Effects of <scp>l</scp>‐arginine on the kidney levels of malondialdehyde in rats submitted to renal ischaemia‐reperfusion

Rhoden, Ernani Luı́s; Lucas, Márcio Luı́s; Pereira-Lima, Luiz; Rhoden, Cláudia Ramos; Souto, Carlos Ary Vargas

doi:10.1046/j.1464-410x.2001.02303.x

Cited by 12 publications

(10 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This highly toxic species reacts with GSH, lipids, proteins and DNA. Moreover, NO production inactivates GSH-Px activity via modification of a cysteine-like essential residue on GSH-Px [24,25].…”

Section: Discussionmentioning

confidence: 99%

“…This could be attributed to increased formation of NO and peroxynitrite, which are potent oxidants inducing depletion of both kidney reduced GSH content and inactivation of kidney GSH-Px, in addition to elevation of lipid peroxidation levels [23,24]. Also, Larginine reduced the kidney platinum accumulation level [24,25]. L-Arginine might antagonize CDDP-induced haemodynamic effects and increase renal blood flow and the glomerular filtration rate through an NO-mediated mechanism by increasing basal NO production by eNOS, which is responsible for renal vasodilation, increased renal plasma flow and regulation of renal O 2 consumption [30,31].…”

Section: Discussionmentioning

confidence: 99%

“…These effects augmented the inactivation of kidney GSH-Px. However, the reduction in the kidney MDA production level could be due to a decrease in the formation of peroxynitrite [24,25].…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Inhibition of Nitric Oxide Synthase Aggravates Cisplatin-Induced Nephrotoxicity: Effect of 2-Amino-4-Methylpyridine

Saad¹,

Najjar²,

Daba³

et al. 2002

Chemotherapy

View full text Add to dashboard Cite

Background: Nitric oxide (NO) has been shown to play a role in maintaining normal renal function. However, the role of NO in cisplatin (CDDP)-induced nephrotoxicity is still unclear. The aim of the present work was to examine the effect of the NO synthase (NOS) inhibitor, 2-amino-4-methylpyridine, on the severity of CDDP-induced nephrotoxicity. Methods: Male Wistar rats were divided into six groups. Three control groups received plain drinking water or water containing 1.5% L-arginine. One of the two groups receiving plain water was treated with an intraperitoneal injection of 2-amino-4-methylpyridine (1 mg/kg in normal saline), and the other two control groups were injected intraperitoneally with normal saline. Another three groups were treated in the same manner and injected with CDDP (6 mg/kg, i.p.). CDDP was injected 1 h after 2-amino-4-methylpyridine treatment. Rats were sacrificed 7 days after CDDP treatment, and serum as well as kidneys were isolated and analysed. Results: CDDP-treated rats showed increases in the kidney weight as a percentage of the total body weight and serum creatinine and urea levels and decreases in serum albumin and calcium levels. Also, CDDP treatment induced reductions in the kidney total nitrate/nitrite (NO_x), reduced glutathione (GSH) and glutathione peroxidase activity (GSH-Px) levels and an increase in the kidney malondialdehyde (MDA) production level. In contrast, 2-amino-4-methylpyridine treatment 1 h prior to CDDP injection induced marked exacerbation of CDDP-induced nephrotoxicity, as manifested by severe aggravation of the indices of nephrotoxicity. Also, 2-amino-4-methylpyridine plus CDDP-treated rats showed exaggeration of the reduction in the kidney total NO_x content and GSH-Px activity and elevation of the kidney platinum accumulation level with normalization of the kidney MDA production level and rebound in the kidney GSH content. Histopathologically, CDDP-treated rats showed marked interstitial nephritis, tubular atrophy and tubular necrosis. However, treatment with 2-amino-4-methylpyridine 1 h prior to CDDP injection revealed marked exacerbation of CDDP-induced histopathological changes. Conclusions: The present findings suggest that NO plays a role in CDDP-induced nephrotoxicity. Administration of 2-amino-4-methylpyridine, an NOS inhibitor, exacerbates CDDP-induced nephrotoxicity.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Inhibition of Nitric Oxide Synthase Aggravates Cisplatin-Induced Nephrotoxicity: Effect of 2-Amino-4-Methylpyridine

