l-Carnitine inhibits cisplatin-induced injury of the kidney and small intestine

Chang, Baojun; Nishikawa, Manabu; Sato, Eisuke F.; Utsumi, Kozo; Inoue, Masayasu

doi:10.1016/s0003-9861(02)00342-9

Cited by 159 publications

(121 citation statements)

References 51 publications

Supporting

Mentioning

111

Contrasting

Unclassified

Order By: Relevance

“…In fact, mitochondrial dysfunction caused by free fatty acids was inhibited by carnitine. 21,22 Furthermore, carnitine strongly inhibited the destruction of the mitochondrial membrane and mitochondrial dysfunction-induced injury in various types of cells. [22][23][24][25] These findings indicate that oxidative stress elicited from abnormally accumulated copper increased the amount of free fatty acids, thereby inducing mitochondrial dysfunction, resulting in cell death and enhanced secondary generation of ROS, which are significantly inhibited by carnitine treatment.…”

Section: Discussionmentioning

confidence: 99%

“…19,20 We previously reported that L-carnitine effectively prevents mitochondrial injury deriving from oxidative damage in vivo. 21 In fact, there are also several reports showing that carnitine effectively inhibited mitochondrial injury induced by oxidative stress and mitochondriadependent apoptosis. [22][23][24][25] It is thought that carnitine shows its protective effects on mitochondria and on whole cells by inhibiting free fatty acid-induced mitochondrial membrane damage and/or its secondary effects.…”

mentioning

confidence: 99%

See 1 more Smart Citation

L‐carnitine inhibits hepatocarcinogenesis via protection of mitochondria

Chang

Nishikawa

Nishiguchi

et al. 2004

Intl Journal of Cancer

Self Cite

View full text Add to dashboard Cite

Hepatocellular carcinoma is usually preceded by chronic inflammation. However, the molecular mechanism in hepatocarcinogenesis is not well known. Recently, we reported that mitochondrial dysfunction plays an important role in hepatocarcinogenesis via the production of free radicals. Furthermore, we proved that L-carnitine effectively protects mitochondrial function in vivo. Therefore, we investigated whether long-term administration of L-carnitine could prevent hepatitis and subsequent hepatocellular carcinoma in Long-Evans Cinnamon rats that are often analyzed as a model of hepatocarcinogenesis. The results indicated that oxidative stress elicited from abnormally accumulated copper increased the amount of free fatty acids, thereby inducing mitochondrial dysfunction, resulting in cell death and enhanced secondary generation of reactive oxygen species, which were significantly inhibited by carnitine treatment. Finally, the occurrence of placental glutathione S-transferase-positive foci as a marker for preneoplastic lesions and hepatocarcinogenesis were significantly inhibited by L-carnitine. These facts suggest that mitochondrial injury plays an essential role in the development of hepatocarcinogenesis and that the clinical use of carnitine has excellent therapeutic potential in individuals with chronic hepatitis.

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

L‐carnitine inhibits hepatocarcinogenesis via protection of mitochondria

Chang

Nishikawa

Nishiguchi

et al. 2004

Intl Journal of Cancer

Self Cite

View full text Add to dashboard Cite

show abstract

“…It has been reported that acetyl-L-carnitine effectively prevents mitochondrial injury resulting from oxidative damage in vivo (Chang et al, 2002). Due to their intrinsic interaction with the bioenergetic processes, carnitines play important roles in mitochondrialrelated functions and it has been suggested that carnitines may have neuroprotective actions in conditions of mitochondrial dysfunction and oxidative stress and possibly in neurodegenerative disorders, such as Parkinson's disease (Beal, 2004).…”

Section: Introductionmentioning

confidence: 99%

Acetyl l-carnitine protects motor neurons and Rohon-Beard sensory neurons against ketamine-induced neurotoxicity in zebrafish embryos

