Melatonin protects against cadmium-induced oxidative damage in different tissues of rat: a mechanistic insight

2019 ◽  
Vol 2 (2) ◽  
pp. 1-21 ◽  
Author(s):  
Elina Mitra ◽  
Bharati Bhattacharjee ◽  
Palash Kumar Pal ◽  
Arnab Kumar Ghosh ◽  
Sanatan Mishra ◽  
...  
Keyword(s):  
Cytochrome C ◽  
Oxidative Damage ◽  
Protein Carbonyl ◽  
Environmental Pollutant ◽  
Glutathione S Transferase ◽  
Protein Carbonyl Content ◽  
Wide Range ◽  
Liver And Kidney ◽  
Nadh Cytochrome ◽  
Cd Exposure

Cadmium (Cd) is a notorious environmental pollutant known for its wide range of toxicities to organisms. Thus, the present study is designed to examine whether melatonin, a potent antioxidant, protects against Cd-induced oxidative damage in the heart, liver and kidney of rats. Cd treatment at a dose of 0.44 mg/kg for 15 days caused severe damage in all these organs. These included significantly increased activities of SGPT, SGOT, lactate dehydrogenase- 1 and 5 and ALP and levels of total lactate, creatinine, lipid peroxidation, protein carbonyl content and reduced glutathione while the activities of superoxide dismutases, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase along with mitochondrial pyruvate dehydrogenase, isocitrate dehydrogenase, α-keto glutarate dehydrogenase, succinate dehydrogenase, NADH-cytochrome-c-oxidoreductase and cytochrome-c-oxidase were significantly reduced by Cd. However, if melatonin was given orally 30 min before Cd injection, all these alterations induced by Cd were significantly preserved by melatonin. Histological observations also demonstrated that Cd exposure caused cellular lesions, promoting necrotic or apoptotic changes. Notably, all these changes were significantly protected by melatonin. The results suggest that melatonin is a beneficial molecule to ameliorate Cd-induced oxidative damage in the heart, liver and kidney tissues of rats with its powerful antioxidant capacity, heavy metal chelating activity and competition of binding sites with Cd to the GSH and catalase.

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.

Modulation of oxidative damage by lipopolysaccharides and antioxidant responses in the freshwater crab Sinopotamon henanense Bott 1967 (Decapoda: Brachyura: Potamonidae) during cadmium exposure

2019 ◽  
Vol 39 (4) ◽  
pp. 477-484
Author(s):  
Yanying Zhou ◽  
Zhengming Luo ◽  
Lan Wang
Keyword(s):  
Oxidative Damage ◽  
Protein Carbonyl ◽  
Freshwater Crab ◽  
Antioxidant Responses ◽  
Carbonyl Derivatives ◽  
Total Antioxidant ◽  
Toxic Pollutant ◽  
Sinopotamon Henanense ◽  
Protein Crosslinks ◽  
Cd Exposure

Abstract Cadmium (Cd) is a toxic pollutant that exerts adverse effects on organisms. We examined oxidative damage and antioxidative parameters in hemocytes of the freshwater crab Sinopotamon henanense Bott 1967 exposed to sublethal levels of Cd for 21 d. We also examined the immunomodulation of lipopolysaccharides (LPS) on oxidation caused by Cd in the crab. Cd induced higher reactive oxygen species (ROS) levels but ROS production in crab hemocytes was down-regulated after LPS injection. The contents of malondialdehyde (MDA) and protein carbonyl derivatives (PCO), DNA-protein crosslinks (DPCs) coefficient in the hemocytes of crabs exposed to Cd increased. LPS injection could decrease these oxidative parameters. The total antioxidant capacity (T-AOC) was significantly inhibited by Cd and LPS enhanced the activity of T-AOC in crab hemocytes. Cd treatment also up-regulated activities of antioxidant enzymes, including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). Only CAT activity decreased when crabs were exposed to Cd followed by LPS stimulation. Peroxidase (POD) activities showed little change after Cd or LPS treatments. The oxidative damage caused by Cd exposure may be reduced by LPS, suggesting its possible use in aquaculture as an immunostimulant for crustaceans.

