Nitric Oxide in Gentamicin-induced Acute Tubular Necrosis in Rats

Nakas-Ićindić, Emina; Avdagić, Nesina; Mijanović, Mirjana; Prašović, Senad; Začiragić, Asija; Hadzović, Almira; Tahirović, Gordan

doi:10.17305/bjbms.2005.3288

Cited by 7 publications

(8 citation statements)

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“…Maldanado et al (2003) have shown increase in nitrosation of tyrosine residues in the proteins of kidney in gentamicin-treated rats. In a recent study, Nakas-Icindic et al (2005) have shown rise in plasma levels of nitric oxide in gentamicin-treated rats. These studies and the present study provide evidence for the role of nitrosative stress in gentamicin-induced renal damage in the rat.…”

Section: Discussionmentioning

confidence: 91%

“…Increased Author for correspondence: Premila Abraham, Department of Biochemistry, Christian Medical College, Bagayam, Vellore 63202, Tamil Nadu, India (fax π91 416 2262268, e-mail premilaabraham/ yahoo.com). nitro tyrosine levels in the kidney and increased nitrite and nitrate levels in the kidney and plasma of gentamicin-treated rats (Rivas-Cabanero et al 1994;Nakas-Icindic et al 2005) have been reported.…”

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confidence: 97%

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Protective Effect of Ebselen, a Selenoorganic Drug, against Gentamicin‐Induced Renal Damage in Rats

Dhanarajan

Abraham²,

Isaac

2006

Basic Clin Pharma Tox

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Gentamicin is an antibiotic that is widely used against serious and life-threatening gram-negative infections. However, its clinical use is limited by its nephrotoxicity. Oxidative stress and nitrosative stress are reported to play important role in gentamicin nephrotoxicity. In the present study we investigated whether ebselen, an inhibitor of oxidative stress and nitrosative stress prevents or reduces gentamicin-induced renal damage in the rat. For this purpose male Wistar rats were divided into five groups and treated as follows. Group 1 (control group): dimethyl sulphoxide, intraperitoneally, Group 2: Gentamicin 100 mg/kg b.wt. subcutaneously, Group 3: 5 mg/g b.wt. ebselen intraperitoneally, Group 4: 2.5 mg/ kg b.wt. ebselen followed by 100 mg/kg b.wt. gentamicin subcutaneously one hour later, and Group 5: 5 mg/kg b.wt. of ebselen followed by 100 mg/kg b.wt. gentamicin one hour later for four consecutive days. Nephrotoxicity was evaluated histopathologically by light microscopy, and biochemically by the measurement of the plasma creatinine and urea levels. Parameters of oxidative stress such as reduced glutathione, malondialdehyde, and activities of superoxide dismutase and glutathione peroxidase were measured in the kidney. Serum nitrite and nitrate were measured as indicators of nitrosative stress. Treatment of rats with gentamicin resulted in statistically significant reduction in reduced glutathione levels (51%) and the activities of antioxidant enzymes superoxide dismutase (56%) and glutathione peroxidase (39%) as compared with the controls in the kidneys. Renal malondialdehyde level was increased significantly (43%) as compared with the controls. Plasma creatinine levels, urea levels and nitrite levels were significantly increased (4, 4.5 and 160% times respectively) as compared with the controls. Histologically, damage to the renal cortex and medulla was observed moderate to severe tubular necrosis and glomerular congestion. Pretreatment with 2.5 mg/kg b.wt. ebselen prevented gentamicin induced damage to medulla; however, renal cortex showed mild damage and biochemically indicators of oxidative stress and nitrosative stress were significantly reduced. Pretreatment with 5 mg/kg b.wt. ebselen prevented gentamicin-induced oxidative damage and nitrosative damage and renal damage almost completely in 78% of the rats, in the other 22% of the rats, ebselen pretreatment reduced gentamicin-induced renal damage. The results of the present study suggest that ebselen may be useful as a nephroprotective agent.

