Occurrence of Textile Dyes and Metals in Tunisian Textile Dyeing Effluent: Effects on Oxidative Stress Status and Histological Changes in Balb/c Mice

Although it is known that textile wastewater contains highly toxic contaminants whose effects in humans represent public health problems in several countries, studies involving mammal species are scarce. This study was aimed to evaluate the toxicity profile of 90-days oral administration of textile dyeing effluent (TDE) on oxidative stress status and histological changes of male mice. The TDE was collected from the textile plant of Monastir, Tunisia and evaluated for the metals, aromatic amines, and textile dyes using analytical approaches. Metal analysis by ICP-MS showed that the tested TDE exhibited very high levels of Cr, As, and Sr, which exceeded the wastewater emission limits prescribed by WHO and Tunisian authority. The screening of TDE through UPLC-MS/MS confirmed the presence of two textile dyes: a triphenylmethane dye (Crystal violet) and a disperse azo dye (Disperse yellow 3). Exposure to TDE significantly altered the malondialdehyde (MDA), Conjugated dienes (CDs), Sulfhydryl proteins (SHP) and catalase levels in the hepatic and renal tissues. Furthermore, histopathology observation showed that hepatocellular and renal lesions were induced by TDE exposure. The present study concluded that TDE may involve induction of oxidative stress which ensues in pathological lesions in several vital organs suggesting its high toxicity. Metals and textile dyes may be associated with the observed toxicological effects of the TDE. These pollutants, which may have seeped into surrounding rivers in Monastir city, can cause severe health malaise in wildlife and humans.

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Dendrobine attenuates isoniazid- and rifampicin-induced liver injury by inhibiting miR-295-5p

Human & Experimental Toxicology ◽

10.1177/0960327120937047 ◽

2020 ◽

Vol 39 (12) ◽

pp. 1671-1680

Author(s):

R Ci ◽

K Zhang ◽

A Zhu ◽

W Zang

Keyword(s):

Oxidative Stress ◽

Liver Injury ◽

Luciferase Reporter ◽

Protective Effects ◽

Histological Changes ◽

Stress Markers ◽

Oxidative Stress Status ◽

Protein Expressions ◽

Polymerase Chain ◽

Underlying Mechanisms

The present study aims to investigate the protective effects of Dendrobine and its underlying mechanisms on liver injury induced by isoniazid (INH) and rifampicin (RIF). A mouse model of liver injury was induced by intragastrically administration of 100 mg/kg INH and 100 mg/kg RIF for 14 days. The mice were intragastrically administrated with Dendrobine (50, 100, and 200 mg/kg) before the administration of INH and RIF. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were determined. Oxidative stress markers including glutathione, superoxide dismutase, and malondialdehyde in the liver were measured and liver histopathological examinations were performed. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blot were applied to determine the mRNA and protein expressions, respectively. Luciferase reporter assay was used to evaluate the interactions between miR-295-5p and CYP1A2. Dendrobine significantly decreased serum ALT and AST and inhibited the liver index and ameliorated the liver histological changes induced by INH and RIF. Besides, Dendrobine also regulated oxidative stress status in the liver by the regulation of CYP1A2. Moreover, mmu-miR-295-5p was identified to target CYP1A2 and to regulate the expression of CYP1A2. In summary, Dendrobine ameliorated INH and RIF induced mouse liver injury by miR-295-5p-mediated CYP1A2 expression.

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Oxidative Stress Status in Patients with Choledocholithiasis: Before and After Endoscopic Sphincterotomy and Biliary Clearance

Revista de Chimie ◽

10.37358/rc.18.8.6493 ◽

2018 ◽

Vol 69 (8) ◽

pp. 2172-2176

Author(s):

Catalin Victor Sfarti ◽

Alin Ciobica ◽

Carol Stanciu ◽

Gheorghe G. Balan ◽

Irina Garleanu ◽

...

Keyword(s):

Oxidative Stress ◽

Endoscopic Sphincterotomy ◽

Specific Activity ◽

Oxidative Stress Marker ◽

Control Group ◽

Oxidative Stress Parameter ◽

Extrahepatic Cholestasis ◽

Biliary Clearance ◽

Oxidative Stress Status ◽

Before And After

Choledocholithiasis may cause biliary obstruction which leads to hepatocellular injury. Oxidative stress has been proposed as a possible mechanism involved in this disorder. This study evaluates the oxidative stress burden in patients with choledocholithiasis and secondary cholestasis, before and after endoscopic sphincterotomy. Experimental part: Patients diagnosed with choledocholithiasis and secondary extrahepatic cholestasis were included in the study between January 1st 2016 and October 31st 2016. In all patients oxidative stress markers were collected within 2 hours before and 48 hours after therapeutic ERCP. Selected markers were superoxide dismutase (SOD), glutathione peroxidase (GPX) and malondialdehyde (MDA). The results were compared to those from a group of 40 healthy subjects. Significantly lower concentrations of SOD (p = 0.03) and GPX (p [ 0.0001) activities, associated with an increased level of MDA level (p [ 0.0001) were shown in patients before biliary clearance compared with the healthy control group. After ERCP the only oxidative stress parameter which showed improvement was the SOD specific activity (p = 0.037). This study shows that extrahepatic cholestasis secondary to choledocholithiasis is associated with increased oxidative stress status. After biliary clearance one oxidative stress marker was significantly improved (SOD), suggesting a possible antioxidant effect of such procedure.

