Epigallocatechin gallate effectively ameliorates fluoride-induced oxidative stress and DNA damage in the liver of rats

2013 ◽  
Vol 91 (7) ◽  
pp. 528-537 ◽  
Author(s):  
Shanmugam Thangapandiyan ◽  
Selvaraj Miltonprabu
Keyword(s):  
Dna Damage ◽  
Green Tea ◽  
Body Mass ◽  
Radical Scavenging ◽  
Epigallocatechin Gallate ◽  
Thiobarbituric Acid ◽  
Protein Carbonyl ◽  
Health Concern ◽  
Lipid Hydroperoxides ◽  
Protein Carbonyl Content

Environmental exposure to sodium fluoride (NaF) compounds is a worldwide health concern. Epigallocatechin gallate (EGCG) is a green tea catechin found in a variety of green tea preparations. The intention of this study was to investigate the hepatoprotective role of EGCG in NaF-intoxicated rats. Rats were orally treated with NaF alone (25 mg·(kg body mass)−1·day−1) or plus EGCG at different doses (20, 40, and 80 mg·(kg body mass)−1·day−1) for 4 weeks. Hepatotoxicity of NaF was determined by increased levels of serum hepatospecific markers and total bilirubin, along with increased levels of thiobarbituric acid reactive substances, lipid hydroperoxides, protein carbonyl content, and conjugated dienes. The hepatotoxic nature of NaF was further evidenced by the decreased activity of enzymatic and nonenzymatic antioxidant levels in liver. NaF-treated rats also showed increased DNA damage and fragmentation in hepatocytes. Administration of EGCG (40 mg·(kg body mass)−1) to NaF-intoxicated rats significantly recuperated the distorted biochemical indices, DNA damage, and pathological changes in the liver tissue. Thus, the results of the present study clearly demonstrate that EGCG has strong free radical scavenging, antioxidant, and antigenotoxic properties that protect against NaF-induced oxidative hepatic injury in rats.

Role of Quercetin in Mitigation of Lindane Induced Toxicity in Terms of Oxidative Responses and Metabolic Status in Mice Brain

2020 ◽  
Vol 16 ◽  
Author(s):  
Anupama Sharma ◽  
Renu Bist ◽  
Hemant Pareek
Keyword(s):  
Citrate Synthase ◽  
Thiobarbituric Acid ◽  
Tca Cycle ◽  
Treated Group ◽  
Protein Carbonyl ◽  
Protein Carbonyl Content ◽  
Mice Brain ◽  
The Brain ◽  
Oxidative Responses

Background:: Current study evaluated the protective potential of quercetin against lindane induced toxicity in mice brain. For investigation, mice were allocated into four groups; First group was control. Second group was administered with oral dose of lindane (25 mg/kg bw) for 4 consecutive days. Third group was exposed to quercetin (40 mg/kg bw) and in fourth group, quercetin was administered 1 hour prior to the exposure of lindane. Objective:: Two major objectives were decided for study. First was to create lesions in the brain by lindane and; second was to evaluate the neuroprotective potential of quercetin. Methods:: To study oxidative responses, level of thiobarbituric acid reactive substances (TBARS), protein carbonyl content (PCC), reduced glutathione (GSH), superoxide dismutase (SOD), Catalase (CAT), and glutathione peroxidase (GPx) were measured in brain homogenates. Three key step regulating enzymes of tricarboxylic acid (TCA) cycle viz citrate synthase (CS), pyruvate dehydrogenase (PDH) and fumarase were also assayed. Results:: Lindane treatment significantly enhanced the levels of TBARS (P<0.001),PCC (P<0.001), GPx (P<0.001), SOD (P<0.05), PDH (P<0.05) and fumarase (P<0.001) in brains of mice compared to control. Meanwhile, it alleviated GSH, CAT and CS (P<0.05) activity. Conclusion:: Pretreatment with quercetin in lindane treated group not only restored, previously altered biochemical parameters after lindane treatment and also significantly improved them too which suggests that quercetin is not only invulnerable rather neuroprotective against lindane intoxication.

