The renoprotective effect of l-carnitine in hypertensive rats is mediated by modulation of oxidative stress-related gene expression

Zambrano, Sonia; Blanca, Antonio J.; Ruiz-Armenta, María V.; Miguel-Carrasco, José L.; Revilla, Elisa; Santa-María, Consuelo; Mate, Alfonso; Vázquez, Carmen M.

doi:10.1007/s00394-012-0470-x

Cited by 44 publications

(27 citation statements)

References 51 publications

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“…The results of the present study, revealed that L-carnitine caused a significant decrease in testicular NF-κB expression and TNF-α and NO production. These effects are in line with previous studies which reported that L-carnitine can block the activation of NF-κB signaling pathway (Arafa, 2008;Zambrano et al, 2013). In addition, Ahmed et al (2014) stated that, Lcarnitine exhibited a powerful down-regulation of mRNA expression of TNF-α and this could be explained in part by its antioxidant activities (Thangasamy et al, 2009) and also by its glucocorticoid-like effect on the expression of pro-inflammatory cytokines (Schetter et al, 2010).…”

Section: Discussionsupporting

confidence: 88%

Protective Effect of L-Carnitine Against Cisplatin-Induced Testicular Toxicity in Rats

Eid

2016

Al-Azhar Journal of Pharmaceutical Sciences

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Testicular damage is one of the most deleterious effects whenever cisplatin (CIS) is employed in cancer chemotherapy. Oxidative stress has been proven to be involved in CIS induced toxicity. Thus, the current study explored the possible protective effect of L-carnitine (L-CAR) against cisplatin-induced testicular damage in rats. L-carnitine (500 mg/kg/day; i.p.) was injected for 15 days, whereas cisplatin (10 mg/kg; i.p.) was injected as a single dose at the 12 th day to induce testicular damage in adult male Sprague-Dawley rats. In the current study, CIS reduced the reproductive organs weight, sperm count, sperm motility and serum testosterone level beside a marked increase in the incidence of sperm abnormalities. In addition, it significantly increased malondialdehyde (MDA) and nitric oxide (NO) along with a marked decrease in testis reduced glutathione (GSH) content and superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities. At the same time, CIS administration resulted in marked elevation in tumor necrosis factor-α (TNF-α) production and nuclear factorkabba B (NF-κB) expression. These results were confirmed by histopathological examination. Treatment with L-CAR markedly attenuated cisplatin-induced injury by suppression of oxidative/nitrosative stress and inflammation, amendment of antioxidant defenses, as well as improvement of steroidogenesis, spermatogenesis and testicular histological features. This study suggests a novel therapeutic application for L-carnitine as a protective agent against cisplatininduced testicular toxicity through its promising anti-inflammatory and antioxidant capacities.

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Section: Discussionsupporting

confidence: 88%

Protective Effect of L-Carnitine Against Cisplatin-Induced Testicular Toxicity in Rats

Eid

2016

Al-Azhar Journal of Pharmaceutical Sciences

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“…The kidney plays an important role in the metabolism of LC (it reabsorbs more than 95% of filtered LC, apart from participating in LC synthesis). LC prevented hypertension-associated renal function damage by reversion of the alterations induced in the activities, protein, and gene expressions of the antioxidant enzymes GPx, GR, and SOD [162]. It also produced up-regulation of eNOS (the enzyme responsible for nitric oxide production), and down-regulation of the renin–angiotensin system (RAS) components and NADPH oxidase subunits NOX2 and NOX4 [163].…”

Section: Cylindrospermopsinmentioning

confidence: 99%

“…LC seemed to improve the oxidative stress response through a specific modulation of nuclear transcription factors kappa B (NF-κB), Nrf2, and peroxisome proliferator-activated receptor alpha (PPARα). Therefore, inhibition of NADPH oxidase led to less production of superoxide anions, which may increase the expression of Nrf2 and PPARα and decrease that of NF-κB, thus enhancing the antioxidant defense systems [162]. In this regard, LC anti-inflammatory properties have also been reported by inhibition of the NF-κB pathway by suppression of ROS formation [164,165].…”

