Depleted nitrite and enhanced oxidative stress in urolithiasis

Bet, Vasavidevi V.; Deshpande, Kishor H.; Suryakar, Adinath N.; Ankush, R. D.; Katkam, R. V.

doi:10.1007/bf02912938

Cited by 12 publications

(7 citation statements)

References 16 publications

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“…Indirect evidence via monitoring biomarkers such as reactive oxygen species, and reactive nitrogen species production, antioxidant defense indicates oxidative damage may be involved in the pathogenesis of these diseases [23,24] Oxidative stress also contributes to tissue injury following irradiation and hyperoxia, as well as in diabetes and is likely to be involved in age-related development of cancer. Infection by Helicobacter pylori which increases the production of reactive oxygen and nitrogen species in human stomach is also thought to be important in the development of gastric cancer [25]. ROS also have been reported to damage cellular components in cartilage by impairing the chondrocyte responses to growth factors and migrating to the sites of cartilage injury leading to osteoarthritis [26].…”

Section: Some Of the Human Disorders Clinically Linked To Oxidative Smentioning

confidence: 99%

“…Increased ROS in human heart is associated with arotic valve stenosis [28]. Excess ROS in human kidney leads to urolithiasis [29]. It was also observed that hyperglycemia triggers the generation of ROS in both mesangial and tubular cells of human kidney, making structural and functional changes in glomeruli causing diabetic nephropathy [30].…”

Section: Some Of the Human Disorders Clinically Linked To Oxidative Smentioning

confidence: 99%

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Oxidative stress and human health

Rahman¹,

Hosen²,

Islam³

et al. 2012

ABB

334

214

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Redox degenerative reactions of the biological system inevitably produce reactive oxygen species (ROS) and their derivatives. Oxidative stress is the result of an imbalance in pro-oxidant/antioxidant homeostasis that leads to the generation of toxic reactive oxygen species (ROS), such as hydrogen peroxide, organic hydro peroxides, nitric oxide, superoxide and hydroxyl radicals etc. Information are accumulating steadily, supporting the general importance of oxidative damage of tissue and cellular components as a primary or secondary causative factor in many different human diseases and aging processes. Many of the recent landmarks in scientific research have shown that in human beings, oxidative stress has been implicated in the progression of major health problems by inactivating the metabolic enzymes and damaging important cellular components, oxidizing the nucleic acids, leading to cardiovascular diseases, eye disorders, joint disorders, neurological diseases (Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis), atherosclerosis, lung and kidney disorders, liver and pancreatic diseases, cancer, ageing, disease of the reproductive system including the male and female infertility etc. The advent of a growing number of in vitro and in vivo models for evaluating the human disease pathology is aiding scientists in deciphering the detailed mechanisms of the point of intersection of the oxidative stress with other cellular components or events in the growing roadmap leading to different human disorders. The toxic effect of reactive oxygen and nitrogen species in human is balanced by the antioxidant action of non-enzymatic antioxidants, as well as by antioxidant enzymes. Such antioxidant defences are extremely important as they represent the direct removal of free radicals (prooxidants), thus providing maximal protection for biological sites. These systems not only assert with the problem of oxidative damage, but also play a crucial role in wellness, health maintenance, and prevention of chronic and degenerative diseases. In this review we have tried to generate a gross picture on the critical role of ROS in deteriorating human health and the importance of antioxidative defense system in ameliorating the toxicity of ROS

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Section: Some Of the Human Disorders Clinically Linked To Oxidative Smentioning

confidence: 99%

Section: Some Of the Human Disorders Clinically Linked To Oxidative Smentioning

confidence: 99%

Oxidative stress and human health

Rahman¹,

Hosen²,

Islam³

et al. 2012

ABB

334

214

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“…However, high concentrations of ROS contribute to the development of various diseases, including kidney stones. Increased prooxidant damage indicators have been observed in the urine of patients with kidney stones [ 34 ]. There are multiple associations between ROS and kidney stone formation, and an imbalance between prooxidants and antioxidants drives kidney stone formation [ 35 ].…”

Section: Discussionmentioning

confidence: 99%

Identification of Resolvin D1 and Protectin D1 as Potential Therapeutic Agents for Treating Kidney Stones

