Effect of sulphated polysaccharides on erythrocyte changes due to oxidative                 and nitrosative stress in experimental hyperoxaluria

Kidney stones are known to haunt humanity for centuries and increase in oxalate is a predominant risk factor for stone formation. The present study was initiated with a notion to study the oxidative and nitrosative stress on erythrocytes under oxalate stress and the putative role of sulphated polysaccharides. Hyperoxaluria was induced in two groups by the administration of 0.75% ethylene glycol in drinking water for 28 days and one of them was treated with sulphated polysaccharides from Fucus vesiculosus from the 8th day to the end of the experimental period of 28 days at a dose of 5 mg/kg body weight subcutaneously. Control and drug control (sulphated polysaccharides alone) were also included in the study. Glycolic and glyoxylic acid levels of urine were analyzed as an index of hyperoxaluria. The plasma enzymic markers of cellular integrity, redox status of red blood cells, osmotic fragility, and 14C-oxalate binding were investigated. Urine and plasma nitric oxide metabolites, expression of inducible nitric oxide synthase protein, and mRNA were assessed in kidney to evaluate the nitrosative stress. Increased levels of glycolic and glyoxylic acid in urine indicated the prevalence of hyperoxaluria in ethylene glycol–administered groups. Plasma aspartate and alanine transaminase were not altered, but alkaline phosphatase and lactate dehydrogenase of hyperoxaluric group were increased indicating tissue damage. Activities of antioxidant enzymes were decreased, whereas erythrocyte membrane lipid peroxidation was increased in hyperoxaluric rats. Moreover, an altered fragility with an increase in oxalate binding activity was observed in hyperoxaluric group. Increase in nitric oxide metabolites levels in urine and plasma along with an increase in expression of inducible nitric oxide synthase protein and mRNA in kidney were observed in hyperoxaluric rats. Administration of sulphated polysaccharides to hyperoxaluric rats averted the abnormal increase in urinary glycolic and glyoxylic acid levels and enzyme activities, decreased lipid peroxidation, and increased the activities of antioxidant enzymes. Furthermore, increased nitrosative stress accompanying hyperoxaluria was also normalized on sulphated polysaccharides treatment. To conclude, sulphated polysaccharide administration was able to maintain the integrity of erythrocyte membrane and decrease the damage to erythrocytes in hyperoxaluria.

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Renoprotective and antihypertensive effects of S-allylcysteine in 5/6 nephrectomized rats

AJP Renal Physiology ◽

10.1152/ajprenal.00235.2007 ◽

2007 ◽

Vol 293 (5) ◽

pp. F1691-F1698 ◽

Cited By ~ 37

Author(s):

Cristino Cruz ◽

Ricardo Correa-Rotter ◽

Dolores Javier Sánchez-González ◽

Rogelio Hernández-Pando ◽

Perla D. Maldonado ◽

...

Keyword(s):

Nitric Oxide ◽

Blood Pressure ◽

Inducible Nitric Oxide Synthase ◽

Renal Damage ◽

Nitrosative Stress ◽

Antioxidant Properties ◽

Oxidative And Nitrosative Stress ◽

Nitric Oxide Synthase 3 ◽

Oxide Synthase ◽

Inducible Nitric Oxide

Progressive renal damage and hypertension are associated with oxidative and nitrosative stress. On the other hand, S-allylcysteine (SAC), the most abundant organosulfur compound in aged garlic extract (AG), has antioxidant properties. The effects of SAC and AG on blood pressure, renal damage, and oxidative and nitrosative stress were studied in five-sixths nephrectomized rats treated with SAC (200 mg/kg ip) and AG (1.2 ml/kg ip) every other day for 30 days. Proteinuria and serum creatinine and blood urea nitrogen concentrations were measured on days 0, 5, 10, 15, and 30, and systolic blood pressure was recorded on days 0, 15, and 30. The degree of glomerulosclerosis and tubulointerstitial damage, the immunostaining for inducible nitric oxide synthase, 3-nitrotyrosine, poly(ADP-ribose), and the subunits of NADPH oxidase p22phox and gp91phox, and the activity of SOD were determined on day 30. SAC and AG reduced hypertension, renal damage, and the abundance of inducible nitric oxide synthase, 3-nitrotyrosine, poly(ADP-ribose), p22phox, and gp91phox and increased SOD activity. Our data suggest that the antihypertensive and renoprotective effects of SAC and AG are associated with their antioxidant properties and that they may be used to ameliorate hypertension and delay the progression of renal damage.