Saad¹,

Najjar²,

Daba³

et al. 2002

Chemotherapy

View full text Add to dashboard Cite

show abstract

“…The measurement of MDA is one of the frequent ways adopted to estimate the levels of LPO. Studies in mice subjected to ischemia reperfusion injury had shown an increase in the level of MDA following pretreatment with L-arginine[29] which was detrimental. The MDA levels in our study showed a marginal decline and this was not statistically significant.…”

Section: Discussionmentioning

confidence: 99%

The effect of L-arginine on arterial stiffness and oxidative stress in chronic kidney disease

et al. 2012

View full text Add to dashboard Cite

Chronic kidney disease (CKD) is a growing problem worldwide. The disproportionate increase in the burden of cardiovascular disease in patients with CKD may be significantly contributed by nontraditional risk factors. Increased arterial stiffness has been recognized as an important player in contributing to this morbidity and mortality. The aim of this study was to report the effect of L-arginine on arterial stiffness and oxidative stress in patients with CKD. Thirty patients with stage II to IV CKD were administered 9 g of L- arginine per day orally for a period of 12 weeks. The parameters evaluated at baseline, at 8 weeks, and at the end of 12 weeks were serum nitric oxide (NO), carotid.femoral pulse wave velocity (cf PWV), and radial artery pulse wave analysis which included aortic augmentation pressure (AP), aortic augmentation index (AIx), aortic augmentation index at heart rate of 75 bpm, subendocardial viability ratio, radial pressures, and central aortic pressure. Serum levels of NO and malondialdehyde (MDA) were estimated at baseline and at the end of 12 weeks. The control group was composed of age- and sex-matched healthy individuals. Twenty-five patients completed the study. Two patients were lost to follow.up; three patients developed adverse events and were excluded. Baseline NO levels were low (13.55 ± 7.49 μM/L) in all the subjects. Administration of L-arginine resulted in improvement in the carotid-radial PWV (m/s) (10.08 ± 1.72 at baseline to 8.56 ± 1.16 by 12 weeks; P < 0.001), cf PWV (m/s) (13.06 ± 2.65 at baseline to 10.62 ± 1.93 at 12 weeks; P < 0.001), Aortic Augmentation Index (%) (32 ± 10.34 at baseline to 17.84 ± 8.05 at 12 weeks; P < 0.001), aortic augmentation pressure (mm of Hg) (14.03 ± 6.53 at baseline to 7.12 ± 3.85 at 12 weeks; P < 0.001), and NO (μM/L) (13.55 ± 7.49 at baseline to 30.22 ± 9.8 at 12 weeks; P < 0.001). There was no significant change in the levels of MDA (nanomol/ml) (20.0 ± 10.14 at baseline and 19.16 ± 9.36 at 12 weeks; P = ns). In conclusion, PWV, an indicator of arterial stiffness, is greatly increased even in the early stages of CKD. Supplementation of L-arginine is a safe, well-tolerated, and effective way of improving endothelial dysfunction in patients with CKD.

show abstract

“…ROS can disrupt the integrity of the endothelium and a¡ect NO production [Rhoden et al, 2001], and ROS (and peroxynitrite) can also cause cellular injury and death via several mechanisms, including peroxidation of membrane lipids, protein denaturation, and DNA damage [Chatterjee et al, 2003]. The observed reduction in eNOS expression may, therefore, be caused by downregulation of the enzyme or to endothelial cell necrosis.…”

Section: Discussionmentioning

confidence: 99%

Changes in nitric oxide production in the rat kidney due to CaOx nephrolithiasis

Huang

Chieh

Chen

2006

Neurourology and Urodynamics

View full text Add to dashboard Cite

show abstract

Effects of l‐arginine on the kidney levels of malondialdehyde in rats submitted to renal ischaemia‐reperfusion

Cited by 12 publications

References 23 publications

Inhibition of Nitric Oxide Synthase Aggravates Cisplatin-Induced Nephrotoxicity: Effect of 2-Amino-4-Methylpyridine

Inhibition of Nitric Oxide Synthase Aggravates Cisplatin-Induced Nephrotoxicity: Effect of 2-Amino-4-Methylpyridine

The effect of L-arginine on arterial stiffness and oxidative stress in chronic kidney disease

Changes in nitric oxide production in the rat kidney due to CaOx nephrolithiasis

Contact Info

Product

Resources

About