scholarly journals Evaluation of isoniazid-oxidative reactions in mice model

2019 ◽  
Vol 9 (6) ◽  
pp. 36-37
Author(s):  
Kamel Mokhnache ◽  
Ahlem Karbab ◽  
Soraya Madoui ◽  
Hanane Khither ◽  
El-Khamsa Soltani ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adverse Effect ◽  
Lipid Peroxidation ◽  
Control Group ◽  
Mice Model ◽  
Oxidative Reactions

In this study the anti-tubercular drug; isoniazid (INH) was investigated for their adverse effect; the oxidative stress. This effect was evaluated by using mice model, at the dose of 151 mg/kg.  We found that oxidative stress induced by INH is associated with lipid peroxidation expressed by the increase in the level of MDA from 76.9 ± 1.74 to 79.61 ± 2.67 nmol/g tissue. The oxidative stress of INH is accompanied by a decrease in reduced GSH level (from 79.9 ± 12 μmol / mg  to 68.48 ± 4.28 μmol / mg compared to of the control group). After treatment with INH at 151 mg/kg, a decrease in CAT activities occurred compared to control (2.53 ± 0.39 U/mg Pr vs 5.07 ± 0.73 U/mg Pr). Keywords: isoniazid, oxidative stress, MDA, GSH, CAT

Resistance of erythrocytes from Brown trout (Salmo trutta m. trutta L.) affected by ulcerative dermal necrosis syndrome

2011 ◽  
Vol 14 (3) ◽  
pp. 443-448 ◽  
Author(s):  
N. Kurhalyuk ◽  
H. Tkachenko ◽  
K. Pałczyńska
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Brown Trout ◽  
Salmo Trutta ◽  
Thiobarbituric Acid ◽  
Control Group ◽  
Thiobarbituric Acid Reactive Substance ◽  
Tbars Level ◽  
Reactive Substance ◽  
Brown Trout Salmo Trutta

Resistance of erythrocytes from Brown trout (Salmo trutta m. trutta L.) affected by ulcerative dermal necrosis syndrome In the present work we evaluated the effect of ulcerative dermal necrosis (UDN) syndrome on resistance of erythrocytes to haemolytic agents and lipid peroxidation level in the blood from brown trout (Salmo trutta m. trutta L.). Results showed that lipid peroxidation increased in erythrocytes, as evidenced by high thiobarbituric acid reactive substance (TBARS) levels. Compared to control group, the resistance of erythrocytes to haemolytic agents was significantly lower in UDN-positive fish. Besides, UDN increased the percent of hemolysated erythrocytes subjected to the hydrochloric acid, urea and hydrogen peroxide. Results showed that UDN led to an oxidative stress in erythrocytes able to induce enhanced lipid peroxidation level, as suggested by TBARS level and decrease of erythrocytes resistance to haemolytic agents.

scholarly journals In Vivo Protective Effects of Gallic Acid Isolated from Peltiphyllum Peltatum Against Sodium Fluoride-Induced Oxidative Stress in Rat Erythrocytes

2013 ◽  
Vol 64 (4) ◽  
pp. 553-559 ◽  
Author(s):  
Seyed Fazel Nabavi ◽  
Solomon Habtemariam ◽  
Antoni Sureda ◽  
Akbar Hajizadeh Moghaddam ◽  
Maria Daglia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Vitamin C ◽  
Gallic Acid ◽  
Sodium Fluoride ◽  
Enzyme Activities ◽  
Control Group ◽  
Rat Erythrocytes ◽  
Pre Treatment

Abstract Gallic acid has been identified as an antioxidant component of the edible and medicinal plant Peltiphyllum peltatum. The present study examined its potential protective role against sodium fluoride (NaF)-induced oxidative stress in rat erythrocytes. Oxidative stress was induced by NaF administration through drinking water (1030.675 mg m-3 for one week). Gallic acid at 10 mg kg-1 and 20 mg kg-1 and vitamin C for positive controls (10 mg kg-1) were administered daily intraperitoneally for one week prior to NaF administration. Thiobarbituric acid reactive substances, antioxidant enzyme activities (superoxide dismutase and catalase), and the level of reduced glutathione were evaluated in rat erythrocytes. Lipid peroxidation in NaF-exposed rats significantly increased (by 88.8 %) when compared to the control group (p<0.05). Pre-treatment with gallic acid suppressed lipid peroxidation in erythrocytes in a dose-dependent manner. Catalase and superoxide dismutase enzyme activities and glutathione levels were reduced by NaF intoxication by 54.4 %, 63.69 %, and 42 % (p<0.001; vs. untreated control group), respectively. Pre-treatment with gallic acid or vitamin C significantly attenuated the deleterious effects. Gallic acid isolated from Peltiphyllum peltatum and vitamin C mitigated the NaF-induced oxidative stress in rat erythrocytes.