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Section: Discussionmentioning

confidence: 91%

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confidence: 97%

Protective Effect of Ebselen, a Selenoorganic Drug, against Gentamicin‐Induced Renal Damage in Rats

Dhanarajan

Abraham²,

Isaac

2006

Basic Clin Pharma Tox

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“…In this study, renal tissue MDA and NO levels were statistically high in AK treated group. Another study has shown that plasma NO levels and the nephrotoxivity was statistically high in gentamicin treated rats 39 .…”

Section: Discussionmentioning

confidence: 96%

Amikacin induced renal damage and the role of the antioxidants on neonatal rats

et al. 2016

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Amikacin (AK) is frequently used on the treatment of Gram-negative infections on neonates, but its usage is restricted because of nephrotoxicity. In this study, on neonatal rats, we aimed to investigate the effects of erythropoietin and vitamin E on AK induced nephrotoxicity. A total of 35 newborn Wistar Albino rats were divided into four groups: (1) injected with saline (serum physiological was administered to placebo controls), (2) injected with AK (1200 mg/kg), (3) injected with AK + vitamin E (150 mg/kg), (4) injected with AK + erythropoietin (EPO) (300 IU/kg/day). In renal tissue, AK levels were significantly high in all groups except the control. Tissue malondialdehyde (MDA) and nitric oxide (NO) levels were statistically higher in AK -treated group than the control. MDA and NO levels were significantly decreased with the administration of vitamin E and EPO. Glutathione peroxidase (GPX) levels were statistically low in AK group compared with the controls. The levels of GPX, in vitamin E group, were increased significantly. However, superoxide dismutase and catalase levels were not significantly different in none of the groups. Insulin-like growth factor-1 values in AK, EPO and vitamin E groups were significantly higher than the control group. Histomorphological changes such as tubular epithelial necrosis were seen in AK treated group. Histopathological improvements observed with EPO and vitamin E administration. AK nephrotoxicity is related to oxidative stress and is supported with biochemical and histopathological findings. Vitamin E and EPO, as antioxidants, can be useful renoprotective agents for ameliorating AK induced nephrotoxicity in neonates.ARTICLE HISTORY

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“…This effect was evident by the decline in renal MDA level, plasma urea, and plasma creatinine Two roles have been played by NO, physiological and pathophysiological roles (Carlstrom et al, 2009) and have a significant role in the function of renal tubular and renal hemodynamics regulation (Patel et al, 1999). Group treated with gentamicin revealed significant increment in the level of NO; acute renal failure occurred due to gentamicin is as a result of the free radical nature of NO (Nakas-Ićindić et al, 2005) Also, NO produced cytotoxic peroxynitrite, as a result of interaction with superoxide radical which resulting in tubular cells injury and renal failure (Christo et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Tribulus terrestris Against Gentamicin Mediated Nephrotoxicity, Oxidative Damage and Apoptosis in Male Rats

Kilany

Abdou

El-Beltagy

et al. 2020

Egyptian Academic Journal of Biological Sciences, B. Zoology

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Gentamicin (GNT) is an aminoglycoside antibiotic that is that's employed in the treatment of diverse forms of bacterial infections. However, gentamicin evoked renal toxicity. Therefore, the present experiment investigated the protecting impact of Tribulus terrestris and vitamin C against GNT-induced renal toxicity in albino rats. Six groups with eight rats each were used for this purpose; they included the normal control group that received physiological saline, the second group received Tribulus terrestris (200 mg kg orally), the third group received Vit. C (200 mg kg, orally). The fourth group injected gentamicin sulfate (100mg/kg I/P). The fifth group received Tribulus terrestris (200 mg kg orally) then injected with gentamicin sulfate, the sixth group received Vit. C (200 mg kg orally) then injected with gentamicin sulfate. The results showed that GNT significantly decreases serum levels of total protein and albumin. On the other hand, there were significant increases in levels of BUN, creatinine, and uric acid. Significant decreases were recorded in the levels of catalase (CAT) and superoxide dismutase (SOD). In addition, there was a substantial increase in the kidney contents of malondialdehyde (MDA). Serum levels of beta 2 microglobulin (β2M), nitric oxide (NO), and kidney injury molecule-1 (KIM-1) were substantially magnified but glutathione S transferase (GST) was significantly declined. Also, GNT caused histopathological changes and increased the expression of caspase-3 in the kidney tissues. However, administration of Tribulus terrestris as well as vitamin C, ameliorated the GNT-induced nephrotoxicity, perhaps via their antioxidant properties.

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Nitric Oxide in Gentamicin-induced Acute Tubular Necrosis in Rats

Cited by 7 publications

References 13 publications

Protective Effect of Ebselen, a Selenoorganic Drug, against Gentamicin‐Induced Renal Damage in Rats

Protective Effect of Ebselen, a Selenoorganic Drug, against Gentamicin‐Induced Renal Damage in Rats

Amikacin induced renal damage and the role of the antioxidants on neonatal rats

Protective Effects of Tribulus terrestris Against Gentamicin Mediated Nephrotoxicity, Oxidative Damage and Apoptosis in Male Rats

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