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Modulatory Role of Riboceine and Vitamin C Supplementation on Altered Oxidative Stress Status of Alloxan-induced Diabetic Wistar Rats

Bioscience Biotechnology Research Communications ◽

10.21786/bbrc/13.4/75 ◽

2020 ◽

Vol 13 (4) ◽

pp. 2130-2138

Author(s):

Akingbade Bamidele Thomas

Keyword(s):

Oxidative Stress ◽

Vitamin C ◽

Wistar Rats ◽

Oxidative Stress Status ◽

Vitamin C Supplementation

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Oxidative stress status: An introduction

Free Radical Biology and Medicine ◽

10.1016/0891-5849(91)90071-a ◽

1991 ◽

Vol 10 (3-4) ◽

pp. 173 ◽

Cited By ~ 13

Author(s):

William A. Pryor ◽

Susan Shipley Godber

Keyword(s):

Oxidative Stress ◽

Oxidative Stress Status

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Curcumin Potentiates α7 Nicotinic Acetylcholine Receptors and Alleviates Autistic-Like Social Deficits and Brain Oxidative Stress Status in Mice

International Journal of Molecular Sciences ◽

10.3390/ijms22147251 ◽

2021 ◽

Vol 22 (14) ◽

pp. 7251

Author(s):

Petrilla Jayaprakash ◽

Dmytro Isaev ◽

Waheed Shabbir ◽

Dietrich E. Lorke ◽

Bassem Sadek ◽

...

Keyword(s):

Oxidative Stress ◽

Nicotinic Acetylcholine Receptors ◽

Acetylcholine Receptors ◽

Pathological Condition ◽

Repetitive Behaviors ◽

Social Deficits ◽

Nicotinic Acetylcholine ◽

Oxidative Stress Status ◽

Inward Currents ◽

Α7 Nachrs

Autistic spectrum disorder (ASD) refers to a group of neurodevelopmental disorders characterized by impaired social interaction and cognitive deficit, restricted repetitive behaviors, altered immune responses, and imbalanced oxidative stress status. In recent years, there has been a growing interest in studying the role of nicotinic acetylcholine receptors (nAChRs), specifically α7-nAChRs, in the CNS. Influence of agonists for α7-nAChRs on the cognitive behavior, learning, and memory formation has been demonstrated in neuro-pathological condition such as ASD and attention-deficit hyperactivity disorder (ADHD). Curcumin (CUR), the active compound of the spice turmeric, has been shown to act as a positive allosteric modulator of α7-nAChRs. Here we hypothesize that CUR, acting through α7-nAChRs, influences the neuropathology of ASD. In patch clamp studies, fast inward currents activated by choline, a selective agonist of α7-nAChRs, were significantly potentiated by CUR. Moreover, choline induced enhancement of spontaneous inhibitory postsynaptic currents was markedly increased in the presence of CUR. Furthermore, CUR (25, 50, and 100 mg/kg, i.p.) ameliorated dose-dependent social deficits without affecting locomotor activity or anxiety-like behaviors of tested male Black and Tan BRachyury (BTBR) mice. In addition, CUR (50 and 100 mg/kg, i.p.) mitigated oxidative stress status by restoring the decreased levels of superoxide dismutase (SOD) and catalase (CAT) in the hippocampus and the cerebellum of treated mice. Collectively, the observed results indicate that CUR potentiates α7-nAChRs in native central nervous system neurons, mitigates disturbed oxidative stress, and alleviates ASD-like features in BTBR mice used as an idiopathic rodent model of ASD, and may represent a promising novel pharmacological strategy for ASD treatment.

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Positive Modulation of PinkNelumbo nuciferaFlowers on Memory Impairment, Brain Damage, and Biochemical Profiles in Restraint Rats

Oxidative Medicine and Cellular Longevity ◽

10.1155/2016/5789857 ◽

2016 ◽

Vol 2016 ◽

pp. 1-11 ◽

Cited By ~ 2

Author(s):

Thawatchai Prabsattroo ◽

Jintanaporn Wattanathorn ◽

Pichet Somsapt ◽

Opass Sritragool

Keyword(s):