Cuevas

Trickler

Guo

et al. 2013

Neurotoxicology and Teratology

View full text Add to dashboard Cite

Ketamine, a non-competitive antagonist of N-methyl-D-aspartate (NMDA) type glutamate receptors is commonly used as a pediatric anesthetic. Multiple studies have shown ketamine to be neurotoxic, particularly when administered during the brain growth spurt. Previously, we have shown that ketamine is detrimental to motor neuron development in the zebrafish embryos. Here, using both wild type (WT) and transgenic (hb9:GFP) zebrafish embryos, we demonstrate that ketamine is neurotoxic to both motor and sensory neurons. Drug absorption studies showed that in the WT embryos, ketamine accumulation was approximately 0.4% of the original dose added to the exposure medium. The transgenic embryos express green fluorescent protein (GFP) localized in the motor neurons making them ideal for evaluating motor neuron development and toxicities in vivo. The hb9:GFP zebrafish embryos (28 h post fertilization) treated with 2 mM ketamine for 20 h demonstrated significant reductions in spinal motor neuron numbers, while co-treatment with acetyl L-carnitine proved to be neuroprotective. In whole mount immunohistochemical studies using WT embryos, a similar effect was observed for the primary sensory neurons. In the ketamine-treated WT embryos, the number of primary sensory Rohon-Beard (RB) neurons was significantly reduced compared to that in controls. However, acetyl L-carnitine co-treatment prevented ketamine-induced adverse effects on the RB neurons. These results suggest that acetyl L-carnitine protects both motor and sensory neurons from ketamine-induced neurotoxicity.

show abstract

“…It was reported that death of tubular cells by necrosis could recruit inflammatory cells including macrophage and leukocytes [26] . Moreover, loss of renal endothelial cells and renal dysfunction in cisplatin nephrotoxicity have been reported [17] , and might be the cause of the extravasation of RBCs, congestion of glomerular and dilatation of peritubular capillaries seen in group II.…”

Section: Discussionmentioning

confidence: 99%

Role of Mesenchymal Stem Cells Versus their Conditioned Medium on Cisplatin-Induced Acute Kidney Injury in Albino Rat. A Histological and Immunohistochemical Study

Zaher

Shawarby

Hammouda

et al. 2017

Egyptian Journal of Histology

View full text Add to dashboard Cite

Introduction: Acute kidney injury (AKI) is a syndrome of rapidly declining renal function. Cisplatin nephrotoxicity is a major cause of AKI in about one third of patients under cisplatin treatment. Stem cell therapy have been suggested as a protective measure against cisplatin-induced AKI. The conditioned medium of the stem cells (serum-free culture medium) has been also found to minimize renal injury and might develop a new therapeutic strategy that avoids stem cells administration. Aim of the Study:This study was conducted to compare the effect of intravenous injection of bone marrow-derived mesenchymal stem cells (BMSCs) versus their conditioned medium (CM) in minimizing the cisplatin-induced acute renal injury. Material and Methods: Sixty adult female albino rats were divided into 4 main groups. Group (I) served as a control group, Group (II) (cisplatin treated group) that were subdivided into two subgroups IIa and IIb, Group (III) (BMSCstreated group) and Group (IV) (CM-treated group). Five young male rats were additionally used for obtaining the BMSCs. Rats of all groups were sacrificed on 4th day of the experiment, except for the rats of subgroup (IIa (which were sacrificed after one day of cisplatin administration. Renal specimens were prepared for histological and immunohistochemical techniques. Morphometrical studies and statistical analysis were performed. Results: Treatment by BMSCs resulted in obvious improvement of renal structure with significant increase in Proliferating Cell Nuclear Antigen (PCNA). However, conditioned medium (CM) was less effective in treatment of acute AKI. Conclusion: BMSCs administration is preferable than their CM in reversing the acute structural damage of the kidney induced by cisplatin.

show abstract

l-Carnitine inhibits cisplatin-induced injury of the kidney and small intestine

Cited by 159 publications

References 51 publications

L‐carnitine inhibits hepatocarcinogenesis via protection of mitochondria

L‐carnitine inhibits hepatocarcinogenesis via protection of mitochondria

Acetyl l-carnitine protects motor neurons and Rohon-Beard sensory neurons against ketamine-induced neurotoxicity in zebrafish embryos

Role of Mesenchymal Stem Cells Versus their Conditioned Medium on Cisplatin-Induced Acute Kidney Injury in Albino Rat. A Histological and Immunohistochemical Study

Contact Info

Product

Resources

About