Section: Cylindrospermopsinmentioning

confidence: 99%

Potential Use of Chemoprotectants against the Toxic Effects of Cyanotoxins: A Review

Guzmán-Guillén

Puerto

Gutiérrez-Praena

et al. 2017

Toxins

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Cyanobacterial toxins, particularly microcystins (MCs) and cylindrospermopsin (CYN), are responsible for toxic effects in humans and wildlife. In order to counteract or prevent their toxicity, various strategies have been followed, such as the potential application of chemoprotectants. A review of the main substances evaluated for this aim, as well as the doses and their influence on cyanotoxin-induced toxicity, has been performed. A search of the literature shows that research on MCs is much more abundant than research on CYN. Among chemoprotectants, antioxidant compounds are the most extensively studied, probably because it is well known that oxidative stress is one of the toxic mechanisms common to both toxins. In this group, vitamin E seems to have the strongest protectant effect for both cyanotoxins. Transport inhibitors have also been studied in the case of MCs, as CYN cellular uptake is not yet fully elucidated. Further research is needed because systematic studies are lacking. Moreover, more realistic exposure scenarios, including cyanotoxin mixtures and the concomitant use of chemoprotectants, should be considered.

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“…Advanced glycation-end products (AGEs) are a group of heterogeneous compounds formed through nonenzymatic oxidative and nonoxidative reactions between proteins and reactive carbonyl compounds derived from carbohydrates and lipids (Peppa and Raptis, 2008). L-carnitine has also been shown to prevent oxidative injury in renal and cardiovascular disease (Zambrano et al, 2013). The antioxidant potential of L-carnitine has been demonstrated (G€ ulçin, 2006;Fatouros et al, 2010), as well as its neuroprotective effect (Ribas et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

“…The antioxidant potential of L-carnitine has been demonstrated (G€ ulçin, 2006;Fatouros et al, 2010), as well as its neuroprotective effect (Ribas et al, 2014). L-carnitine has also been shown to prevent oxidative injury in renal and cardiovascular disease (Zambrano et al, 2013). Carnicor, a natural supplement of L-carnitine, is usually administered to most of the ESRD patients after each dialysis session to recover the amount lost during the dialysis process.…”

Section: Introductionmentioning

confidence: 99%

Influence of Carnicor, Venofer, and Sevelamer on the levels of genotoxic damage in end‐stage renal disease patients

Pastor

Coll

Rodríguez-Ribera

et al. 2018

Environ and Mol Mutagen

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End-stage renal disease (ESRD) patients present high levels of phosphorus and calcium products in serum, which contribute to the development of vascular calcification and cardiovascular disease, and to low iron stores and carnitine deficiency. For these reasons, ESRD patients are generally supplemented with different medicines. Some of the most common treatments include the use of Carnicor, Venofer, and Sevelamer drugs. Carnicor is used as a source of L-carnitine, acting as antioxidant and neuroprotector. Venofer is used to reduce the deficit of iron. Sevelamer is used to treat hyperphosphatemia. To determine the potential harmful genotoxic effects of these drugs, a group of 214 patients included in a hemodialysis program with different intakes of Carnicor, Venofer, and Sevelamer were evaluated. The levels of basal and oxidative DNA damage, as well as chromosomal damage, were measured in all individuals using the comet and the micronucleus assays, respectively. Our results indicate that Carnicor administration was associated with low but significant increases in the frequency of basal DNA damage and micronuclei. Environ. Mol. Mutagen. 59:302-311, 2018. © 2018 Wiley Periodicals, Inc.

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The renoprotective effect of l-carnitine in hypertensive rats is mediated by modulation of oxidative stress-related gene expression

Abstract: Our results might support the use of LC to prevent hypertension-induced renal damage.

Cited by 44 publications

References 51 publications

Protective Effect of L-Carnitine Against Cisplatin-Induced Testicular Toxicity in Rats

Protective Effect of L-Carnitine Against Cisplatin-Induced Testicular Toxicity in Rats

Potential Use of Chemoprotectants against the Toxic Effects of Cyanotoxins: A Review

Influence of Carnicor, Venofer, and Sevelamer on the levels of genotoxic damage in end‐stage renal disease patients

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