Protective Effects of Vitamin C, Alone or in Combination with Vitamin A, on Endotoxin-Induced Oxidative Renal Tissue Damage in Rats

Kanter, Mehmet; Çoşkun, Ömer; Armutçu, Ferah; Uz, Yeşim Hülya; Kizilay, Gulnur

doi:10.1620/tjem.206.155

Cited by 37 publications

(30 citation statements)

References 24 publications

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“…Finally, it should be mentioned that several animal and clinical studies suggest that antioxidant administration might be an attractive approach to attenuate extensive oxidative attack within vital organs (Sisto et al 1995;Metin et al 2002;Liu et al 2004;Kanter et al 2005).…”

Section: Discussionmentioning

confidence: 99%

Persistent Oxidative Stress after Myocardial Infarction Treated by Percutaneous Coronary Intervention

Nikolić-Heitzler

Rabuzin

Tatzber

et al. 2006

Tohoku J. Exp. Med.

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[247][248][249][250][251][252][253][254][255] Acute myocardial infarction causing cardiac ischemia is responsible for the majority of cardiac related deaths. Medical interventions that ensure rapid reperfusion, such as percutaneous coronary intervention, are aimed to allow myocardial re-oxygenation. However, this generates reactive oxygen species, resembling ischemiareperfusion type of injury based on oxidative stress. In the present study we monitored dynamic changes of total serum peroxides, total antioxidant capacity and soluble intercellular adhesion molecule-1 as well as the titer of antibodies against oxidized low-density lipoproteins in the blood during the convalescence period of 32 patients with acute myocardial infarction treated by percutaneous coronary intervention. Samples were taken at admittance and at two hours, four hours, three days and seven days following percutaneous coronary intervention. Total antioxidant capacity dropped to 82% ( p < 0.05). The titer of antibodies against oxidized low-density lipoproteins transiently decreased within the first three days, and increased afterwards. The values of serum peroxides and soluble intercellular adhesion molecule-1 increased continuously in respect to the initial levels reaching the maximum at the time of release from hospital. These findings indicate a persistent oxidative stress that might be associated with intravascular inflammation in patients during convalescence and release from hospital. myocardial infarction; percutaneous coronary intervention; inflammation; soluble intercellular adhesion molecule-1; lipid peroxidation © 2006 Tohoku University Medical Press While oxidative stress has been shown to be related with the age and living habits (Ozbay and Dulker 2002), it plays an important role in the development of vascular diseases that affect vital organs, in particular brain and heart (Zarkovic 2003;Zarkovic et al. 2004;Madamanchi et al.

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Section: Discussionmentioning

confidence: 99%

Persistent Oxidative Stress after Myocardial Infarction Treated by Percutaneous Coronary Intervention

Nikolić-Heitzler

Rabuzin

Tatzber

et al. 2006

Tohoku J. Exp. Med.

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“…Endotoxin is a highly conserved cell wall component that is recognized by the immune system of higher vertebrates as a pathogen-associated molecular pattern (PAMP) and can elicit a systemic inflammatory response [2,3].…”

Section: Introductionmentioning

confidence: 99%

“…Vitamins are ideal antioxidants to increase tissue protection from oxidative stress due to their easy, effective and safe dietary administration in a large range of concentrations [3,14]. Vitamin E (-Tocopherol [(-Toc]) is the primary membrane bound, lipid-soluble, chain-breaking antioxidant that protects cell membranes against lipid peroxidation [15][16][17][18].…”

Section: Introductionmentioning

confidence: 99%

Vitamin E Supplementation Modulates Endotoxin-induced Liver Damage in a Rat Model

Bharrhan¹,

Chopra²,

Rishi³

2010

Am. J. Biomed. Sci.

