with focus on inflammation. Sepsis was induced in female C57BL/6 mice by cecal ligation and puncture (CLP), 20 nm cit-AuNP or saline were intravenously (IV) injected 2 h after induction of sepsis and experiments performed 6 h after induction. Intravital microscopy was used for leukocyte and platelet adhesion study in brain, blood brain barrier (BBB) permeability carried out by Evans blue assay, cytokines measured by ELISA and real time PCR, cell adhesion molecules (CAMs) by flow cytometry and immunohistochemistry, and transcription factors, by western blotting. Results 20 nm cit-AuNP treatment reduced leukocyte and platelet adhesion to cerebral blood vessels, prevented BBB failure, reduced TNF- concentration in brain, and ICAM-1 expression both in circulating polymorphonuclear (PMN) leukocytes and cerebral blood vessels of mice with sepsis. Furthermore, 20 nm cit-AuNP did not interfere with the antibiotic effect on the survival rate of mice with sepsis. Conclusions Cit-AuNP showed important anti-inflammatory properties in the brain of mice with sepsis, being a potential candidate to be used as adjuvant drug along with antibiotics in the treatment of sepsis to avoid SAE

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Tualang Honey Attenuates Noise Stress-Induced Memory Deficits in Aged Rats

Oxidative Medicine and Cellular Longevity ◽

10.1155/2016/1549158 ◽

2016 ◽

Vol 2016 ◽

pp. 1-11 ◽

Cited By ~ 10

Author(s):

Khairunnuur Fairuz Azman ◽

Rahimah Zakaria ◽

Che Badariah Abdul Aziz ◽

Zahiruddin Othman

Keyword(s):

Oxidative Stress ◽

Memory Performance ◽

Acetylcholinesterase Activity ◽

Protein Carbonyl ◽

Protective Effects ◽

Aged Rats ◽

Stress Exposure ◽

Object Recognition Test ◽

Noise Stress ◽

Tualang Honey

Ageing and stress exposure may lead to memory impairment while oxidative stress is thought to be one of the underlying mechanisms involved. This study aimed to investigate the potential protective effects of Tualang honey supplementation on memory performance in aged rats exposed to noise stress. Tualang honey supplementation was given orally, 200 mg/kg body weight for 28 days. Rats in the stress group were subjected to loud noise, 100 dB(A), 4 hours daily for 14 days. All rats were subjected to novel object recognition test for evaluation of memory performance. It was observed that the rats subjected to noise stress exhibited significantly lower memory performance and higher oxidative stress as evident by elevated malondialdehyde and protein carbonyl levels and reduction of antioxidant enzymes activities compared to the nonstressed rats. Tualang honey supplementation was able to improve memory performance, decrease oxidative stress levels, increase brain-derived neurotrophic factor (BDNF) concentration, decrease acetylcholinesterase activity, and enhance neuronal proliferation in the medial prefrontal cortex (mPFC) and hippocampus. In conclusion, Tualang honey protects against memory decline due to stress exposure and/or ageing via enhancement of mPFC and hippocampal morphology possibly secondary to reduction in brain oxidative stress and/or upregulation of BDNF concentration and cholinergic system.

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Folic Acid Attenuated Learning and Memory Impairment via Inhibition of Oxidative Damage and Acetylcholinesterase Activity in Hypothyroid Rats

10.21203/rs.3.rs-383794/v1 ◽

2021 ◽

Author(s):

Sabiheh Amirahmadi ◽

Mahmoud Hosseini ◽

Somaieh Ahmadabady ◽

Mahsa Akbarain ◽

Kataneh Abrari ◽

...