Effects of diallyl tetrasulfide on cadmium-induced oxidative damage in the liver of rats

2007 ◽  
Vol 26 (6) ◽  
pp. 527-534 ◽  
Author(s):  
P. Murugavel ◽  
L. Pari
Keyword(s):  
Lipid Peroxidation ◽  
Body Weight ◽  
Oxidative Damage ◽  
Antioxidant Defense ◽  
Protective Efficacy ◽  
Thiobarbituric Acid ◽  
Protein Carbonyl ◽  
Vital Role ◽  
Glutathione S Transferase ◽  
Glucose 6 Phosphate Dehydrogenase

The protective efficacy of diallyl tetrasulfide (DTS) from garlic on liver injury induced by cadmium (Cd) was investigated. In this study, Cd (3 mg/kg body weight) was administered subcutaneously for 3 weeks to induce toxicity. DTS was administered orally (10, 20 and 40 mg/kg body weight) for 3 weeks with subcutaneous (sc) injection of Cd. Cd-induced liver damage was evidenced from increased activities of serum hepatic enzymes, namely aspartate transaminase, alanine transaminase, alkaline phosphatase and lactate dehydrogenase, with significant elevation of lipid peroxidation indices (thiobarbituric acid reactive substances and hydroperoxides) and protein carbonyl groups in the liver. Rats subjected to Cd toxicity also showed a decline in the levels of total thiols, reduced glutathione (GSH), vitamin C and vitamin E, accompanied by an increased accumulation of Cd, and significantly decreased activities of superoxide dismutase, catalase (CAT), glutathione peroxidase, glutathione-S-transferase (GST), glutathione reductase, and glucose-6-phosphate dehydrogenase in the liver. Administration of DTS at 40 mg/kg body weight significantly normalised the activities of hepatic marker enzymes, compared to other doses of DTS (10 and 20 mg/kg body weight). In addition, DTS (40 mg/kg body weight) significantly reduced the accumulation of Cd and the level of lipid peroxidation, and restored the level of antioxidant defense in the liver. Histological studies also showed that administration of DTS to Cd-treated rats resulted in a marked improvement of hepatocytes morphology with mild portal inflammation. Our results suggest that DTS might play a vital role in protecting Cd-induced oxidative damage in the liver. Human & Experimental Toxicology(2007) 26, 527—534

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 Dietary quercetin abrogates hepatorenal oxidative damage associated with dichloromethane exposure in rats

2019 ◽  
Author(s):  
Solomon E Owumi ◽  
Olabisi F Danso ◽  
Magdalene E Effiong
Keyword(s):  
Oxidative Damage ◽  
Protective Role ◽  
Gamma Glutamyl Transferase ◽  
Glutathione S Transferase ◽  
Histological Changes ◽  
Chlorinated Solvent ◽  
Household Products ◽  
Liver And Kidney ◽  
Glutamyl Transferase

Exposure to dichloromethane (DCM), a commonly used chlorinated solvent in industrial settings and for the production of many household products, reportedly elicits detrimental effects in animals and humans. The present study investigated the protective role of dietary quercetin on DCM-induced hepatorenal damage in rats. Experimental rats were orally administered with DCM (150 mg/kg) and 30 min later with quercetin at 10, 20 and 40 mg/kg or none for 7 consecutive days. The results indicated that DCM-mediated significant (p<0.05) increases in serum alanine aminotransferase, aspartate aminotransferase, gamma glutamyl transferase and alkaline phosphatase activities as well as urea and creatinine levels were dose-dependently normalized to the control values in rats co-treated with quercetin. Further, quercetin co-treatment ameliorated DCM-mediated decrease in the hepatic and renal activities of superoxide dismutase, catalase, glutathione peroxidase and glutathione S-transferase as well as glutathione level in the treated rats. Moreover, quercetin co-treatment markedly reduced lipid peroxidation level and protected against histological changes in liver and kidney of the treated rats. Taken together, quercetin abrogated hepatorenal oxidative damage in DCM-treated rats via improvement of antioxidant status and suppression of oxidative damage.

Mitochondria-Mediated Apoptosis Induced Testicular Dysfunction in Diabetic Rats: Ameliorative Effect of Resveratrol

Endocrinology ◽  
2021 ◽  
Vol 162 (4) ◽  
Author(s):  
Hamdy A A Aly
Keyword(s):  
Cytochrome C ◽  
Sperm Count ◽  
Protein Carbonyl ◽  
Diabetic Rats ◽  
Serum Testosterone Level ◽  
H2o2 Production ◽  
Testicular Damage ◽  
Protein Carbonyl Content ◽  
Testicular Dysfunction ◽  
Ameliorative Effect