Expression Analysis of 4-Hydroxynonenal Modified Proteins in Schizophrenia Brain; Relevance to Involvement in Redox Dysregulation

2021 ◽  
Vol 18 ◽  
Author(s):  
Sobia Manzoor ◽  
Ayesha Khan ◽  
Beena Hasan ◽  
Shamim Mushtaq ◽  
Nikhat Ahmed
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Thiobarbituric Acid ◽  
Brain Regions ◽  
Protein Adducts ◽  
Antioxidant Systems ◽  
Control Group ◽  
Tbars Level ◽  
Elevated Expression ◽  
Modified Proteins

Background: Oxidative damage contributes to the pathophysiology of schizophrenia (SZ). Redox imbalance may lead to increased lipid peroxidation, which produces toxic aldehydes like 4-hydroxynonenal (4-HNE) ultimately leading to oxidative stress. Conversely, implications of oxidative stress points towards an alteration in HNE-protein adducts and activities of enzymatic and antioxidant systems in schizophrenia. Objectives: Present study focuses on identification of HNE-protein adducts and its related molecular consequences in schizophrenia pathology due to oxidative stress, particularly lipid peroxidation. Material and Methods: Oxyblotting was performed on seven autopsied brain samples each from cortex and hippocampus region of schizophrenia patients and their respective normal healthy controls. Additionally, thiobarbituric acid substances (TBARS), reduced glutathione (GSH) levels and catalase (CAT) activities associated with oxidative stress, were also estimated. Results: Obtained results indicates substantially higher levels of oxidative stress in schizophrenia patients than healthy control group represented by elevated expression of HNE-protein adducts. Interestingly, hippocampus region of schizophrenia brain shows increased HNE protein adducts compared to cortex. An increase in catalase activity (4.8876 ± 1.7123) whereas decrease in antioxidant GSH levels (0.213 ± 0.015µmol/ml) have been observed in SZ brain. Elevated TBARS level (0.3801 ± 0.0532ug/ml) were obtained in brain regions SZ patients compared with their controls that reflects an increased lipid peroxidation (LPO). Conclusion: Conclusion: We propose the role of HNE modified proteins possibly associated with the pathology of schizophrenia. Our data revealed increase lipid peroxidation as a consequence of increased TBARS production. Furthermore, altered cellular antioxidants pathways related to GSH and CAT also highlight the involvement of oxidative stress in schizophrenia pathology.

Butylated hydroxyanisole alleviates ferric nitrilotriacetate induced nephrotoxicity in rats by abrogation of oxidative stress

2013 ◽  
Vol 3 (2) ◽  
pp. 65-70
Author(s):  
Sabah Ansar ◽  
Mohammad Iqbal ◽  
Noura Al Jameil
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Lipid Peroxidation ◽  
Body Weight ◽  
Antioxidant Enzymes ◽  
Control Group ◽  
Butylated Hydroxyanisole ◽  
Chemopreventive Agent ◽  
Microsomal Lipid Peroxidation ◽  
Hydrogen Peroxide Generation