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Oxidative and nitrosative stress in acute renal ischemia

AJP Renal Physiology ◽

10.1152/ajprenal.0071.2001 ◽

2001 ◽

Vol 281 (5) ◽

pp. F948-F957 ◽

Cited By ~ 203

Author(s):

Eisei Noiri ◽

Akihide Nakao ◽

Koji Uchida ◽

Hirokazu Tsukahara ◽

Minoru Ohno ◽

...

Keyword(s):

Nitric Oxide ◽

Lipid Peroxidation ◽

Dna Damage ◽

Oxidative Dna Damage ◽

Nitrosative Stress ◽

Oxidative And Nitrosative Stress ◽

Reperfusion Period ◽

Series Of Experiments ◽

Acute Renal Ischemia ◽

Oxide Synthase

First Published July 12, 2001; 10.1152/ajprenal.0071.2001.—Generation of reactive oxygen species and nitric oxide in hypoxia-reperfusion injury may form a cytotoxic metabolite, peroxynitrite, which is capable of causing lipid peroxidation and DNA damage. This study was designed to examine the contribution of oxidative and nitrosative stress to the renal damage in ischemic acute renal failure (iARF). iARF was initiated in rats by 45-min renal artery clamping. This resulted in lipid peroxidation, DNA damage, and nitrotyrosine modification confirmed both by Western and immunohistochemical analyses. Three groups of animals were randomly treated with an inhibitor of inducible nitric oxide synthase (NOS),l- N 6-(1-iminoethyl)lysine (l-Nil), cell-permeable lecithinized superoxide dismutase (SOD), or both. Each treatment resulted in amelioration of renal dysfunction, as well as reduced nitrotyrosine formation, lipid peroxidation, and DNA damage, thus suggesting that peroxynitrite rather than superoxide anion is responsible for lipid peroxidation and DNA damage. Therefore, in a separate series of experiments, a scavenger of peroxynitrite, ebselen, was administered before the reperfusion period. This treatment resulted in a comparable degree of amelioration of iARF. In conclusion, the present study provides the first attempt to elucidate the role of peroxynitrite in initiation of the cascade of lipid peroxidation and DNA damage to ischemic kidneys. The results demonstrate that l-Nil , lecithinized SOD, and ebselen treatments improve renal function due to their suppression of peroxynitrite production or its scavenging, consequently preventing lipid peroxidation and oxidative DNA damage.

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D(+) galactosamine induced oxidative and nitrosative stress-mediated renal damage in rats via NF-κB and inducible nitric oxide synthase (iNOS) pathways is ameliorated by a polyphenol xanthone, mangiferin

Free Radical Research ◽

10.3109/10715762.2011.644240 ◽

2012 ◽

Vol 46 (2) ◽

pp. 116-132 ◽

Cited By ~ 35

Author(s):

Manoranjan Ghosh ◽

Joydeep Das ◽

Parames C. Sil

Keyword(s):

Nitric Oxide ◽

Nitric Oxide Synthase ◽

Inducible Nitric Oxide Synthase ◽

Renal Damage ◽

Nitrosative Stress ◽

Oxidative And Nitrosative Stress ◽

Oxide Synthase ◽

Inducible Nitric Oxide

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Adiponectin reduces carotid atherosclerotic plaque formation in ApoE−/− mice: Roles of oxidative and nitrosative stress and inducible nitric oxide synthase

Molecular Medicine Reports ◽

10.3892/mmr.2014.2947 ◽

2014 ◽

Vol 11 (3) ◽

pp. 1715-1721 ◽

Cited By ~ 16

Author(s):

XIAOJUN CAI ◽

XUAN LI ◽

LI LI ◽

XIAO-ZHEN HUANG ◽

YU-SHENG LIU ◽

...