Abstract The molecular mechanism underlying diabetes-induced testicular damage has not been thoroughly elucidated. The present study was conducted to elucidate the role of mitochondria-mediated apoptosis in diabetes-induced testicular dysfunction in rats and to explore the ameliorative effect of resveratrol. Diabetes suppressed sperm count, motility, and viability and increased sperm abnormalities. It decreased serum testosterone level and testicular mitochondrial membrane potential. The level of Bax and caspase-3 and -9 activities were increased in the testicular cytosol, while the level of Bcl-2 was decreased. Diabetes increased the Bax/Bcl-2 ratio. The cytochrome C level was decreased in the mitochondrial fraction, while its level was increased in the cytosol, a result that was supported by the immunohistochemistry of cytochrome C. Diabetes resulted in deleterious alterations in the architecture of testicular tissue, suppressed antioxidant enzymes, and increased H2O2 production, protein carbonyl content, and lipid peroxidation. However, administration of resveratrol at a dose of 50 mg kg/day for 4 successive weeks post diabetic induction, successfully ameliorated the testicular dysfunction. In conclusion, these findings strongly reveal that diabetes induces testicular damage, at least in part, by inducing mitochondrial-mediated apoptosis and oxidative stress. Administration of resveratrol to diabetic rats improves the diabetes-induced testicular damage. These impacts could be mediated through resveratrol antioxidant and anti-apoptotic effects.

scholarly journals The Effect ofBabesia divergensInfection on the Spleen of Mongolian Gerbils

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Mohamed A. Dkhil ◽  
Saleh Al-Quraishy ◽  
Mohamed S. Al-Khalifa
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Protein Carbonyl ◽  
Splenic Tissue ◽  
Cellular Damage ◽  
Mongolian Gerbils ◽  
Protein Carbonyl Content ◽  
Wide Range ◽  
Cell Cycle Alteration ◽  
Nitrite Nitrate

Babesiosis is caused by intraerythrocytic protozoan parasites transmitted by ticks and affects a wide range of domestic and wild animals and occasionally humans. The current study aimed to investigate the effect ofB. divergensinfected erythrocytes on spleen histopathology, cell cycle alteration, and the presence of oxidative stress. Mongolian gerbils were challenged with 5 × 106  Babesia divergensinfected erythrocytes. Parasitemia reached approximately 77% at day 5 postinfection. Infection also induced injury of the spleen. This was evidenced with (i) increases in cellular damage of the spleen, (ii) decrease in antioxidant capacity as indicated by decreased glutathione, catalase, and superoxide dismutase levels, (iii) increased production of malondialdehyde and nitric oxide derived products (nitrite/nitrate), and (iv) increased lactic acid dehydrogenase activity and protein carbonyl content in the spleen. Infection interfered with normal cell cycle of the spleen cells at G0/G1, S, and G2/M phases. On the basis of the above results it can be hypothesized thatB. divergensinfected erythrocytes could alter the spleen histopathology and cause cell cycle alteration and induce oxidative stress in splenic tissue.

scholarly journals Does Ischemia with Reperfusion Lead to Oxidative Damage to Proteins in the Brain?

1993 ◽  
Vol 13 (1) ◽  
pp. 145-152 ◽  
Author(s):  
Jaroslava Folbergrová ◽  
Yoshihiro Kiyota ◽  
Kerstin Pahlmark ◽  
Hajime Memezawa ◽  
Maj-Lis Smith ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Soluble Protein ◽  
Protein Fraction ◽  
Contralateral Side ◽  
Protein Carbonyl ◽  
Carbonyl Content ◽  
Soluble Protein Fraction ◽  
Protein Carbonyl Content ◽  
Oxidative Damage To Proteins ◽  
H Protein

Recent results suggest that even relatively brief periods of ischemia in gerbils (10 min) lead to oxidative damage to brain proteins, reflected in an increased carbonyl content in the soluble protein fraction and a decreased glutamine synthetase (GS) activity. Since we failed to reproduce these findings in rats subjected to 15 min of transient ischemia, we explored whether oxidative damage to proteins could be observed after longer ischemic periods. To that end, one middle cerebral artery was occluded in rats for either 1 or 3 h, with recirculation periods of 0 min, 15 min, 1 h, and 6 h. Protein carbonyl content and GS activity were determined in focal and perifocal tissues and compared with values obtained in the same areas on the contralateral side. Ischemia, particularly of 3-h duration, followed by various reperfusion periods was accompanied by a significant (16–35%) decrease in the concentration of proteins of the soluble protein fraction. However, in no group was there an increased carbonyl content of the remaining proteins in this fraction. When expressed per milligram of protein, GS activity remained unchanged or rose somewhat. An inconsistent (and moderate) decrease in GS activity was present only if GS activity was expressed per milligram of wet tissue. The present findings, which fail to document oxidative damage to proteins following focal ischemia of 1- or 3-h duration, are thus radically different from those obtained in gerbils. The results suggest that appreciable species differences exist and raise the question of whether free radical–mediated oxidation of proteins is an invariable component of ischemic brain damage.