Oxidative Stress ◽

Monoamine Oxidase ◽

Spatial Memory ◽

Brain Damage ◽

Memory Deficit ◽

Ki67 Expression ◽

Mao B ◽

Serum Corticosterone ◽

Neuron Density ◽

Oxidative Stress Status

Due to the crucial role of oxidative stress in the stress-induced memory deficit, the benefit of substance possessing antioxidant effect is focused. Since no data are available, we aimed to determine the effect ofNelumbo nuciferaflowers extract on spatial memory and hippocampal damage in stressed rats. Male Wistar rats, weighing 250–350 g, were orally givenN. nuciferaextract at doses of 10, 10, and 200 mg·kg−145 minutes before the exposure to 12-hour restraint stress. The spatial memory and serum corticosterone were assessed at 7 and 14 days of study period. At the end of study, acetylcholinesterase (AChE), monoamine oxidase type A and monoamine oxidase type B (MAO-A and MAO-B), oxidative stress status, neuron density, and Ki67 expression in hippocampus were also assessed. The results showed thatN. nuciferaextract decreased memory deficit and brain damage, serum corticosterone, oxidative stress status, AChE, and MAO-A and MAO-B activities but increased neuron density and Ki67 expression in hippocampus. These suggested that the improved oxidative stress status, adult neurogenesis, and cholinergic and monoaminergic functions might be responsible for the protective effect against stress-related brain damage and dysfunction of the extract. Therefore,N. nuciferaextract is the potential neuroprotective and memory enhancing agent. However, further researches are still required.

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Autistic-Like Behaviors, Oxidative Stress Status, and Histopathological Changes in Cerebellum of Valproic Acid Rat Model of Autism Are Improved by the Combined Extract of Purple Rice and Silkworm Pupae

Oxidative Medicine and Cellular Longevity ◽

10.1155/2016/3206561 ◽

2016 ◽

Vol 2016 ◽

pp. 1-10 ◽

Cited By ~ 13

Author(s):

Nartnutda Morakotsriwan ◽

Jintanaporn Wattanathorn ◽

Woranan Kirisattayakul ◽

Kowit Chaisiwamongkol

Keyword(s):

Oxidative Stress ◽

Valproic Acid ◽

Purkinje Cell ◽

Rat Model ◽

Cell Loss ◽

Hot Plate ◽

Hot Plate Test ◽

Silkworm Pupae ◽

Oxidative Stress Status ◽

Purkinje Cell Loss

Due to the crucial role of oxidative stress on the pathophysiology of autism and the concept of synergistic effect, the benefit of the combined extract of purple rice and silkworm pupae (AP1) for autism disorder was the focus. Therefore, we aimed to determine the effect of AP1 on autistic-like behaviors, oxidative stress status, and histopathological change of cerebellum in valproic acid (VPA) rat model of autism. VPA was injected on postnatal day (PND) 14 and the animals were orally given AP1 at doses of 50, 100, and 200 mg·kg−1BW between PND 14 and PND 40. The autism-like behaviors were analyzed via hot-plate, rotarod, elevated plus-maze, learning, memory, and social behavior tests. Oxidative stress and the histological change in the cerebellum were assessed at the end of study. AP1 treated rats improved behaviors in all tests except that in hot-plate test. The improvement of oxidative stress and Purkinje cell loss was also observed in the cerebellum of VPA-treated rats. Our data suggest that AP1 partially reduced autism-like behaviors by improving oxidative stress and Purkinje cell loss. Further research is required to identify the active ingredients in AP1 and gender difference effect.

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QSYQ Attenuates Oxidative Stress and Apoptosis Induced Heart Remodeling Rats through Different Subtypes of NADPH-Oxidase

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2013/824960 ◽

2013 ◽

Vol 2013 ◽

pp. 1-8 ◽

Cited By ~ 6

Author(s):

Yong Wang ◽

Chun Li ◽

Yuli Ouyang ◽

Tianjiao Shi ◽

Xiaomin Yang ◽

...

Keyword(s):

Oxidative Stress ◽

Heart Failure ◽

Nadph Oxidase ◽

Caspase 3 ◽

Ventricular Remodeling ◽

Cardiac Injury ◽

Myocardial Tissue ◽

Therapeutic Effects ◽

Histological Changes ◽

Nadph Oxidase 4

We aim to investigate the therapeutic effects of QSYQ, a drug of heart failure (HF) in clinical practice in China, on a rat heart failure (HF) model. 3 groups were divided: HF model group (LAD ligation), QSYQ group (LAD ligation and treated with QSYQ), and sham-operated group. After 4 weeks, rats were sacrificed for cardiac injury measurements. Rats with HF showed obvious histological changes including necrosis and inflammation foci, elevated ventricular remodeling markers levels(matrix metalloproteinases-2, MMP-2), deregulated ejection fraction (EF) value, increased formation of oxidative stress (Malondialdehyde, MDA), and up-regulated levels of apoptotic cells (caspase-3, p53 and tunnel) in myocardial tissue. Treatment of QSYQ improved cardiac remodeling through counter-acting those events. The improvement of QSYQ was accompanied with a restoration of NADPH oxidase 4 (NOX4) and NADPH oxidase 2 (NOX2) pathways in different patterns. Administration of QSYQ could attenuate LAD-induced HF, and AngII-NOX2-ROS-MMPs pathway seemed to be the critical potential targets for QSYQ to reduce the remodeling. Moreover, NOX4 was another key targets to inhibit the p53 and Caspase3, thus to reduce the hypertrophy and apoptosis, and eventually provide a synergetic cardiac protective effect.

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