Lead induced oxidative DNA damage in battery-recycling child workers from Bangladesh

2018 ◽  
Vol 34 (4) ◽  
pp. 213-218 ◽  
Author(s):  
Mohammad Arif ◽  
MM Towhidul Islam ◽  
Hossain Uddin Shekhar
Keyword(s):  
Dna Damage ◽  
Lead Exposure ◽  
Oxidative Dna Damage ◽  
Lead Concentration ◽  
Threshold Level ◽  
Protein Carbonyl ◽  
The Body ◽  
Lipid Peroxidation Product ◽  
Protein Carbonyl Content ◽  
Battery Recycling

Lead exposure can damage cells directly by effecting DNA or indirectly by modifying proteins and enzymes. In Bangladesh, many working children are exposed to a very high level of lead during their early life due to their involvement with lead-oriented professions. This imposes a severe threat to the growth and development of the children. Therefore to study the effect of lead, we enrolled 60 age-matched male children, from an area of old Dhaka city, where battery-recycling shops are located, depending on their blood lead concentration. If the children had a plasma lead concentration above the WHO recommended threshold level of 10 µg/dl, we grouped them as test subjects and others as control subjects to determine the effect of lead on different biochemical parameters of the body. Compared to the controls, acculumlation of the lipid peroxidation product, malondialdehyde, increased significantly in test subjects ( p < 0.01). Lead exposure also increased the protein carbonyl content ( p < 0.05) and significantly decreased the plasma glutathione levels of test subjects compared to the controls ( p < 0.05). While comparing the lead-exposed group against controls, it was found that the percentage of damaged DNA, as measured using the Comet assay, significantly increased in tail ( p < 0.01) and decreased in head regions. All of these results suggest that high-plasma lead content may induce an oxidative stress to the study population, which may lead to DNA damage.

Metabolization of nifurtimox and benznidazole in cellular fractions of rat mammary tissue

2010 ◽  
Vol 29 (10) ◽  
pp. 813-822 ◽  
Author(s):  
Laura Cecilia Bartel ◽  
María Montalto de Mecca ◽  
Carmen Rodríguez de Castro ◽  
Florencia Matilde Bietto ◽  
José Alberto Castro
Keyword(s):  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Protein Carbonyl ◽  
Reduced Form ◽  
Mammary Tissue ◽  
Intragastric Administration ◽  
Lipid Hydroperoxides ◽  
Sprague Dawley ◽  
Protein Carbonyl Content ◽  
Sprague Dawley Rats ◽  
Protein Sulfhydryl

Two nitroheterocyclic drugs, nifurtimox (NFX) and benznidazole (BZ), used in the treatment of Chagas’ disease have serious side effects attributed to their nitroreduction to reactive metabolites. Here, we report that these drugs reach the mammary tissue and there they could undergo in situ bioactivation. Both were detected in mammary tissue from female Sprague-Dawley rats after their intragastric administration. Only NFX was biotransformed by pure xanthine-oxidoreductase and from tissue cytosol. These activities were purine dependent and were inhibited by allopurinol. Also, only NFX was biotransformed by microsomes in the presence of β-nicotinamide adenine dinucleotide phosphate, reduced form (NADPH), and was inhibited by carbon monoxide and partially by diphenyleneiodonium. NFX treatment produced significant decrease in protein sulfhydryl content after 1, 3 and 6 hours; no increases in protein carbonyl content at any time tested and significantly higher levels of lipid hydroperoxides at 3 and 6 hours; besides, ultrastructural observations after 24 hours showed significant differences in epithelial cells compared to control. These findings indicate that NFX might be more deleterious to mammary tissue than BZ and could correlate with early reports on its ability to promote rat mammary tissue toxicity.

scholarly journals DNA Damage in Lymphocytes in Hypertensive Subjects in Bangladesh

2013 ◽  
Vol 5 (3) ◽  
pp. 535-543
Author(s):  
M. Saiedullah ◽  
S. Hayat ◽  
M. R. Zamir ◽  
M. Arif ◽  
Z. H. Howlader ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Dna Damage ◽  
Superoxide Dismutase ◽  
Oxidative Dna Damage ◽  
Protein Carbonyl ◽  
Protein Carbonyl Content ◽  
Ribonucleic Acids ◽  
Stress Oxidative ◽  
Bangladeshi Population

