Unilateral ureteral obstruction impairs renal antioxidant enzyme activation during sodium depletion

Kinter, Michael; Wolstenholme, Jennifer T.; Thornhill, Barbara A.; Newton, Elizabeth; McCormick, Michael L.; Chevalier, Robert L.

doi:10.1046/j.1523-1755.1999.00358.x

Cited by 61 publications

(33 citation statements)

References 26 publications

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“…Most interesting was the finding that stretching proximal tubular cells in vitro suppressed catalase expression, suggesting that mechanical forces imposed on tubular epithelial cells in the obstructed kidney could contribute to renal oxidant injury [90]. Since obstructive nephropathy can result in significant sodium wasting and volume contraction, we examined the effect of sodium depletion on renal antioxidant enzyme activity in rats subjected to chronic UUO [91]. We found that while sodium depletion increased several renal antioxidant enzymes in intact rats, UUO not only reduced baseline antioxidant activities, but also prevented the normal response to sodium depletion [91].…”

Section: Progressive Renal Injury Resulting From Urinary Tract Obstrumentioning

confidence: 99%

Molecular and cellular pathophysiology of obstructive nephropathy

Chevalier¹

1999

Pediatric Nephrology

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118

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Congenital obstructive nephropathy remains one of the most-important causes of renal insufficiency in children. This review focuses on the unique interactions that result from urinary tract obstruction during the period of renal development in the neonatal rodent. Following unilateral ureteral obstruction (UUO), growth of the obstructed kidney is impaired and compensatory growth by the intact opposite kidney is related directly to the duration of obstruction. Development of the renal vasculature is delayed by UUO, and the activity of the intrarenal renin-angiotensin system is enhanced throughout the period of obstruction. Glomerular maturation is also delayed by UUO, and nephrogenesis is permanently impaired. The effects of UUO on the developing tubule are also profound, with a suppression of proliferation, stimulation of apoptosis, and the maintenance of an immature phenotype by tubular epithelial cells. Expression of tubular epidermal growth factor is suppressed and transforming growth factor-beta1 and clusterin are increased. Maturation of interstitial fibroblasts is delayed, with progression of tubular atrophy and interstitial fibrosis resulting in part from continued activation of the renin-angiotensin system and oxygen radicals. Future efforts to prevent the consequences of congenital urinary tract obstruction must account for the dual effects of obstruction: interference with normal renal development and progression of irreversible tubulointerstitial injury.

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Section: Progressive Renal Injury Resulting From Urinary Tract Obstrumentioning

confidence: 99%

Molecular and cellular pathophysiology of obstructive nephropathy

Chevalier¹

1999

Pediatric Nephrology

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118

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“…Tissue GPx activity increased in almost all groups compared to the sham groups. Kinter et al showed that increased sodium wasting in rats in which they induced unilateral CUO did not change antioxidant enzyme CAT levels but did cause a slight increase in GPx (14).…”

Section: Discussionmentioning

confidence: 99%

The effect of trimetazidine on renal oxidative stress in partialand complete ureteral obstructions in a rat model