In this study the effect of butylated hydroxyanisole (BHA), a phenolic antioxidantused in food on Ferric‐Nitrilotriacetate (Fe–NTA) induced nephrotoxicity is reported. Fe‐NTA (9 mg Fe/kg body weight, intraperitoneally) treatment enhanced the renal microsomal lipid peroxidation and hydrogen peroxide generation to ~2‐2.5 folds compared to saline‐treated control and glutathione levels and the activities of antioxidant enzymes decreased to a range of 2–2.5 fold in kidney. These changes were reversed significantly in animals receiving a pretreatment of BHA. Pretreatment with BHA prior to Fe‐ NTA treatment reduced microsomal lipid peroxidation and hydrogen peroxide generation to 1.3‐1.5 fold compared to control group and glutathione and the activities of antioxidant enzymes increased to a range of 1.5‐2 folds in kidney. Fe‐NTA administration enhanced value of blood urea nitrogen and creatinine to 3.7 and 2.5 fold respectively as compared to their corresponding control group. Administration of Fe‐NTA to rats receiving a pretreatment of BHA led to a significant diminution in both of these values. The results indicate that BHA is a potent chemopreventive agent and suppresses Fe‐NTA induced nephrotoxicity in rats.

scholarly journals Effect of corticosteroid (triamcinolone acetonide) and chlorhexidin on chemotherapy- induced oxidative stress in buccal mucosa of rats

2020 ◽  
pp. 014556131989440
Author(s):  
Sami Gümüş ◽  
Murat Yarıktaş ◽  
Mustafa Nazıroğlu ◽  
Abdülhadi Cihangir Uğuz ◽  
Giray Aynali ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Triamcinolone Acetonide ◽  
Buccal Mucosa ◽  
Inflammatory Cell ◽  
Chemotherapeutic Agent ◽  
Oxidative Injury ◽  
Cheek Pouch ◽  
Control Group ◽  
Ulcerative Lesions

Oral mucositis (OM) refers to erythematous and ulcerative lesions of the oral mucosa. This pathology can occur by various causes. Cancer therapy is one of the well-known causes of OM such as chemotherapy and/or with radiation therapy. It has been widely mentioned that oxidative stress parameters such as lipid peroxidation (LP) levels increase during cancer process. Glutathione (GSH) is one of the major intracellular enzymes to detoxify oxidant molecules. The aim of this study was to investigate and compare the effects of Triamcinolone Acetonide (TA), a synthetic steroid chlorhexidine (CHX), a chemical antiseptic, on 5- fluorouracil (5-FU), a chemotherapeutic agent and soft abrasion induced OM in buccal mucosa of rats. OM was induced in rats through a combination of 5-FU treatment and mild abrasion of the cheek pouch with a wire brush. Buccal mucosa lipid peroxidation (LP) levels were higher (p< 0.05) in 5-FU group than in control although LP levels were lower (p<0.05) in TA group than in control group. The reduced glutathione levels were lower (p<0.05) in 5-FU group than in the control group although its level was higher (p<0.05) in TA and CHX groups than in the 5-FU group. Glutathione peroxidase activity was also higher (p<0.05) in TA group than the 5- FU group. In histopathological analyses, treatment with TA reduced 5-FU induced inflammatory cell infiltration and ulceration (p<0.001) but not with CHX. In conclusion, we observed that TA and CHX treatment modulated chemotherapy induced oxidative injury in the rat OM. However, only TA histopathologically ameliorated the 5-FU induced OM of rats. These findings suggest that TA is a useful agent for management of experimental oxidative injury and OM caused by the chemotherapy.

Lipid Peroxidation, Protein Oxidation, Gelatinases, and Their Inhibitors in a Group of Adults with Obesity

2019 ◽  
Vol 51 (06) ◽  
pp. 389-395 ◽  
Author(s):  
Gregorio Caimi ◽  
Baldassare Canino ◽  
Maria Montana ◽  
Caterina Urso ◽  
Vincenzo Calandrino ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Protein Oxidation ◽  
Thiobarbituric Acid ◽  
Protein Carbonyl ◽  
The Body ◽  
Control Group ◽  
The Matrix ◽  
Markers Of Oxidative Stress ◽  
Obese Subjects

