Effect of Acetyl-L-Carnitine on Leukemia L1210 Resistant to Mitoxantrone

Niang, Mohamed; Mĕlka, M

doi:10.14712/18059694.2019.125

Cited by 2 publications

(2 citation statements)

References 17 publications

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“…L-CAR as a monotherapy had an inhibitory effect on tumor volume. 58 Niang and Melka 59 0.05: significant a using ANOVA followed by Tukey-Kramer as a post ANOVA test.a: significantly different from the control group. TAM (10 mg/kg, i.p.)…”

Section: Discussionmentioning

confidence: 99%

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Modulatory effects of l-carnitine on tamoxifen toxicity and oncolytic activity

et al. 2013

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The aim of this study was to investigate the protective effect of l-carnitine (l-CAR) in tamoxifen (TAM)-induced toxicity and antitumor activity. Adult female rats were randomly divided into four groups. Group I was served as control, groups II and III were treated with TAM (10 mg/kg, periorally) and l-CAR (300 mg/kg, intraperitoneally), respectively, while group IV was treated with both compounds. The treatment continued daily for 28 days. Administration of TAM resulted in significant increase in serum lipid profiles, liver enzymes, and bilirubin level. TAM produced a significant increase in lipid peroxides (LPO) level and nonsignificant change in nitrogen oxide (NO( x)) level accompanied with significant decrease in superoxide dismutase (SOD) activity of hepatic and uterus tissues and significant decrease in glutathione (GSH) content of uterus tissue. Administration of l-CAR for 1 h prior to TAM treatment decreased serum lipids and liver enzymes significantly and significantly increased SOD activity in liver and uterus tissues compared with TAM-treated group. Furthermore, it restored LPO and GSH levels and increased NO( x) level in uterus tissue. DNA fragmentation and the apoptotic marker, caspase-3, were not detected in the liver of all treated groups. Histopathologically, alterations in the liver and uterus structures after TAM treatment, which was attenuated after l-CAR administration. The antitumor effect and survival of the combined treatment of Ehrlich ascites carcinoma (EAC)-bearing mice was less than each one alone. l-CAR interestingly increased survival rate of EAC-bearing mice more than TAM-treated group. In conclusion, l-CAR has beneficial effects regarding TAM toxicity; however, it interferes with its antitumor effect.

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Section: Discussionmentioning

confidence: 99%

“…l -CAR as a monotherapy had an inhibitory effect on tumor volume. 58 Niang and Melka 59 reported that acetyl- l -CAR prolonged the survival of mice with the ascitic form of leukemia L1210 and l -CAR treatment prolonged survival of rats with adriamycin-induced heart failure by improving the myocardial metabolism of fatty acids. 60…”

Section: Discussionmentioning

confidence: 99%

Modulatory effects of l-carnitine on tamoxifen toxicity and oncolytic activity

et al. 2013

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Biochemical and Pharmacological Effects of Mitoxantrone and Acetyl-L-Carnitine in Mice with a Solid Form of Ehrlich Tumour

Niang¹,

Soukup²,

Živný

et al. 2011

Chemotherapy

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Background: Dysfunction of the carnitine system in non-tumour tissue following anticancer therapy has been reported. In this setting, supplementation with carnitine derivatives might increase the general metabolic activity of normal cells so that they might better withstand the adverse effects of chemotherapy aimed at tumour cells. Here we investigated the effect of acetyl-L-carnitine (ALC) alone and in combination with the antineoplastic agent mitoxantrone (MX) in an animal cancer model. Methods: The effects of MX and MX-ALC were assessed based on gain or loss of body weight and on local growth of a solid form of Ehrlich tumour inoculated into mice. We also performed biochemical analyses like serum activities of some enzymes signalling the functioning of the liver, aspartate aminotransferase (AST), and alanine aminotransferase (ALT). Total protein, albumin and bilirubin were also determined in serum. Under favourable conditions, the Ehrlich tumour readily forms metastases, and this is the reason why we performed histological studies of samples of both the liver and heart in order to identify changes that may have mediated the observed effect of the treatment. In addition to those studies, the survival time of treated animals against controls was also noted. Results: MX monotherapy was associated with lower body weight gain, fewer metastases, smaller tumour size, and lower dissemination. ALC alone promoted survival, but had no potentiating effect on MX therapy in terms of survival. Serum biochemistry changes associated with MX-ALC treatment consisted of a significant (p < 0.05) increase in AST with MX at 6 or 9 mg·kg^–1 plus ALC 200 mg·kg^–1 and a significant (p < 0.05) reduction in total protein compared to the corresponding MX group; serum albumin and bilirubin remained unchanged. Conclusion: ALC in combination with MX, regardless of the dose of MX, led to higher occurrences of metastases with dissemination to the kidneys, lungs, heart, and mediastinum compared to MX treatment alone. These histological findings indicate that ALC is inappropriate to combine with MX in the treatment of a solid cancer. The protective effect of ALC in combination therapy with the cytostatic drug MX was not supported in this study by our findings that the agent did not improve the therapeutic outcomes of MX therapy.

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Effect of Acetyl-L-Carnitine on Leukemia L1210 Resistant to Mitoxantrone

Cited by 2 publications

References 17 publications

Modulatory effects of l-carnitine on tamoxifen toxicity and oncolytic activity

Modulatory effects of l-carnitine on tamoxifen toxicity and oncolytic activity

Biochemical and Pharmacological Effects of Mitoxantrone and Acetyl-L-Carnitine in Mice with a Solid Form of Ehrlich Tumour

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