PROTECTIVE EFFECTS OF <scp>l</scp>‐CARNITINE ON MYOGLOBINURIC ACUTE RENAL FAILURE IN RATS

Aydoğdu, Nurettin; Atmaca, Gülizar; Yalçın, Ömer; Taskiran, Recep; Taştekin, Ebru; Kaymak, Kadir

doi:10.1111/j.1440-1681.2006.04336.x

Cited by 61 publications

(59 citation statements)

References 36 publications

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“…The protective role of nitric oxide (NO) in different models of renal failure has been documented [136], including glycerol-induced renal failure [137] and nephrolithiasis induced by ethylene glycol [138]. These studies have demonstrated that levels of NO are decreased in glycerol-induced renal failure and different agents have shown to produce renoprotection by increasing the NO production [120].…”

Section: Pomegranate (Punica Granatum L)mentioning

confidence: 99%

Prevention of Nephropathy by Some Natural Sources of Antioxidants

Azab¹,

Albasha²,

Elsayed³

2017

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Nephrotoxicity is one of the most common kidney problems and occurs when the body is exposed to a drug or toxin. Natural sources of antioxidants may serve as a vital source of potentially useful new compounds for the development of an effective therapy to combat a variety of kidney problems. Natural antioxidants have a variety of biochemical actions such as inhibition of reactive oxygen species production, scavenging of free radicals. The present review aims to summarize the recent articles which studied some of the nephrotoxic agents, and alleviation of nephrotoxicity using of some natural products possessing antioxidant properties. Our review shows the oxidative damage and renal disorders induced in human and experimental animals by nephrotoxic agents such as gentamicin, alcohol, nicotine, adenine, glycerol, ethylene glycol, sodium nitrite, mercuric chloride, AlCl 3 , lead acetate, carbon tetrachloride (CCl 4 ), furosemide, carbendazim, diazinon, heat stress, and γ-radiation. Also, nephrotic disorders caused in diabetic rats, patients, cirrhotic ascetic patients, and ischemia-reperfusion. Administration of natural sources of antioxidants such as curcumin, garlic, fenugreek, parsley, peppermint, pomegranate, propolis, olive leaves, rosemary, and sesame attenuated both physiological and histopathological alterations induced in the kidney by the nephrotoxic agent and certain diseases. The nephroprotective effect of the former natural sources of antioxidants may be due to the enhancement of antioxidant activity and inhibition of tissue lipid peroxidation. It can be concluded that administration of curcumin, garlic, fenugreek, parsley, peppermint, pomegranate, propolis, olive leaves, rosemary, and sesame showed a remarkable kidney protection against nephrotoxic agents, and diseases induced renal dysfunctions in human and experimental animals. So, the present study recommended that the consumption of these natural sources of antioxidants may be useful for human exposure to nephrotoxic agents and patients who suffer from renal diseases.

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Section: Pomegranate (Punica Granatum L)mentioning

confidence: 99%

Prevention of Nephropathy by Some Natural Sources of Antioxidants

Azab¹,

Albasha²,

Elsayed³

2017

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“…The effects of LC on the metabolism of tissues in organs such as the heart [15], brain [16], and liver [13] have been studied widely. Current reports suggest that LC may play a significant role in balancing antioxidative systems and has an antiperoxidative effect on some tissues [17,18]. The aim of this study was to investigate possible protective effects of exogenous LC supplementation on CDDP-induced oxidative organ injuries, and its effects on the levels of antioxidant enzymes and lipid peroxidation, as well as histological changes.…”