Keyword(s):

Oxidative Stress ◽

Folic Acid ◽

Oxidative Damage ◽

Learning And Memory ◽

Cognitive Performance ◽

Ache Activity ◽

Acetylcholinesterase Activity ◽

Protective Effects ◽

Thiol Content ◽

Oxidative Stress Indicators

Abstract Hypothyroidism has been associated with cognitive decline. Considering the role that has been suggested for folic acid (FA) in cognitive performance, the present study was designed to investigate the effects of FA against hypothyroidism-induced cognitive impairment, oxidative damage and acetylcholinesterase (AChE) activity alterations in propylthiouracil (PTU)-induced hypothyroid rats. In this study, PTU (0.05% in drinking water) and FA (5, 10, and 15 mg/kg, oral gavage) were administered to the rats for a period of 7 weeks. Then, behavioral performance was tested using Morris water maze (MWM) and passive avoidance (PA) tasks. Finally, oxidative stress indicators and AChE activity were assayed in the brain tissues. The impairing effect of hypothyroidism on cognitive performance was markedly alleviated by FA especially at the higher doses. In the MWM test, FA reduced escape latency and travelled distance, compared to the non-treated hypothyroid group. In the PA test, the latency to enter the dark chamber was significantly enhanced by FA as compared to the non-treated hypothyroid group (p < 0.05-p < 0.001). Besides, FA attenuated AChE activity and malondialdehyde level but increased superoxidase dismutase enzyme activity and total thiol content (p < 0.05-p < 0.001). In conclusion, FA could improve learning and memory ability in hypothyroid rats. The observed protective effects may be mediated through regulation of oxidative stress and AChE activity.

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Oxidative Stress and BPA Toxicity: An Antioxidant Approach for Male and Female Reproductive Dysfunction

Antioxidants ◽

10.3390/antiox9050405 ◽

2020 ◽

Vol 9 (5) ◽

pp. 405 ◽

Cited By ~ 6

Author(s):

Rosaria Meli ◽

Anna Monnolo ◽

Chiara Annunziata ◽

Claudio Pirozzi ◽

Maria Carmela Ferrante

Keyword(s):

Oxidative Stress ◽

Molecular Mechanisms ◽

Hormone Receptors ◽

Redox Homeostasis ◽

Consumer Products ◽

Target Cells ◽

Protective Effects ◽

Male And Female ◽

Methyl Donors ◽

Cell Signaling Pathways

Bisphenol A (BPA) is a non-persistent anthropic and environmentally ubiquitous compound widely employed and detected in many consumer products and food items; thus, human exposure is prolonged. Over the last ten years, many studies have examined the underlying molecular mechanisms of BPA toxicity and revealed links among BPA-induced oxidative stress, male and female reproductive defects, and human disease. Because of its hormone-like feature, BPA shows tissue effects on specific hormone receptors in target cells, triggering noxious cellular responses associated with oxidative stress and inflammation. As a metabolic and endocrine disruptor, BPA impairs redox homeostasis via the increase of oxidative mediators and the reduction of antioxidant enzymes, causing mitochondrial dysfunction, alteration in cell signaling pathways, and induction of apoptosis. This review aims to examine the scenery of the current BPA literature on understanding how the induction of oxidative stress can be considered the “fil rouge” of BPA’s toxic mechanisms of action with pleiotropic outcomes on reproduction. Here, we focus on the protective effects of five classes of antioxidants—vitamins and co-factors, natural products (herbals and phytochemicals), melatonin, selenium, and methyl donors (used alone or in combination)—that have been found useful to counteract BPA toxicity in male and female reproductive functions.

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Cotreatment of Small Gold Nanoparticles Protects Against the Increase in Cerebral Acetylcholinesterase Activity and Oxidative Stress Induced by Acute Ethanol Exposure in the Zebrafish

Neuroscience ◽

10.1016/j.neuroscience.2021.01.011 ◽

2021 ◽

Vol 457 ◽

pp. 41-50

Author(s):

Carolina Antunes Torres ◽

Niuany Viel Mendes ◽

Samira Leila Baldin ◽

Henrique Teza Bernardo ◽

Karine Medeiros Vieira ◽

...