Oxidative stress due to imbalance between the production of reactive oxygen species and their dismutation is claimed to be higher in hypertensive subjects than normotensive subjects. In hypertensive subjects oxidative stress may damage deoxy-ribonucleic acids (DNA). In this study plasma superoxide dismutase (SOD) activities, protein carbonyl contents (PCCs) and extent of DNA damage in lymphocytes were measured in specimens obtained from 86 subjects to compare oxidative stress and oxidative DNA damage between normotensive and hypertensive subjects and to assess their relationship with the degree of blood pressure. Results were expressed as mean±SD. Two-tailed unpaired t test and Pearson’s correlation test were done to compare or to determine the relationship between groups or variables. SOD activities were 2.85±0.12 unit/mg protein and 3.84±0.45 unit/mg protein (p<0.05) in hypertensive and normotensive groups respectively. PCCs were 4.77±0.36 nmol/mg protein and 3.75±0.23 nmol/mg protein in hypertensive and normotensive groups respectively. Olive tail moments (OTM) were 124.7±11.69 units and 108.9±9.27 units in hypertensive and normotensive groups respectively. The correlation coefficient of OTM was 0.3924 (p<0.05) for diastolic blood pressure and 0.3618 (p<0.05) for systolic blood pressure. Oxidative stress and DNA damage was higher in hypertensives than normotensives and DNA damage correlated positively with blood pressure. Keywords: Superoxide dismutase, Protein carbonyl content, Oxidative stress, Oxidative DNA damage, Hypertension, Bangladeshi population. © 2013 JSR Publications. ISSN: 2070-0237 (Print); 2070-0245 (Online). All rights reserved. doi: http://dx.doi.org/10.3329/jsr.v5i3.15022 J. Sci. Res. 5 (3), 535-543 (2013)  

scholarly journals Heat Killing of Bacillus subtilis Spores in Water Is Not Due to Oxidative Damage

1998 ◽  
Vol 64 (10) ◽  
pp. 4109-4112 ◽  
Author(s):  
Barbara Setlow ◽  
Peter Setlow
Keyword(s):  
Bacillus Subtilis ◽  
Oxidative Damage ◽  
Radical Scavenging ◽  
Protein Carbonyl ◽  
Free Radical Scavenging ◽  
Wild Type ◽  
Carbonyl Content ◽  
Protein Carbonyl Content ◽  
Spore Killing ◽  
High Concentrations

ABSTRACT The heat resistance of wild-type spores of Bacillus subtilis or spores (termed α−β−) lacking DNA protective α/β-type small, acid-soluble spore proteins was not altered by anaerobiosis or high concentrations of the free radical scavenging agents ethanethiol and ethanedithiol. Heat-killed wild-type and α−β− spores exhibited no increase in either protein carbonyl content or oxidized bases in DNA. These data strongly suggest that oxidative damage to spore macromolecules does not contribute significantly to spore killing by heat.

Exercise-induced oxidative stress leads hemolysis in sedentary but not trained humans

2005 ◽  
Vol 99 (4) ◽  
pp. 1434-1441 ◽  
Author(s):  
Ümit Kemal Şentürk ◽  
Filiz Gündüz ◽  
Oktay Kuru ◽  
Günnur Koçer ◽  
Yaşar Gül Özkaya ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Osmotic Fragility ◽  
Thiobarbituric Acid ◽  
Protein Carbonyl ◽  
Antioxidant Vitamin ◽  
Thiobarbituric Acid Reactive Substance ◽  
Protein Carbonyl Content ◽  
Trained Subjects ◽  
Exercise Induced ◽  
Sedentary Subjects

Intravascular hemolysis is one of the most emphasized mechanisms for destruction of erythrocytes during and after physical activity. Exercise-induced oxidative stress has been proposed among the different factors for explaining exercise-induced hemolysis. The validity of oxidative stress following exhaustive cycling exercise on erythrocyte damage was investigated in sedentary and trained subjects before and after antioxidant vitamin treatment (A, C, and E) for 2 mo. Exercise induced a significant increase in thiobarbituric acid-reactive substance and protein carbonyl content levels in sedentary subjects and resulted in an increase of osmotic fragility and decrease in deformability of erythrocytes, accompanied by signs for intravascular hemolysis (increase in plasma hemoglobin concentration and decrease in haptoglobulin levels). Administration of antioxidant vitamins for 2 mo prevented exercise-induced oxidative stress (thiobarbituric acid-reactive substance, protein carbonyl content) and deleterious effects of exhaustive exercise on erythrocytes in sedentary subjects. Trained subjects' erythrocyte responses to exercise were different from those of sedentary subjects before antioxidant vitamin treatment. Osmotic fragility and deformability of erythrocytes, plasma hemoglobin concentration, and haptoglobulin levels were not changed after exercise, although the increased oxidative stress was observed in trained subjects. After antioxidant vitamin treatment, functional and structural parameters of erythrocytes were not altered in the trained group, but exercise-induced oxidative stress was prevented. Increased percentage of young erythrocyte populations was determined in trained subjects by density separation of erythrocytes. These findings suggest that the exercise-induced oxidative stress may contribute to exercise-induced hemolysis in sedentary humans.

scholarly journals l-carnosine (β-alanyl-l-histidine) and carcinine (β-alanylhistamine) act as natural antioxidants with hydroxyl-radical-scavenging and lipid-peroxidase activities