AbstractThe association between obesity and cardiovascular diseases has a multifactorial pathogenesis, including the synthesis of inflammatory molecules, the increase in oxidative stress and the dysregulation of the matrix metalloprotease (MMP) concentration and activity. In a group of adults with obesity, divided in 2 subgroups according to the body mass index (BMI), we examined lipid peroxidation, expressed as thiobarbituric acid-reactive substances (TBARS), protein oxidation, expressed as protein carbonyl groups (PCs), plasma gelatinases (MMP-2 and MMP-9), and their tissue inhibitors (TIMP-1 and TIMP-2). In the whole group, as well as in the 2 subgroups (with BMI 30–35 or BMI>35) of obese subjects, we observed an increase in TBARS, PCs, MMP-2, and MMP-9, and also TIMP-1 and TIMP-2 in comparison with the control group. A positive correlation between TBARS and PCs emerged in obese subjects and persisted after dividing obese subjects according to BMI. The correlation between MMP-2 and TIMP-2 was not statistically significant, while a significant correlation was present between MMP-9 and TIMP-1. The correlations between the markers of oxidative stress (TBARS and PCs) and those of the MMP/TIMP profile indicated a more marked influence of protein oxidation on MMPs and TIMPs in comparison with TBARS. The innovative aspect of our study was the simultaneous evaluation of oxidative stress markers and MMP/TIMP profile in adult obese subjects. We observed significant alterations and correlations that may negatively influence the clinical course of the disease.

scholarly journals Evaluation of Salivary and Serum Total Antioxidant Capacity and Lipid Peroxidation in Postmenopausal Women

2020 ◽  
Vol 2020 ◽  
pp. 1-5
Author(s):  
Fatemeh Zovari ◽  
Hadi Parsian ◽  
Ali Bijani ◽  
Ameneh Moslemnezhad ◽  
Atena Shirzad
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Antioxidant Capacity ◽  
Postmenopausal Women ◽  
Total Antioxidant Capacity ◽  
Premenopausal Women ◽  
Control Group ◽  
Antioxidant Power ◽  
Whole Saliva ◽  
Total Antioxidant

Objective. In menopause, reduction of estrogen hormone affects oxidative stress process in serum. Oxidative stress in saliva plays a significant role in the pathogenesis of oral diseases. The aim of this study was to investigate the total antioxidant capacity and lipid peroxidation in the serum and saliva of premenopausal and postmenopausal women. Methods. In this case control study, 50 postmenopausal women (case group) and 48 premenopausal women (control group) were selected. The unstimulated whole saliva and serum of the postmenopausal and premenopausal women were collected. The total antioxidant capacity (TAC) of the saliva and serum was measured by ferric reducing antioxidant power (FRAP). Also, malondialdehyde (MDA) was measured by thiobarbituric acid reactive substance (TBARS) method for serum and saliva. Then, the obtained data were analyzed by SPSS 17, whereby Mann–Whitney test and Spearman’s correlation test were used. P < 0.05 was considered statistically significant. Results. The postmenopausal group had significantly lower mean serum TAC and higher mean serum MDA than the control group ( P < 0 < 001 and P < 0.01 , respectively). The mean salivary TAC and MDA, however, did not differ significantly between the case and control group ( P = 0.64 and P = 0.08 , respectively). Conclusion. In postmenopausal women, with elevation of serum MDA and reduction of serum TAC, the extent of serum oxidative stress grows, but MDA and TAC levels of saliva do not change.

Hepatoprotection by carotenoids in isoniazid–rifampicin induced hepatic injury in rats

2010 ◽  
Vol 88 (5) ◽  
pp. 819-834 ◽  
Author(s):  
S. V. Rana ◽  
R. Pal ◽  
K. Vaiphei ◽  
R. P. Ola ◽  
K. Singh
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Alkaline Phosphatase ◽  
Superoxide Dismutase ◽  
Body Mass ◽  
Hepatic Injury ◽  
Control Group ◽  
Adult Rats ◽  
Partial Protection ◽  
Phosphatase Treatment

This study evaluates the hepatoprotective effect of carotenoids against isoniazid (INH) and rifampicin (RIF). Thirty-six adult rats were divided into the following 4 groups: (1) control group treated with normal saline; (2) INH + RIF group treated with 50 mg·(kg body mass)–1·day–1 of INH and RIF each; (3) INH + RIF+ carotenoids group treated with 50 mg·(kg body mass)–1·day–1 of INH and RIF each and 10 mg·(kg body mass)–1·day–1 of carotenoids; and (4) carotenoids group treated with 10 mg·(kg body mass)–1·day–1 of carotenoids for 28 days intragastrically. Oxidative stress and antioxidant levels in liver and blood, liver histology and change in transaminases were measured in all the above-mentioned groups. There was an increase in lipid peroxidation with a reduction in thiols, catalase, and superoxide dismutase (SOD) in the liver and blood of rats accompanied by an increase in transaminases, bilirubin, and alkaline phosphatase. Treatment with carotenoids along with INH + RIF partially reversed lipid peroxidation, thiols, catalase, and SOD in the liver and blood of rats. Elevated levels of the enzymes in serum were also reversed partially by this treatment. The degree of necrosis, portal triaditis, and inflammation were also lowered in the carotenoids group. In conclusion, carotenoids supplementation in INH + RIF treated rats showed partial protection.