Keyword(s):

Oxidative Stress ◽

Gold Nanoparticles ◽

Acetylcholinesterase Activity ◽

Ethanol Exposure ◽

Acute Ethanol ◽

And Oxidative Stress

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Taurine represses oxidative stress in the liver and kidney following exposure to atrazine in Wistar rats

International Journal of Biological Research ◽

10.14419/ijbr.v7i1.29815 ◽

2019 ◽

Vol 7 (1) ◽

pp. 7

Author(s):

Olusegun Kayode Afolabi ◽

Dasola Teslim Folarin ◽

Felix Olusola Aderibigbe ◽

Abimbola Arinola

Keyword(s):

Oxidative Stress ◽

Wistar Rats ◽

Reduced Glutathione ◽

Antioxidant Property ◽

High Dose ◽

Protective Effects ◽

Biochemical Assays ◽

Total Antioxidant ◽

Liver And Kidney ◽

Essential Nutrient

Background: Taurine is a conditional essential nutrient in man, with proven antioxidant property. This study was designed to evaluate the protective effects of taurine against atrazine (ATZ)-induced hepatic and renal oxidative toxicity in rats.Methods: Wistar rats were orally exposed to ATZ (1/10 LD50) alone or in combination with taurine at 1.5% w/v and 3% w/v in their drinking water for 30 days. After treatment, the liver and kidney were excised for biochemical assays by spectrophotometric methods.Results: Exposure to ATZ significantly elevated hepatic and renal malondialdehyde (MDA) levels when compared to control (p < 0.05). Advanced oxidized protein products (AOPP) were equally increased in these tissues on exposure to ATZ. In addition, reduced glutathione (GSH) and total antioxidant capacity (TAC) were markedly depleted in both organs on exposure to ATZ. Furthermore, activities of the antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT) were inhibited by ATZ compared to the control. However, co-treatment with taurine attenuated the oxidative responses generated by ATZ exposure in the rats, with the high dose of the amino acid normalizing most of the toxic effects.Conclusion: The study suggested that taurine can protect against ATZ-induced oxidative stress.

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Antioxidant and Anti-Inflammatory Effects of Coenzyme Q10 on L-Arginine-Induced Acute Pancreatitis in Rat

Oxidative Medicine and Cellular Longevity ◽

10.1155/2016/5818479 ◽

2016 ◽

Vol 2016 ◽

pp. 1-8 ◽

Cited By ~ 24

Author(s):

Seyed Abbas Mirmalek ◽

Ala Gholamrezaei Boushehrinejad ◽

Hassan Yavari ◽

Bahareh Kardeh ◽

Yekta Parsa ◽

...

Keyword(s):

Oxidative Stress ◽

Acute Pancreatitis ◽

Coenzyme Q10 ◽

Histopathological Examination ◽

Antioxidant Property ◽

Control Group ◽

Protective Effects ◽

Sprague Dawley ◽

Serum Lipase ◽

Anti Inflammatory

This study was aimed at evaluating the protective effect of coenzyme Q10 on L-arginine-induced acute pancreatitis in rats regarding biomarkers and morphologic changes. Thirty-two male Sprague-Dawley rats were divided into 4 equal groups. Control group received intraperitoneal normal saline, while in sham and experimental groups 1 and 2 pancreatitis was induced with L-arginine. E1 and E2 groups were treated with a single dose of 100 and 200 mg/kg Q10, respectively. Serum lipase and amylase, along with pancreas IL-10, IL-1β, and TNF-α, were measured. For evaluation of oxidative stress, pancreatic superoxide dismutase (SOD), glutathione (GSH), malondialdehyde (MDA), and myeloperoxidase (MPO) were assessed. Histopathological examination for morphologic investigation was conducted. Serum amylase and lipase, as well as TNF-αand IL-1βcytokines, reverted with administration of Q10 in consistence with dosage. In contrast, Q10 assisted in boosting of IL-10 with higher dosage (200 mg/kg). A similar pattern for oxidative stress markers was noticed. Both MDA and MPO levels declined with increased dosage, contrary to elevation of SOD and GSH. Histopathology was in favor of protective effects of Q10. Our findings proved the amelioration of pancreatic injury by Q10, which suggest the anti-inflammatory and antioxidant property of Q10 and its potential therapeutic role.

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