1994 ◽  
Vol 304 (2) ◽  
pp. 509-516 ◽  
Author(s):  
M A Babizhayev ◽  
M C Seguin ◽  
J Gueyne ◽  
R P Evstigneeva ◽  
E A Ageyeva ◽  
...  
Keyword(s):  
Linoleic Acid ◽  
Direct Reduction ◽  
Radical Scavenging ◽  
Thiobarbituric Acid ◽  
Natural Antioxidants ◽  
Peroxyl Radicals ◽  
Lipid Phase ◽  
Oh Radicals ◽  
Thiobarbituric Acid Reactive Substance ◽  
Lipid Hydroperoxides

Carnosine (beta-alanyl-L-histidine) and carcinine (beta-alanylhistamine) are natural imidazole-containing compounds found in the non-protein fraction of mammalian tissues. Carcinine was synthesized by an original procedure and characterized. Both carnosine and carcinine (10-25 mM) are capable of inhibiting the catalysis of linoleic acid and phosphatidylcholine liposomal peroxidation (LPO) by the O2(-.)-dependent iron-ascorbate and lipid-peroxyl-radical-generating linoleic acid 13-monohydroperoxide (LOOH)-activated haemoglobin systems, as measured by thiobarbituric-acid-reactive substance. Carcinine and carnosine are good scavengers of OH. radicals, as detected by iron-dependent radical damage to the sugar deoxyribose. This suggests that carnosine and carcinine are able to scavenge free radicals or donate hydrogen ions. The iodometric, conjugated diene and t.l.c. assessments of lipid hydroperoxides (13-monohydroperoxide linoleic acid and phosphatidylcholine hydroperoxide) showed their efficient reduction and deactivation by carnosine and carcinine (10-25 mM) in the liberated and bound-to-artificial-bilayer states. This suggests that the peroxidase activity exceeded that susceptible to direct reduction with glutathione peroxidase. Imidazole, solutions of beta-alanine, or their mixtures with peptide moieties did not show antioxidant potential. Free L-histidine and especially histamine stimulated iron (II) salt-dependent LPO. Due to the combination of weak metal chelating (abolished by EDTA), OH. and lipid peroxyl radicals scavenging, reducing activities to liberated fatty acid and phospholipid hydroperoxides, carnosine and carcinine appear to be physiological antioxidants able to efficiently protect the lipid phase of biological membranes and aqueous environments.

scholarly journals ANTI-OXIDATIVE, ANTI-INFLAMMATORY AND ANTI-ATHEROSCLEROTIC EFFECT OF TAURINE ON HYPERCHOLESTEROLEMIA INDUCED ATHEROSCLEROTIC RATS

2018 ◽  
Vol 10 (3) ◽  
pp. 145
Author(s):  
Harsha Sharma ◽  
Ankita Joshi ◽  
Harsha Lad ◽  
Deepak Bhatnagar
Keyword(s):  
Dna Damage ◽  
Experimental Atherosclerosis ◽  
Protein Carbonyl ◽  
Atherogenic Diet ◽  
Inflammatory Activity ◽  
Glutathione S Transferase ◽  
Protein Carbonyl Content ◽  
Oral Supplementation ◽  
Normal Rat ◽  
Anti Inflammatory

Objective: The present study evaluates the antioxidant, anti-inflammatory and anti-atherosclerotic potency of taurine (2-amino ethane sulfonic acid) when administered orally to hypercholesterolemia induced atherosclerotic rats.Methods: The experimental atherosclerosis was induced by feeding rats with an atherogenic diet comprising of the normal rat chow supplemented with 4 % cholesterol, 1 % cholic acid and 0.5 % thiouracil (CCT diet) for 20 d. Treatment with atorvastatin (10 mg/kg body weight) and taurine (2 % in drinking water) was given to atherosclerotic rats to study antioxidant enzymes (superoxide dismutase, catalase, glutathione-S-transferase), lipid peroxidation in liver, glutathione reductase and protein carbonyl content, extent of DNA damage using the alkaline comet assay, assaying pro-inflammatory cytokines and quantifying atherosclerotic lesions.Results: Oral supplementation of 2 % taurine to hypercholesterolemic rats modulated antioxidant status and significantly reduced malondialdehyde (MDA) content (P<0.05). The extent of DNA damage was also significantly reduced as observed by a reduction in the comet tail index (P<0.05). Taurine exhibited anti-inflammatory activity by significantly inhibiting TNF-α (tumor necrosis factor) and IL-1α (inter leukine) and also inhibited atherosclerotic lesions by clearing lipid deposits on the intimal surface of the rat aorta.Conclusion: Oral administration of taurine to rats showed antioxidant and anti-inflammatory activity by modulating oxidants in favor of reducing oxidative stress and also showed anti-atherosclerotic activity in hypercholesterolemia-induced atherosclerosis.

