The Effect of L-Carnitine on Oxidative Stress Responses of Experimental          Contrast-Induced Nephropathy in Rats

Boyacıoğlu, Murat; Turgut, Hülya; Akgüllü, Çağdaş; Eryılmaz, Ufuk; Kum, Cavit; Onbasili, Osman Alper

doi:10.1292/jvms.13-0202

Cited by 36 publications

(40 citation statements)

References 54 publications

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“…Treatment of carnitine significantly reduced MDA and activate the antioxidant status which consistent with Boyacioglu et al, (2014) who stated that renal and serum MDA decreased and GSH increased after carnitine treatment in contrast mediainduced acute renal insufficiency. It has been suggested that improved GSH levels after L-carnitine addition in rats may also be attributed to increased nicotinamide adenine dinucleotide phosphate hydrogen (NADPH) generation through increased fatty acid metabolism (Thangasamy et al .,2009).…”

Section: Discussionsupporting

confidence: 87%

Impact of L-Carnitine on Bisphenol A-Induced Kidney Damage in Rats

Edres¹,

Taha²,

Mandour³

et al. 2018

AJVS

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Key words:Bisphenol A, L-carnitine, Malondialdehyde, Hydronephrosis, GlutathioneThe present study aimed to explore the protective effects of L-carnitine on the oxidative stress induced by Bisphenol A (BPA) in rat kidneys. Forty male adult rats were allocated into four groups (10 rats each); placebo, BPA (50 mg/kg bwt per os), Lcarnitine (500 mg/kg bwt i.p), and the BPA/L-carnitine-treated group. After 70 days, blood and kidneys were collected for measurement of renal function, oxidative/antioxidative status, histopathological analyses, and gene expression of nrf2. BPA significantly increased serum urea and carnitine levels suggesting renal damage evidenced by hydropic degenerative changes and hydronephrosis. The level of malondialdehyde (MDA) in kidney was elevated along with decline in renal total antioxidant capacity (TAC) and reduced glutathione (GSH) concentrations following challenged with BPA. Notably, the expression of nrf2 mRNA transcript in kidney tissues was down-regulated after BPA-induced toxicity. L-carnitine treatment ameliorates the damaged effects of BPA on kidneys as indicated by low levels of serum urea and carnitine, and renal MDA. Further, L-carnitine enhances the antioxidants (TAC, and GSH), with up-regulation of nrf2 expression in kidney tissues. Our results suggest the renoprotective activity of L-carnitine in BPA-induced kidney injuries through induction of antioxidant system and modulation of oxidative stress.

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Section: Discussionsupporting

confidence: 87%

Impact of L-Carnitine on Bisphenol A-Induced Kidney Damage in Rats

Edres¹,

Taha²,

Mandour³

et al. 2018

AJVS

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“…Many disease-related renal fibroblasts originate from transdifferentiated tubular epithelia cells at the sites of injury [18], and L-carnitine has been studied for its protective effects against renal oxidative injury and fibrotic process [13,19], so we set out to determine whether L-carnitine could alleviate COM-induced cell dedifferentiation.…”

Section: L-carnitine Protects Mdck Cells From Com-induced Dedifferentmentioning

confidence: 99%

L-Carnitine Protects Renal Tubular Cells Against Calcium Oxalate Monohydrate Crystals Adhesion Through Preventing Cells From Dedifferentiation

