Redox status and lipid peroxidation in alcoholic hypertensive patients and alcoholic hypertensive patients with diabetes

Ramanathan, Veerappan; Selvaraj, Senthil; Rao, M. Ramakrishna; Ramesh, R.; Pugalendi, Kodukkur Viswanathan

doi:10.1016/j.cccn.2003.11.004

Cited by 30 publications

(14 citation statements)

References 26 publications

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“…Enhanced H 2 O 2 excretion [27,37] and lower GPx activity [31,36] has been reported in adult SHR when compared with normotensive WKY rats. Reduced GPx activity [7,30] and enhanced H 2 O 2 levels [13] have also been reported in patients with hypertension. Interestingly, normotensive volunteers with a family history of hypertension have been found to have higher plasma H 2 O 2 levels than those in normotensives without a family history of hypertension [14].…”

Section: Discussionmentioning

confidence: 90%

Glutathione system in young spontaneously hypertensive rats

et al. 2010

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Glutathione (GSH) forms a part of the antioxidant system that plays a vital role in preventing oxidative stress, and an imbalance in the oxidant/antioxidant system has been linked to the pathogenesis of hypertension. The aim of this study was to investigate the status of the GSH system in the kidney of spontaneously hypertensive rats (SHR). Components of the GSH system, including glutathione peroxidase (GPx), glutathione reductase (GR), glutathione-S-transferase (GST), and total GSH content, were measured in the kidneys of 4, 6, 8, 12, and 16 weeks old SHR and Wistar-Kyoto (WKY) rats. Systolic blood pressure of SHR was significantly higher from the age of 6 weeks onwards compared with age-matched WKY rats. GPx activity in the SHR was significantly lower from the age of 8 weeks onwards when compared to that in age-matched WKY rats. No significant differences were evident in the GPx-1 protein abundance, and its relative mRNA levels, GR, GST activity, and total GSH content between SHR and age-matched WKY rats. The lower GPx activity suggests of an impairment of the GSH system in the SHR, which might be due to an abnormality in its protein rather than non-availability of a cofactor. Its role in the development of hypertension in SHR however remains unclear.

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Section: Discussionmentioning

confidence: 90%

Glutathione system in young spontaneously hypertensive rats

et al. 2010

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“…The present study mainly showing the ameliorating effect of cranberry' polyphenols on Diclofenac induced renal toxicity in studied groups. The decreased concentration of lipid hydroperoxides and thiobarbituric acid reactive substances ensure the ameliorating effect of cranberry polyphenols antioxidant [46]. Diclofenac sodium increases functional abnormalities and cellular damage in renal tissue by the process of lipid peroxidation [12] [38].…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Cranberry Extracts against Oxidative Stress and DNA Damage Induced by Diclofenac Sodium in Kidney of Male Albino Rate

Hassan¹,

Sabry²,

Hussein³

2017

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This work aimed to find the effect of cranberry extract (75 and 150 mg/kg•b•w) and vit. C (1 g/kg•b•w orally) on renal toxicity induced by Diclofenac sodium in male albino rats. Treated rats with diclofenac sodium with a concentration 150 mg/kg•b•w, expressed a significant increase in several parameters includes, plasma total cholesterol, LDL-cholesterol, and triglyceride as well as renal nitric oxide (NO), tumor necrosis factor-alfa (TNF-α) and TBARS. In addition, a significant reduction in renal superoxide dismutase (SOD), GSH, catalase (CAT) and plasma HDL. The present results explain that, using cranberry extract and vit. C resulted in increasing the level of GSH, CAT and SOD as well as gene expression of renal SOD, CAT and IL-22 and reduce the level of TBARs significantly which led to preventing renal tissue damage. Our results also revealed that cranberry extract can protect DNA from damage as obtained from comet essay. TM-U was elevated in DCLF treated group when compared with normal. However cranberry extract was able to reduce this elevation in dose dependant manner. Histological features in H&E taken to different groups also mirrors this findings. DCLF causes many changes in renal tissue include infiltration by inflammatory cells, attenuated glomeruli, apoptosis in tubular epithelia. Keywords

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“…Normally, the cell is protected by virtue of an intricate antioxidative system, consisting of enzymic and nonenzymic systems, to maintain redox status homeostasis. Enzymic superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) and nonenzymic vitamins C and E and reduced glutathione (GSH) play an important role during the process of scavenging ROS or preventing their formation (Kabuto et al 2003;Veerappan et al 2004).…”

Section: Introductionmentioning

confidence: 99%

“…The enzymic antioxidants SOD, CAT, GPx, and GST play a vital role during the process of scavenging ROS or preventing their formation (Kabuto et al 2003;Veerappan et al 2004). However, when the excessive ROS impairs antioxidant defense or exceeds the scavenging ability of the antioxidant defense system, oxidative stress and injury may be unavoidable.…”

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confidence: 99%

Beneficial Effect of Caffeic Acid on Alcohol-Induced Alterations in Lipid Peroxidation and Antioxidant Defense in Rats

Karthikesan

Pari

2007

Toxicology Mechanisms and Methods

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We studied the effect of caffeic acid on alcohol-induced oxidative stress in alcohol-induced toxicity in rats. The elevation in the levels of lipid peroxidation in alcohol administration was accompanied by a significant decrease in the levels of vitamins C and E, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH), and glutathione S-transferase (GST) in the liver and kidney. Oral administration of caffeic acid at a dose of 12 mg/kg/body weight for 45 days significantly reduced the severe oxidative stress in alcohol toxicity as evidenced by the decrease in the levels of lipid peroxidation with a simultaneous increase in the level of enzymic and nonenzymic antioxidants in liver and kidney. Histological studies in the liver and kidney also showed that administration of caffeic acid to alcohol-treated rats resulted in a marked reduction in alcohol-induced pathological changes. These results suggest that administration of caffeic acid to alcohol-supplemented rats alleviates the alcohol-induced oxidative damage in the liver and kidney.

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Redox status and lipid peroxidation in alcoholic hypertensive patients and alcoholic hypertensive patients with diabetes

Cited by 30 publications

References 26 publications

Glutathione system in young spontaneously hypertensive rats

Glutathione system in young spontaneously hypertensive rats

Protective Effect of Cranberry Extracts against Oxidative Stress and DNA Damage Induced by Diclofenac Sodium in Kidney of Male Albino Rate

Beneficial Effect of Caffeic Acid on Alcohol-Induced Alterations in Lipid Peroxidation and Antioxidant Defense in Rats

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