scholarly journals Grx5 Glutaredoxin Plays a Central Role in Protection against Protein Oxidative Damage inSaccharomyces cerevisiae

1999 ◽  
Vol 19 (12) ◽  
pp. 8180-8190 ◽  
Author(s):  
Maria Teresa Rodríguez-Manzaneque ◽  
Joaquim Ros ◽  
Elisa Cabiscol ◽  
Albert Sorribas ◽  
Enrique Herrero
Keyword(s):  
Oxidative Damage ◽  
Active Site ◽  
Synthetic Lethality ◽  
Growth Conditions ◽  
Protein Carbonyl ◽  
Cysteine Residue ◽  
Yeast Cells ◽  
Protein Carbonyl Content ◽  
Highly Sensitive ◽  
Specific Proteins

ABSTRACT Glutaredoxins are members of a superfamily of thiol disulfide oxidoreductases involved in maintaining the redox state of target proteins. In Saccharomyces cerevisiae, two glutaredoxins (Grx1 and Grx2) containing a cysteine pair at the active site had been characterized as protecting yeast cells against oxidative damage. In this work, another subfamily of yeast glutaredoxins (Grx3, Grx4, and Grx5) that differs from the first in containing a single cysteine residue at the putative active site is described. This trait is also characteristic for a number of glutaredoxins from bacteria to humans, with which the Grx3/4/5 group has extensive homology over two regions. Mutants lacking Grx5 are partially deficient in growth in rich and minimal media and also highly sensitive to oxidative damage caused by menadione and hydrogen peroxide. A significant increase in total protein carbonyl content is constitutively observed in grx5cells, and a number of specific proteins, including transketolase, appear to be highly oxidized in this mutant. The synthetic lethality of the grx5 and grx2 mutations on one hand and ofgrx5 with the grx3 grx4 combination on the other points to a complex functional relationship among yeast glutaredoxins, with Grx5 playing a specially important role in protection against oxidative stress both during ordinary growth conditions and after externally induced damage. Grx5-deficient mutants are also sensitive to osmotic stress, which indicates a relationship between the two types of stress in yeast cells.

Lycopene attenuates dichlorvos-induced oxidative damage and hepatotoxicity in rats

2015 ◽  
Vol 35 (6) ◽  
pp. 654-665 ◽  
Author(s):  
AM Abu El-Saad ◽  
MM Ibrahim ◽  
AA Hazani ◽  
GA El-Gaaly
Keyword(s):  
Protective Efficacy ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Protein Carbonyl ◽  
Lipoprotein Cholesterol ◽  
Glutathione S Transferase ◽  
Protein Carbonyl Content ◽  
The Status ◽  
Treatment Administration ◽  
Serum Transaminases

Because of the widespread use of dichlorvos (DDVP) for domestic applications, evaluation of their toxic effects is of major concern to public health. Lycopene may lower oxidative stress by a mechanism that is not fully elucidated. The present study was undertaken to evaluate the protective efficacy of lycopene in terms of normalization of altered biochemical parameters following DDVP treatment in rats. Animals were divided into four groups. The first group was used as control, while groups 2, 3, and 4 were orally treated with lycopene (10 mg kg−1 body weight (b.w.)), DDVP (1.6 mg kg−1 b.w.), and DDVP plus lycopene, respectively. Results showed that oral administration of DDVP for 30 days increased the levels of lipid peroxidation markers such as malondialdehyde, 4-hydroxynonanal, and protein carbonyl content in liver. Also, a decrease in levels of vitamin C, vitamin E, and reduced glutathione was detected due to DDVP administration. These were accompanied by a decrease in the activities of antioxidant enzymes superoxide dismutase, catalase, glutathione peroxidase, and glutathione- S-transferase in the liver tissue. Moreover, DDVP increased the activities of serum transaminases, alkaline phosphatase, lactate dehydrogenase, and lipoxygenase, and the levels of bilirubin, total cholesterol, low-density lipoprotein cholesterol, triglyceride and DNA–protein crosslinks, and 8-hydroxy-2-deoxyguanosine, while decreased the level of high-density lipoprotein cholesterol. Our results provide new insights into the biochemical studies of relation between DDVP hepatotoxicity and lycopene treatment. Administration of lycopene to DDVP-treated rats reverted the status of hepatic markers to near-normal levels. These data suggest that lycopene can protect against the liver damage induced by DDVP.

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