Effect of Cyclosporin a on Tissue Lipid Peroxidation and Membrane Bound Phosphatases in Hyperoxaluric Rat and the Protection by Vitamin E Pretreatment

Marimuthu, A.; Selvam, Ramasamy

doi:10.7883/yoken1952.50.9

Cited by 15 publications

(12 citation statements)

References 6 publications

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“…Similarly, when buthionine sulfoximine treatment was combined with ethylene glycol, there was more deposition of crystals in the tubules damaged with denudation and shedding of epithelial lining of the tubules [65]. Similar observations were also seen in the cyclosporin-treated ammonium oxalate-fed rats [1] and ethylene glycol-fed rats [46]. Studies by Thamilselvan et al [114] also revealed that oxidative damage was more related to the hyperoxaluria and crystalluria rather than to tissue crystal deposits.…”

Section: Lipid Peroxidationmentioning

confidence: 71%

“…Furthermore, the concentrations of free radical scavengers, vitamin E, ascorbic acid, GSH, and protein thiol also decreased [1,3,14,15,65,73,74,76,94,96,97,98,102] (Table 1, Table 2). Similar to experimental urolithic rats, stone patients also showed enhanced plasma LPO products, TBARS, hydro peroxides, and lipofuscin, and depletion of antioxidant scavengers [4,7,75] (Table 3).…”

Section: Antioxidant Enzymes and Scavengers In Urolithiasismentioning

confidence: 98%

“…Irrespective of the nature of urolithic agents used to induce either hyperoxaluria or calcium oxalate crystal deposition in experimental rats by administration of sodium oxalate [93], feeding sodium glycolate either in the diet or drinking water [14,94,96], vitamin B 6 -deficient diet [73,74,76,98], ethylene glycol (EG) [15,114], ammonium oxalate [1], and dehydroascorbic acid [97], enhanced LPO products that were always commonly observed in kidney, liver, and plasma (Table 1). When the animals were treated with a glutathione-depleting agent such as buthionine sulfoximine or nephrotoxin, and cyclosporine along with a calculi-producing agent, still higher LPO products were released [15,65] ( Table 2).…”

Section: Lipid Peroxidationmentioning

confidence: 99%

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Calcium oxalate stone disease: role of lipid peroxidation and antioxidants

Selvam

2002

Urological Research

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185

105

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Membrane injury facilitated the fixation of calcium oxalate crystals and subsequent growth into kidney stones. Oxalate-induced membrane injury was mediated by lipid peroxidation reaction through the generation of oxygen free radicals. In urolithic rat kidney or oxalate exposed cultured cells, both superoxide anion and hydroxyl radicals were generated in excess, causing cellular injury. In hyperoxaluric rat kidney, both superoxide and H2O2-generating enzymes such as glycolic acid oxidase (GAO) and xanthine oxidase (XO) were increased, and hydroxyl radical and transition metal ions, iron, and copper were accumulated. The lipid peroxidation products, thiobarbituric acid-reactive substances (TBARS), hydroperoxides, and diene conjugates were excessively released in tissues of urolithic rats and in plasma of rats as well as stone patients. The accumulation of these products was concomitant with the decrease in the antioxidant enzymes, superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), and glucose-6 phosphate dehydrogenase (G6PD) as well as radical scavengers, vitamin E, ascorbic acid, reduced glutathione (GSH), and protein thiol. All the above parameters were decreased in urolithic condition, irrespective of the agents used for the induction of urolithiasis. Oxalate binding activity and calcium oxalate crystal deposition were markedly pronounced, along with decreased adenosine triphosphatase (ATPase) activity. Lipid peroxidation positively correlated with cellular oxalate, oxalate binding, gamma-glutamyl carboxylase, and calcium level and negatively correlated with GSH, vitamin E. ascorbic acid, and total protein thiol. Antioxidant therapy to urolithic rats with vitamin E, glutathione monoester, methionine, lipoic acid, or fish oil normalised the cellular antioxidant system, enzymes and scavengers, and interrupted membrane lipid and protein peroxidation reaction, ATPase inactivation, and its associated calcium accumulation. Antioxidant therapy prevented calcium oxalate precipitation in the rat kidney and reduced oxalate excretion in stone patients. Similarly, calcium oxalate crystal deposition in vitro to urothelium was prevented by free radical scavengers such as phytic acid and mannitol by protecting the membrane from free radical-mediated damage. All these observations were suggestive of the active involvement of free radical-mediated lipid peroxidation-induced membrane damage in the pathogenesis of calcium oxalate crystal deposition and retention.