Li¹,

Wu²,

Duan³

et al. 2016

Kidney Blood Press Res

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Background/Aims: The interactions between calcium oxalate monohydrate (COM) crystals and renal tubular epithelial cells are important for renal stone formation but still unclear. This study aimed to investigate changes of epithelial cell phenotype after COM attachment and whether L-carnitine could protect cells against subsequent COM crystals adhesion. Methods: Cultured MDCK cells were employed and E-cadherin and Vimentin were used as markers to estimate the differentiate state. AlexaFluor-488-tagged COM crystals were used in crystals adhesion experiment to distinguish from the previous COM attachment, and adhesive crystals were counted under fluorescence microscope, which were also dissolved and the calcium concentration was assessed by flame atomic absorption spectrophotometry. Results: Dedifferentiated MDCK cells induced by transforming growth factor β1 (TGF-β1) shown higher affinity to COM crystals. After exposure to COM for 48 hours, cell dedifferentiation were observed and more subsequent COM crystals could bind onto, mediated by Akt/GSK-3β/Snail signaling. L-carnitine attenuated this signaling, resulted in inhibition of cell dedifferentiation and reduction of subsequent COM crystals adhesion. Conclusions: COM attachment promotes subsequent COM crystals adhesion, by inducing cell dedifferentiation via Akt/GSK-3β/Snail signaling. L-carnitine partially abolishes cell dedifferentiation and resists COM crystals adhesion. L-carnitine, may be used as a potential therapeutic strategy against recurrence of urolithiasis.

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“…and multiple organ damage by the contrast agent. 28 Our research also manifested that the LC reduced eryptosis by inhibiting oxidative stress. It is necessary to probe the best concentration and effective acting time.…”

Section: Discussionmentioning

confidence: 54%

L-Carnitine inhibits eryptosis induced by uremic serum and the related mechanisms

Sun

Liu

et al. 2015

Renal Failure

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Objective: To investigate whether L-carnitine (LC) inhibits eryptosis induced by uremic serum and the related mechanism. Methods: One percent erythrocyte suspension was cultured by three kinds of mediums in vitro, which was included in the control group (Group C, phosphate buffered saline [PBS]), the uremic serum group (Group U, 30% uremic serum + 70% PBS) and the LC group (Group L, 30% uremic serum + 70% PBS + 200 umol/L LC), respectively. Erythrocytes were collected at 24 and 48 h, respectively. Phosphatidylserine (PS) was estimated from Annexin-V-binding and reactive oxygen species (ROS) by flow cytometry, glutathione (GSH) was estimated from Enzyme linked immunosorbent assays (ELISA) by Microplate reader. Results: Eryptosis in Group C increased as the incubating time extended (3.43 ± 0.37 at 24 h, 4.21 ± 0.44 at 48 h). Eryptosis increased in Group U compared with Group C (6.5 1 ± 0.71 at 24 h, p50.01; 8.55 ± 0.76 at 48 h, p50.01), while decreased in Group L compared with Group U (5.80 ± 0.69 at 24 h, p50.05; 7.87 ± 0.76 at 48 h, p50.05). Meanwhile, ROS of erythrocytes increased in Group U compared with Group C (33.12 ± 1.61 versus 14.83 ± 2.22 at 24 h, p50.01; 42.06 ± 1.81 versus 20.94 ± 1.78 at 48 h, p50.01), and GSH decreased in Group U compared with Group C (25.66 ± 0.32 versus 31.27 ± 0.38 at 24 h, p50.01; 8.53 ± 0.59 versus 17.29 ± 0.54 at 48 h, p50.01). ROS of erythrocytes decreased in Group L compared with Group C (26.29 ± 1.69 at 24 h, p50.01; 36.21 ± 2.00 at 48 h, p50.01). GSH increased in Group L compared with Group U (27.54 ± 0.60 at 24 h, p50.01; 15.18 ± 0.42 at 48 h, p50.01). Conclusions: LC inhibits eryptosis induced by uremic serum, which possibly relates to oxidative stress in part.

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The Effect of L-Carnitine on Oxidative Stress Responses of Experimental Contrast-Induced Nephropathy in Rats

Cited by 36 publications

References 54 publications

Impact of L-Carnitine on Bisphenol A-Induced Kidney Damage in Rats

Impact of L-Carnitine on Bisphenol A-Induced Kidney Damage in Rats

L-Carnitine Protects Renal Tubular Cells Against Calcium Oxalate Monohydrate Crystals Adhesion Through Preventing Cells From Dedifferentiation

L-Carnitine inhibits eryptosis induced by uremic serum and the related mechanisms

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