Mild Oxidative Stress: Cellular Mode of Mitogenic Effect

Goligorsky, Michael S.; Morgan, M.; H, Suh; Safirstein, Robert; Johnson, Roger B.

doi:10.3109/08860229209106646

Cited by 8 publications

(3 citation statements)

References 13 publications

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“…For example, renal tubular epithelial cells express protooncogenes and proliferate in response to low doses of hydrogen peroxide [32,33]. Quite low doses of hydrogen peroxide or ter-butyl hydroperoxide stimulate the growth of hamster kidney fibroblasts in vitro [29].…”

Section: Oxidants and Growth Responsesmentioning

confidence: 99%

The Involvement of Oxidative Stress in the Progression of Renal Injury

Haugen

Nath²

1999

Blood Purif

120

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That reactive oxygen species are involved in progressive renal injury is supported by several lines of evidence: increased generation of oxidants occurs in chronic renal injury; various antioxidant strategies exert beneficial effects in models of chronic renal injury; and, oxidative stress can induce changes in the otherwise unmanipulated kidney that resemble those seen in chronic renal disease. Oxidants may contribute to progressive renal disease by virtue of their renal haemodynamic actions, by impairing glomerular permselective properties, by inducing inordinate or aberrant growth responses, by inducing loss of cellular phenotype and apoptosis, and finally, by promoting acute and chronic inflammatory responses. Certain adhesion molecules and proinflammatory mediators, and the transcription factor NFκB, can be upregulated by oxidants. Oxidants can also induce the fibrogenic cytokine, TGFβ1, one that is widely incriminated in progressive renal injury. Reduction in renal oxidative stress by dietary or pharmacologic approaches provides an appealing target for therapies directed towards the retardation of progressive renal injury.

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Section: Oxidants and Growth Responsesmentioning

confidence: 99%

The Involvement of Oxidative Stress in the Progression of Renal Injury

Haugen

Nath²

1999

Blood Purif

120

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“…First, RS are suggested to induce processes known to be involved in chronic renal scaring, such as cell proliferation, apoptosis, inflammation and vascular injury. For instance, mitogenesis and hypertrophy of tubular cells are controlled by RS [30,31]. Apoptosis of mesangial and tubular cells is also mediated by RS [32].…”

Section: Oxidative Hypothesis Of Kidney Diseasesmentioning

confidence: 99%

Antioxidants: A Possible Role in Kidney Protection

Tylicki

Rutkowski

Hörl

2003

Kidney Blood Press Res

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Oxidative stress contributes to the pathophysiology of kidney injury. Beneficial renal effects of some medications, such as angiotensin-converting enzyme inhibitors, angiotensin II type 1 receptor antagonists, calcium channel blockers, β-blockers and lipid lowering agents depend at least partially on the ability to alleviate oxidative stress. The administration of various natural or synthetic antioxidants has been shown to be of benefit in prevention and attenuation of renal scaring in numerous animal models of kidney diseases. These include vitamins, N-acetylcysteine, α-lipoic acid, melatonin, dietary flavonoids and phytoestrogens, and many others. Human studies are limited in this regard. Under certain conditions, surprisingly, the antioxidant supplements may exhibit pro-oxidant properties and even worsen renal damage. To date, the evidence is insufficient to recommend antioxidant supplements in patients with kidney disease. Prospective, controlled clinical trials on safety and effectiveness of different therapeutic antioxidant strategies are indispensable.

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“…First, RS are suggested to induce processes known to be involved in chronic renal scarring, such as cell proliferation, apoptosis, inflammation and vascular injury [18][19][20][21] . RS also participate in vascular smooth muscle cell growth and migration [22] , impairment of endothelial-dependent vascular relaxation [23] and the development of atherosclerosis [24] , processes closely related to vascular injury.…”

Section: Discussionmentioning

confidence: 99%

The Effect of N-Acetylcysteine on Proteinuria and Markers of Tubular Injury in Non-Diabetic Patients with Chronic Kidney Disease

Renke

Tylicki²,

Rutkowski³

et al. 2008

Kidney Blood Press Res

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Background: Inhibition of the renin-angiotensin-aldosterone system with angiotensin-converting enzyme inhibitors (ACEI) and/or angiotensin II subtype 1 receptor antagonists (ARB) constitutes a strategy in the management of patients with chronic kidney disease. There is still no optimal therapy which can stop the progression of chronic kidney disease. Antioxidants such as N-acetylcysteine (NAC) have been reported as a promising strategy in this field. Methods: In a placebo-controlled, randomized, open, 2-period cross-over study, we evaluated the influence of NAC (1,200 mg/day) added to renin-angiotensin-aldosterone system blockade on proteinuria and surrogate markers of tubular injury and renal fibrosis in 20 non-diabetic patients with proteinuria (0.4–6.36 g/24 h) with normal or decreased kidney function (estimated glomerular filtration rate 61–163 ml/min). Subjects entered the 8-week run-in period during which the therapy using ACEI and/or ARB was established with blood pressure below 130/80 mm Hg. Next, patients were randomly assigned to 1 of 2 treatment sequences: NAC/washout/placebo or placebo/washout/NAC. Clinical evaluation and laboratory tests were performed at the randomization point and after each period of the study. Results: No significant changes in laboratory tests were observed. Conclusion: NAC had no effect on proteinuria, surrogate markers of tubular injury or renal fibrosis in non-diabetic patients with chronic kidney disease.

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Mild Oxidative Stress: Cellular Mode of Mitogenic Effect

Cited by 8 publications

References 13 publications

The Involvement of Oxidative Stress in the Progression of Renal Injury

The Involvement of Oxidative Stress in the Progression of Renal Injury

Antioxidants: A Possible Role in Kidney Protection

The Effect of N-Acetylcysteine on Proteinuria and Markers of Tubular Injury in Non-Diabetic Patients with Chronic Kidney Disease

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