Ayyıldız

Benli̇

et al. 2017

Turk J Med Sci

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IntroductionObstructive uropathy results from the blockage of urinary flow at any point in the urinary system. If the obstruction is not relieved in time, it leads to loss of kidney function. The most widespread cause of unilateral ureteral obstruction (UUO) in adult humans is sudden blockage leading to acute obstruction in a ureter. It generally appears with ureteral stones. An obstruction-related increase in retrograde hydrostatic pressure triggers tubular cell death due to apoptosis and necrosis, interstitial inflammation, decreased capillary numbers, and progressive fibrosis (1).Oxidative stress causes injury and functional losses in many tissues, including the kidney. Clinical and experimental studies have shown that oxidative stress causes glomerular, tubulointerstitial, and endothelial changes in the kidneys and mediates the development of several kidney diseases, such as acute kidney failure, rhabdomyolysis, obstructive nephropathy, glomerular injury, and chronic kidney failure (2).Reactive oxygen species (ROS) are highly reactive molecules derived from the mitochondrial electron transport chain (3). Overproduction of ROS and/or insufficiency in the antioxidant mechanism leads to compromise of the oxidant/ antioxidant balance and thus to oxidative stress (4-6). The most important ROS include superoxide (O 2 -), hydroxyl (OH), hydrogen peroxide, singlet oxygen, and nitric oxygen radicals (6). Since reactive oxygen products have a rather unstable structure due to their unpaired electron, they can damage these structures by reacting with all elements in the environment in order to achieve stability (3-6). Excessive ROS formation in the body can lead to changes in the structure of DNA, resulting in activation of transcription factors induced by various stresses, production of pro-and antiinflammatory cytokines, and modification of lipids (4).Background/aim: Renal oxidative stress occurs in ureteral obstructions. The purpose of this study was to investigate the effect of the antioxidant and antiischemic agent trimetazidine (TMZ) on oxidative stress following ureteral obstruction. Materials and methods:Ten groups were established. Sham groups were checked as controls after 1 and 3 weeks. The other 8 groups had partial or complete ureteral obstruction while receiving or not receiving trimetazidine (TMZ) at 5 mg/kg daily and were evaluated after either 1 week or 3 weeks. Creatinine and cystatin C measurements were performed in the serum. Malondialdehyde, myeloperoxidase, catalase, and glutathione peroxidase activity were measured in renal tissue and serum. Results:In the 1-week groups, tissue malondialdehyde, serum myeloperoxidase, and glutathione peroxidase activity increased significantly with obstruction and TMZ use compared to the control group (P < 0.005). In the 3-week TMZ group, cystatin C, tissue malondialdehyde, serum and tissue myeloperoxidase, and tissue glutathione peroxidase differed significantly (P < 0.05). There was no significant difference in all parameters after 3 weeks of partial obstruction (...

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“…Oxidative stress is believed to mediate a wide range of kidney disorders, including renal impairment, acute renal failure [18,19], obstructive nephropathy [20], hyperlipidemia [21] and glomerular damage [22]. As HT and its metabolites have been shown to be present in the kidney in relatively high amounts [15], and express antioxidant activity in vitro and in vivo [23][24][25][26][27][28], they may be able to exert a degree of protection against oxidative kidney injury.…”

Section: Introductionmentioning

confidence: 99%

Involvement of ERK, Akt and JNK signalling in H₂O₂‐induced cell injury and protection by hydroxytyrosol and its metabolite homovanillic alcohol

Incani

Deiana

Corona

et al. 2010

Molecular Nutrition Food Res

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The olive oil polyphenol, hydroxytyrosol (HT), is believed to be capable of exerting protection against oxidative kidney injury. In this study we have investigated the ability of HT and its O-methylated metabolite, homovanillic alcohol (HVA) to protect renal cells against oxidative damage induced by hydrogen peroxide. We show that both compounds were capable of inhibiting hydrogen peroxide-induced kidney cell injury via an ability to interact with both MAP kinase and PI3 kinase signalling pathways, albeit at different concentrations. HT strongly inhibited death and prevented peroxide-induced increases in ERK1/2 and JNK1/2/3 phosphorylation at 0.3 microM, whilst HVA was effective at 10 microM. At similar concentrations, both compounds also prevented peroxide-induced reductions in Akt phosphorylation. We suggest that one potential protective effect exerted by olive oil polyphenols against oxidative kidney cell injury may be attributed to the interactions of HT and HVA with these important intracellular signalling pathways.

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Unilateral ureteral obstruction impairs renal antioxidant enzyme activation during sodium depletion

Cited by 61 publications

References 26 publications

Molecular and cellular pathophysiology of obstructive nephropathy

Molecular and cellular pathophysiology of obstructive nephropathy

The effect of trimetazidine on renal oxidative stress in partialand complete ureteral obstructions in a rat model

Involvement of ERK, Akt and JNK signalling in H₂O₂‐induced cell injury and protection by hydroxytyrosol and its metabolite homovanillic alcohol

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Unilateral ureteral obstruction impairs renal antioxidant enzyme activation during sodium depletion

Cited by 61 publications

References 26 publications

Molecular and cellular pathophysiology of obstructive nephropathy

Molecular and cellular pathophysiology of obstructive nephropathy

The effect of trimetazidine on renal oxidative stress in partialand complete ureteral obstructions in a rat model

Involvement of ERK, Akt and JNK signalling in H2O2‐induced cell injury and protection by hydroxytyrosol and its metabolite homovanillic alcohol

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Involvement of ERK, Akt and JNK signalling in H₂O₂‐induced cell injury and protection by hydroxytyrosol and its metabolite homovanillic alcohol