Keyword(s):

Nitric Oxide ◽

Inducible Nitric Oxide Synthase ◽

Atherosclerotic Plaque ◽

Nitrosative Stress ◽

Plaque Formation ◽

Carotid Atherosclerotic Plaque ◽

Oxidative And Nitrosative Stress ◽

Atherosclerotic Plaque Formation ◽

Oxide Synthase ◽

Inducible Nitric Oxide

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Mechanisms of Thymoquinone Hepatorenal Protection in Methotrexate-Induced Toxicity in Rats

Mediators of Inflammation ◽

10.1155/2015/859383 ◽

2015 ◽

Vol 2015 ◽

pp. 1-12 ◽

Cited By ~ 45

Author(s):

Azza A. K. El-Sheikh ◽

Mohamed A. Morsy ◽

Ahlam M. Abdalla ◽

Azza H. Hamouda ◽

Ibrahim A. Alhaider

Keyword(s):

Nitric Oxide ◽

Nitrosative Stress ◽

Oxidative And Nitrosative Stress ◽

Liver Functions ◽

Apoptotic Effect ◽

Liver And Kidney ◽

Hepatic Histology ◽

Oxide Synthase ◽

Necrosis Factor ◽

Inducible Nitric Oxide

To investigate mechanisms by which thymoquinone (TQ) can prevent methotrexate- (MTX-) induced hepatorenal toxicity, TQ (10 mg/kg) was administered orally for 10 days. In independent rat groups, MTX hepatorenal toxicity was induced via 20 mg/kg i.p. at the end of day 3 of experiment, with or without TQ. MTX caused deterioration in kidney and liver function, namely, blood urea nitrogen, creatinine, alanine aminotransferase, and aspartate aminotransferase. MTX also caused distortion in renal and hepatic histology, with significant oxidative stress, manifested by decrease in reduced glutathione and catalase, as well as increase in malondialdehyde levels. In addition, MTX caused nitrosative stress manifested by increased nitric oxide, with upregulation of inducible nitric oxide synthase. Furthermore, MTX caused hepatorenal inflammatory effects as shown by increased tumor necrosis factor-α, besides upregulation of necrosis factor-κB and cyclooxygenase-2 expressions. MTX also caused apoptotic effect, as it upregulated caspase 3 in liver and kidney. Using TQ concurrently with MTX restored kidney and liver functions, as well as their normal histology. TQ also reversed oxidative and nitrosative stress, as well as inflammatory and apoptotic signs caused by MTX alone. Thus, TQ may be beneficial adjuvant that confers hepatorenal protection to MTX toxicity via antioxidant, antinitrosative, anti-inflammatory, and antiapoptotic mechanisms.

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Application of L-arginine and aminoguanidine for correction of liver at acute experimental pеritonitis

Medical and Clinical Chemistry ◽

10.11603/mcch.2410-681x.2015.v17.i3.5059 ◽

2015 ◽

Vol 17 (3) ◽

Author(s):

V. V. Chernyashova

Keyword(s):

Nitric Oxide ◽

Lipid Peroxidation ◽

Antioxidant Enzymes ◽

Selective Inhibitor ◽

Mature Male ◽

Male Rats ◽

Acute Peritonitis ◽

Similar Scheme ◽

Oxide Synthase ◽

Inducible Nitric Oxide

The precursor of the synthesis of nitric oxide – L-arginine at acute peritonitis (intrabdominally administration nonlinear mature male rats, 25 mg/kg, 30 minutes before and 12, 24 and 36 h after modeling pathology) promoted of increasing of nitrite anion content to inhibition of lipid peroxidation background processes, activating the mitochondrial and antioxidant enzymes in the liver, reducing indices of endogenous intoxication. Application of experimental peritonitis selective inhibitor of inducible nitric oxide synthase – aminoguanidine (intrabdominally, 10 mg/kg, the introduction of a similar scheme) accompanied the progression of liver disease on the background of inhibition of the synthesis of nitric oxide.

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