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Section: Lipid Peroxidationmentioning

confidence: 71%

Section: Antioxidant Enzymes and Scavengers In Urolithiasismentioning

confidence: 98%

Section: Lipid Peroxidationmentioning

confidence: 99%

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Calcium oxalate stone disease: role of lipid peroxidation and antioxidants

Selvam

2002

Urological Research

Self Cite

185

105

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“…Nephrotoxicity of cyclosporine has been attributed to the enhanced formation of free radicals. Ascorbate-induced lipid peroxidation was reported to increase in cyclosporine A-administered rats [22]. In kidney cortex mitochondria and microsomes, ascorbate was observed to increase cyclosporine A-induced lipid peroxidation and viability loss similar to the effect of ferrous iron [23].…”

Section: Pro-oxidant Effects Of Ascorbate Via Reduction Of Cellular mentioning

confidence: 87%

Vitamin C in Chronic Kidney Disease and Hemodialysis Patients

Deicher

Hörl

2003

Kidney Blood Press Res

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Increments of oxidative stress have been addressed as one potential cause for the accelerated atherosclerosis of chronic kidney disease patients. Ascorbate represents one of the most prominent antioxidants both in plasma as well as intracellulary, exerting beneficial effects by an inhibition of lipid peroxidation and by reducing endothelial dysfunction. However, in the presence of transition metals like iron, ascorbate may give rise to an increased generation of oxidants, and ascorbylation may impose additional carbonyl stress to uremic patients. Unsupplemented dialysis patients have reportedly lower plasma levels of ascorbate in comparison to healthy controls, mostly due to a loss into the dialysate or, in case of not dialyzed patients, increased urinary losses. Currently, 60 mg of ascorbate are recommended for chronic kidney disease patients, and 1–1.5 g of oral ascorbate/week in case of suspected subclinical ascorbate deficiency or 300 mg parenteral ascorbate/dialysis session, respectively. Ascorbate’s role in modifying arterial blood pressure remains unclear, but anemic patients with functional iron deficiency might benefit from short-term, moderately dosed ascorbate supplements.

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“…ATPases are lipid dependent, membrane-bound enzymes involved in actively transporting sodium, potassium, calcium, and magnesium (Kimelberg, 1977). Enhanced susceptibility of membranes to lipid peroxides can lead to loss of protein thiol, thereby changing membrane functions (Adhirai & Selvam, 1997).…”

Section: Discussionmentioning

confidence: 99%

Influence of kaempferol, a flavonoid compound, on membrane-bound ATPases in streptozotocin-induced diabetic rats

Al‐Numair

Veeramani

Alsaif

et al. 2015

Pharmaceutical Biology

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Context: Kaempferol is a flavonoid found in many edible plants (e.g. tea, cabbage, beans, tomato, strawberries, and grapes) and in plants or botanical products commonly used in traditional medicine. Numerous preclinical studies have shown that kaempferol have a wide range of pharmacological activities, including antioxidant, anti-inflammatory, anticancer, cardioprotective, neuroprotective, and antidiabetic activities. Objective: The present study investigates the effect of kaempferol on membrane-bound ATPases in erythrocytes and in liver, kidney, and heart of streptozotocin (STZ)-induced diabetic rats. Materials and methods: Diabetes was induced into adult male albino rats of the Wistar strain, by intraperitoneal administration of STZ (40 mg/kg body weight (BW)). Kaempferol (100 mg/kg BW) or glibenclamide (600 mg/kg BW) was administered orally once daily for 45 d to normal and STZinduced diabetic rats. The effects of kaempferol on membrane-bound ATPases (total ATPase, Na + /K + -ATPase, Ca 2+ -ATPase, and Mg 2+ -ATPase) activity in erythrocytes and in liver, kidney, and heart were determined. Results: In our study, diabetic rats had significantly (p50.05) decreased activities of total ATPases, Na + /K + -ATPase, Ca 2+ -ATPase, and Mg 2+ -ATPase in erythrocytes and tissues. Oral administration of kaempferol (100 mg/kg BW) or glibenclamide (600 mg/kg BW) for a period of 45 d resulted in significant (p50.05) reversal of these enzymes' activities to near normal in erythrocytes and tissues when compared with diabetic control rats. Discussion and conclusion: Thus, obtained results indicate that administration of kaempferol has the potential to restore deranged activity of membrane-bound ATPases in STZ-induced diabetic rats. Further detailed investigation is necessary to discover kaempferol's action mechanism.

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Effect of Cyclosporin a on Tissue Lipid Peroxidation and Membrane Bound Phosphatases in Hyperoxaluric Rat and the Protection by Vitamin E Pretreatment

Cited by 15 publications

References 6 publications

Calcium oxalate stone disease: role of lipid peroxidation and antioxidants

Calcium oxalate stone disease: role of lipid peroxidation and antioxidants

Vitamin C in Chronic Kidney Disease and Hemodialysis Patients

Influence of kaempferol, a flavonoid compound, on membrane-bound ATPases in streptozotocin-induced diabetic rats

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