scholarly journals Is Oxidative Stress in Mice Brain Regions Diminished by 2-[(2,6-Dichlorobenzylidene)amino]-5,6-dihydro-4H-cyclopenta[b]thiophene-3-carbonitrile?

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
A. C. Fortes ◽  
A. A. C. Almeida ◽  
G. A. L. Oliveira ◽  
P. S. Santos ◽  
W. De Lucca Junior ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Western Blot ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Brain Regions ◽  
Saline Control ◽  
Control Group ◽  
Nitrite Content

2-[(2,6-Dichlorobenzylidene)amino]-5,6-dihydro-4H-cyclopenta[b]thiophene-3-carbonitrile, 5TIO1, is a new 2-aminothiophene derivative with promising pharmacological activities. The aim of this study was to evaluate its antioxidant activity in different areas of mice central nervous system. Male Swiss adult mice were intraperitoneally treated with Tween 80 dissolved in 0.9% saline (control group) and 5TIO1 (0.1, 1, and 10 mg kg−1). Brain homogenates—hippocampus, striatum, frontal cortex, and cerebellum—were obtained after 24 h of observation. Superoxide dismutase and catalase activities, lipid peroxidation and nitrite content were measured using spectrophotometrical methods. To clarify the 5TIO1’s mechanism on oxidative stress, western blot analysis of superoxide dismutase and catalase was also performed. 5TIO1 decreased lipid peroxidation and nitrite content in all brain areas and increased the antioxidant enzymatic activities, specially, in cerebellum. The data of Western blot analysis did not demonstrate evidence of the upregulation of these enzymes after the administration of this compound. Our findings strongly support that 5TIO1 can protect the brain against neuronal damages regularly observed during neuropathologies.

scholarly journals The possibilities of pharmacological correction of ademol oxidative stress in rates with traumatic brain injury

2021 ◽  
Vol 25 (2) ◽  
pp. 192-195
Author(s):  
S. I. Semenenko
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Lipid Peroxidation ◽  
Antioxidant Enzymes ◽  
Brain Injury ◽  
Oxidative Degradation ◽  
Male Rats ◽  
Control Group ◽  
Nacl Solution ◽  
Amantadine Sulfate

Annotation. An important measure of intensive care in patients with traumatic brain injury (TBI) is the use of pharmacotherapeutic agents with antioxidant properties. The aim of this study was to evaluate the effect of ademol compared with amantadine sulfate and 0.9% NaCl solution on the course of oxidative stress in the brain of TBI rats. The experiments were performed on 28 white male rats weighing 160-190 g. The experimental TBI model of severe severity was caused by the action of a carbon dioxide flow under pressure created using a gas balloon pneumatic gun. The therapeutic effect of ademol on model TBI was evaluated with a 2 mg/kg dose. The pseudoperated animals and control group received a 0.9% solution of NaCl and amantadine sulfate at a dose of 2 ml/kg and 5 mg/kg i/v. Data were processed using StatPlus 2009. We used the parametric criterion of t-Student, non-parametric criterion of W. White, paired criterion Ť. Wilcoxon, Fisher's angular transformation at p <0,05. In the course of the experiment, it was found that treatment of rats with TBI ademol leads to a decrease in the activity of lipid peroxidation and oxidative degradation of proteins (p<0.05) and promotes the normalization of the activity of antioxidant enzymes in cells of traumatically damaged brain (p<0.05). The use of ademol compared to amantadine sulfate and 0.9% NaCl solution was accompanied by a more significant decrease in the activity of lipid peroxidation and oxidative degradation of proteins and an improvement in the level of antioxidant enzymes in damaged brain of animals with TBI (p<0.05).

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