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Vitamin E (-Tocopherol [-Toc]) is the primary membrane bound, lipid-soluble, chain-breaking antioxidant that has been reported to protect against lipid peroxidation-induced tissue damage. Therefore, the present study was designed to investigate the protection afforded by α-Tocopherol (vitamin E), if any, on LPS-induced liver injury in Wistar rats and to study the underlying mechanism of protection. Bacterial endotoxin (10 mg/Kg body weight-prestandardized dose) was injected intraperitoneally and animals were sacrificed 8 h post-challenge. Vitamin E (35 mg/Kg body weight) was administered orally for 15 days prior to endotoxin challenge. Challenge with LPS resulted in a significant increase in the activities of serum transaminases and alkaline phosphatase along with histological alterations in the liver. These responses were associated with elevated levels of malondialdehyde (MDA) and reduced levels of glutathione, superoxide dismutase and catalase along with increased levels of tumor necrosis factor alpha (TNF-α) in the liver homogenates. However, vitamin E supplementation attenuated the oxidative stress by reducing the levels of MDA, restoring the levels of glutathione, superoxide dismutase and catalase and decreasing the levels of TNF-α. Decreased TNF-α levels after vitamin E supplementation might have resulted into the modulation of above mentioned biochemical changes resulting into amelioration of hepatic architecture. Vitamin E, therefore, seems to have a promising role for clinical manifestations due to oxidative stress.

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“…28 However, some current researches show that the cytoprotective properties of a-tocopherol are mostly related to gene regulation rather over to antioxidant activity in toxin-induced cell death in tissues such as liver. 29 Vit C alone or in combination with vit A can protect the oxidative kidney damage induced by lipopolysaccharide in rats, 30 and vit C is beneficial in the treatment of paracetamol induced renal damage. 31 Although vit A alone does not change histopathologic appearance, vit C alone or in combination with vit A prevent the renal tissue damage in endotoxic rats.…”

Section: Discussionmentioning

confidence: 99%

Protective effects of antioxidant combination against D‐galactosamine‐induced kidney injury in rats

Çatal

Saçan

Yanardağ

et al. 2010

Cell Biochemistry & Function

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The protective effects of an antioxidant combination in kidney injury induced by the injection of D-galactosamine (D-GaIN) were examined in the present study. Sprague Dawley female rats were used and divided into four groups as follows: (1) animals injected physiological saline solution, intraperitoneally, (2) animals treated with the combination of ascorbic acid (100 mg kg(-1) day(-1)), beta-carotene (15 mg kg(-1) day(-1)), alpha-tocopherol (100 mg kg(-1) day(-1)), and sodium selenate (0.2 mg kg(-1) day(-1)) for three days orally, (3) rats injected D-GaIN (500 mg kg(-1)) intraperitoneally as a single dose, and (4) animals treated with the antioxidant combination for three days, then injected D-GaIN. The tissue and blood samples of animals were collected for morphological and biochemical evaluations. Histopathological injury in kidney tissues was observed together with a significant increase in tissue lipid peroxidation (LPO) level, myeloperoxidase (MPO), lactate dehydrogenase, catalase and superoxide dismutase (SOD) activities, and serum creatinine and urea levels, and a significant decrease in glutathione level and glutathione peroxidase activity in D-GaIN injected rats. However, a decrease in the degenerative changes was detected in the kidney tissue of D-GaIN + antioxidant group, and biochemical results showed reversed effects. In conclusion, it seems reasonable to conclude that the treatment of the antioxidant combination has a protective effect on D-GaIN-induced kidney injury of rats.

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Protective Effects of Vitamin C, Alone or in Combination with Vitamin A, on Endotoxin-Induced Oxidative Renal Tissue Damage in Rats

Cited by 37 publications

References 24 publications

Persistent Oxidative Stress after Myocardial Infarction Treated by Percutaneous Coronary Intervention

Persistent Oxidative Stress after Myocardial Infarction Treated by Percutaneous Coronary Intervention

Vitamin E Supplementation Modulates Endotoxin-induced Liver Damage in a Rat Model

Protective effects of antioxidant combination against D‐galactosamine‐induced kidney injury in rats

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