Section: Introductionmentioning

confidence: 99%

Protective effect of L-carnitine against cisplatin-induced liver and kidney oxidant injury in rats

et al. 2009

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AbstractThe present study was designed to investigate the protective effects of L-carnitine (LC) on changes in the levels of lipid peroxidation and endogenous antioxidants induced by cisplatin (cis-diamminedichloroplatinum II, CDDP) in the liver and kidney tissues of rats. Twenty-four Sprague Dawley rats were equally divided into four groups of six rats each: control, cisplatin, L-carnitine, and L-carnitine plus cisplatin. The degree of protection produced by L-carnitine was evaluated by determining the level of malondialdehyde (MDA). The activity of glutathione (GSH), glutathione peroxidase (GSH-Px), glutathione S-transferase (GST), and superoxide dismutase (SOD) were estimated from liver and kidney homogenates, and the liver and kidney were histologically examined as well. L-carnitine elicited significant liver and kidney protective activity by decreasing the level of lipid peroxidation (MDA) and elevating the activity of GSH, GSHPx, GST, and SOD. Furthermore, these biochemical observations were supported by histological findings. In conclusion, the present study indicates a significant role for reactive oxygen species (ROS) and their relation to liver and kidney dysfunction, and points to the therapeutic potential of LC in CDDP-induced liver and kidney toxicity.

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“…Besides, carnitine also prevents increase in MDA levels in IR damage in several organs and in renal damage caused by several agents. 23,24,28,29,32 According to all these findings, it is possible to say carnitine prevents lipid peroxidation in infrarenal AIR models in doserelated fashion and this effect of carnitine also contributes in the prevention of possible renal damage.…”

Section: Discussionmentioning

confidence: 99%

“…[23][24][25][26][27] Carnitine also decreases renal damage developed because of several agents. [28][29][30][31][32] Although carnitine has been shown to decrease lung damage in infrarenal AIR models, effect of carnitine on renal damage in this model has not been studied. 33 This study was designed to investigate the effect of carnitine, an antioxidant agent, in rat models in decreasing IR damage developing in kidneys following infrarenal aortic occlusion-reperfusion and in preventing kidneys from this kind of damage.…”

Section: Introductionmentioning

confidence: 99%

The Role of Carnitine in Preventing Renal Damage Developed as a Result of Infrarenal Aortic Ischemia–Reperfusion

et al. 2011

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Background: This study was designed to use carnitine for preventing deposition of end products of lipid peroxidation in rat models in the prevention of ischemia-reperfusion (IR) damage frequently seen following operations of infrarenal abdominal aorta (AA). Methods: Forty male rats of Sprague-Dawley type were evenly (n = 8) randomized to five groups: sham laparotomy (SHAM), carnitine control (CC), aortic IR (AIR), AIR + low-dose carnitine (AIR+LDC), and AIR + high-dose carnitine (AIR+HDC). Results: Compared to other groups, serum creatinine levels of AIR group were significantly higher. Also tissue malondialdehyde (MDA) levels of AIR group were significantly higher compared to SHAM, CC, and AIR+HDC groups. In histopathological examination, although tubular necrosis atrophy and tubular degeneration observed in AIR group showed regression with low-dose carnitine, tubular necrosis atrophy, tubular degeneration, glomerular damage, and vascular congestion thrombosis decreased with high-dose carnitine. Total score of histological damage was significantly higher in AIR, AIR+LDC, and AIR+HDC groups compared to SHAM and CC groups. Moreover, total score of histological damage was significantly lower in AIR+HDC group than AIR+LDC group. Conclusions: In this study, we showed carnitine can partially prevent renal damage in infrarenal AIR models of rats. This result may open new prospects to us in the prevention of renal IR damage during surgery of aorta.

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PROTECTIVE EFFECTS OF l‐CARNITINE ON MYOGLOBINURIC ACUTE RENAL FAILURE IN RATS

Cited by 61 publications

References 36 publications

Prevention of Nephropathy by Some Natural Sources of Antioxidants

Prevention of Nephropathy by Some Natural Sources of Antioxidants

Protective effect of L-carnitine against cisplatin-induced liver and kidney oxidant injury in rats

The Role of Carnitine in Preventing Renal Damage Developed as a Result of Infrarenal Aortic Ischemia–Reperfusion

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