Wang

Wei

Huangfu

et al. 2022

Oxidative Medicine and Cellular Longevity

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Intrarenal calcium oxalate (CaOx) crystals induce renal tubular epithelial cell (TEC) inflammatory and oxidative injury. This study is aimed at exploring potential therapeutic lipid components in kidney stones because lipids are involved in the development of several diseases and indicate the risk of kidney stones. Serum specimens were collected from 35 kidney stone patients and 35 normal controls. The lipid components in serum were measured, and differences were analyzed. The documented biological importance was comprehensively reviewed to identify lipids that differed significantly between the two groups to find potential agents associated with kidney stones. CaOx nephrocalcinosis mouse model was established to examine the therapeutic effects of specific lipids on CaOx deposition and CaOx-induced oxidative renal injury. Several lipids with significantly different levels were present in the serum of patients with stones and normal controls. Resolvin D1 (RvD1) (4.93-fold change, P < 0.001 ) and protectin D1 (PD1) (5.06-fold change, P < 0.001 ) were significantly decreased in the serum of patients with kidney stones, and an integrative review suggested that these factors might be associated with inflammatory responses, which is a crucial mechanism associated with stone damage. The administration of RvD1 and PD1 significantly inhibited kidney CaOx deposition and suppressed CaOx-induced renal tubular cell inflammatory injury and necrosis in a CaOx nephrocalcinosis mouse model. Furthermore, RvD1 and PD1 facilitated the expression of the oxidative indicator superoxide dismutase 2 (SOD2), inhibited NADPH oxidase 2 (NOX2) expression, and diminished intracellular reactive oxygen species (ROS) levels. This study preliminarily elucidated the role of lipids in kidney stones. The inhibitory effects of RvD1 and PD1 on oxidative damage induced by CaOx deposition provide a promising perspective for kidney stone treatment strategies.

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“…Thus, pro-oxidant and antioxidant imbalance may contribute to the development of kidney stones. Consequently, patients with kidney stones were characterised by increased lipid peroxides, while nitrite and α-tocopherol levels were reduced in the serum [66]. Previous studies proved that patients with nephrolithiasis were characterised by an increased level of pro-oxidative damage markers in urine, including 8-hydroxydeoxyguanosine (8-oxoG, a marker of DNA oxidative damage) and thiobarbituric acid-reactive substances (TBARS, a marker of lipid peroxidation) [67].…”

Section: Oxidative Stressmentioning

confidence: 99%

“…On the other hand, surgical removal of the renal calculus may contribute to a decrease in malonyl dialdehyde (MDA, 29%) and an increase in Gpx activity (by 50%), reaching values close to the levels of the control group [74]. Previous studies have suggested that an elevated peroxidation and depletion of thiol level may contribute to an increase in the oxalate binding activity and damage to the renal tubular cells, which in turn promotes nucleation, crystal adherence and aggregation of stones [66]. Therefore, in idiopathic CaOx stone cases, a high urine level of renal enzymes indicative of renal tubular damage was observed, such as γ-glutamyl transpeptidase, angiotensin 1 converting enzyme, β-galactosidase and N-acetyl-beta-Dglucosaminidase (NAG), and products of lipid peroxidation, including MDA.…”

Section: Oxidative Stressmentioning

confidence: 99%

The Molecular Aspect of Nephrolithiasis Development

Wigner

Grębowski

Bijak

et al. 2021

Cells

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Urolithiasis is the third most common urological disease after urinary tract infections and prostate diseases, and it is characterised by an occurrence rate of about 15%, which continues to rise. The increase in the incidence of kidney stones observed in recent decades, is most likely caused by modifications in dietary habits (high content of protein, sodium and sugar diet) and lifestyle (reduced physical activity) in all industrialised countries. Moreover, men are more likely than women to be diagnosed with kidney stones. A growing body of evidence suggests that inflammation, oxidant–antioxidant imbalance, angiogenesis, purine metabolism and urea cycle disorders may play a crucial role in nephrolithiasis development. Patients with urolithiasis were characterised by an increased level of reactive oxygen species (ROS), the products of lipid peroxidation, proinflammatory cytokines as well as proangiogenic factors, compared to controls. Furthermore, it has been shown that deficiency and disorders of enzymes involved in purine metabolism and the urea cycle might be causes of deposit formation. ROS generation suggests that the course of kidney stones might be additionally potentiated by inflammation, purine metabolism and the urea cycle. On the other hand, ROS overproduction may induce activation of angiogenesis, and thus, allows deposit aggregation.

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Depleted nitrite and enhanced oxidative stress in urolithiasis

Abstract: ABSTRACT

Cited by 12 publications

References 16 publications

Oxidative stress and human health

Oxidative stress and human health

Identification of Resolvin D1 and Protectin D1 as Potential Therapeutic Agents for Treating Kidney Stones

The Molecular Aspect of Nephrolithiasis Development

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