scholarly journals Co-Carcinogenicity of Arsenic: Probable Mechanisms

2021 ◽  
Vol 10 (11) ◽  
pp. 294-305
Author(s):  
Archismaan Ghosh Sutapa Mukherjee ◽  
Madhumita Roy
Keyword(s):  
Lipid Peroxidation ◽  
Dna Damage ◽  
Inflammatory Cytokines ◽  
Total Antioxidant Capacity ◽  
Protein Carbonyl ◽  
Ros Generation ◽  
Carbonyl Content ◽  
Protein Carbonyl Content ◽  
Total Antioxidant ◽  
Pro Inflammatory Cytokines

Presence of carcinogens, like Polycyclic Aromatic Hydrocarbons (PAH), in the form of cigarette smoke, vehicular emission and industrial emissions in our immediate surroundings is a potent health hazard. Arsenic, a carcinogenic metalloid, omnipresent in the environment, can act as co-carcinogen, where it enhances the carcinogenicity of other carcinogens. In the present study, the co-carcinogenic effect of Arsenic has been investigated, upon the 7,12-dimethylbenz[a]-anthracene (DMBA), a PAH, induced skin cancer model, in Swiss albino mice. Histological analysis revealed earlier development of invasive carcinoma in the DMBA and arsenic treated group in comparison to the DMBA treated mice alone. To understand this phenomena, ROS generation, DNA damage, lipid peroxidation, protein carbonyl content, total antioxidant capacity and activity of pro-inflammatory cytokines (TNF-α, IL6, IL17a, IL22) and their downstream modulators (NF-κB) was assessed. The results suggested that arsenic in the presence of DMBA induced higher ROS generation, greater DNA damage, elevated lipid peroxidation, increased protein carbonyl content, upregulated activity of pro-inflammatory cytokines and their downstream regulators as well as down regulated the total antioxidant capacity in comparison to DMBA alone. These findings hint at the co-carcinogenic potential of arsenic, as it significantly enhances the carcinogenicity of DMBA and hastens carcinogenesis.

ROLE OF 7-CHLORO-4-(PHENYLSELANYL) QUINOLINE IN THE TREATMENT OF OXALIPLATIN-INDUCED HEPATIC TOXICITY IN MICE

2020 ◽  
Author(s):  
Briana Barros Lemos ◽  
Ketlyn Pereira Motta ◽  
Jaini Janke Paltian ◽  
Angélica S Reis ◽  
Gustavo Bierhals Blodorn ◽  
...  
Keyword(s):  
Therapeutic Strategy ◽  
Histopathological Examination ◽  
Thiobarbituric Acid ◽  
Protein Carbonyl ◽  
Organoselenium Compound ◽  
Protein Carbonyl Content ◽  
Therapeutic Alternatives ◽  
Dehydratase Activity ◽  
Alanine Aminotransferase Activity

There is an increasing incidence of oxaliplatin (OXA)-induced hepatotoxicity. Therefore researchers’ attention has been drawn to therapeutic alternatives that may decrease OXA-induced hepatotoxicity. Studies indicate that oxidative stress plays a major role in OXA-induced liver injury. Since several pharmacological effects of 7-chloro-4-(phenylselanyl) quinole (4-PSQ) involve its antioxidant action, the hypothesis that this organoselenium compound could be promising for the treatment or prevention of hepatotoxicity induced by treatment with OXA was investigated. To test this hypothesis, male Swiss mice received OXA (10 mg/kg), on days 0 and 2, followed by the oral administration of 4-PSQ (1 mg/kg), on days 2 to 14. 4-PSQ reduced the plasma aspartate and alanine aminotransferase activity increased by exposure to OXA. The histopathological examination of the liver showed that 4-PSQ markedly improved OXA-induced hepatic injury. In addition, treatment with 4-PSQ reduced the oxidation of lipids and proteins (thiobarbituric acid reactive species levels and protein carbonyl content) and attenuated the increase of hepatic catalase and glutathione peroxidase activity caused by OXA. The inhibition of hepatic δ-aminolevulinic dehydratase activity induced by OXA was reverted by 4-PSQ. In conclusion, results indicate that 4-PSQ may be a good therapeutic strategy for attenuating OXA-induced liver damage.

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