Action of vinca alraloides on calcium movements through mitochondrial membrane

Tarı, Canan; Fournier, Nancy; Briand, Claudette; Ducet, Gaston; Crevat, A.

doi:10.1016/0031-6989(86)90147-5

Cited by 25 publications

(8 citation statements)

References 3 publications

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“…However, previous studies have shown a differential effect for VBL on bone marrow cell as compared to fetal liver cells [ 17 ]. Additionally, VBL was shown to alter calcium homeostasis via mitochondrial membranes leading to substantiated cyto-toxicity as compared to VCR [ 38 ].…”

Section: Discussionmentioning

confidence: 99%

Assessment of genotoxicity of vincristine, vinblastine and vinorelbine in human cultured lymphocytes: a comparative study

Mhaidat

Al-Zoubi

Khabour

et al. 2016

Balkan Journal of Medical Genetics

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Vincristine (VCR), vinblastine (VBL) and vinorelbine (VRL) are anticancer agents from the Vinca alkaloid family that have the potential to induce genotoxic effect. The aim of the present study was to compare the genotoxic effect of VCR, VBL and VRL. Levels of 8-hydroxy-2-deoxy guanosine (8-OHdG) and sister chromatid exchanges (SCEs) were measured in cultured human blood lymphocytes treated with VCR, VBL and VRL at concentrations of 0.01 and 0.1 μg/mL. Results showed that VCR, VBL and VRL significantly increased the 8-OHdG levels (p <0.05), whereas it did not cause a significant increase in the frequencies of SCEs in human blood lymphocytes as compared to controls. On the other hand, all three agents significantly increased cells mitotic index (p <0.05). At both tested concentrations, the magnitude of the increase in 8-OHdG was VBL>VCR>VRL. In conclusion, VCR, VBL and VRL induce DNA damage as indicated by the increase in the 8-OHdG biomarker but with different magnitude.

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Section: Discussionmentioning

confidence: 99%

Assessment of genotoxicity of vincristine, vinblastine and vinorelbine in human cultured lymphocytes: a comparative study

Mhaidat

Al-Zoubi

Khabour

et al. 2016

Balkan Journal of Medical Genetics

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“…Vinca alkaloids can alter calcium homeostasis through the dysregulation and structural modification of mitochondria, decreasing the amount and rate of calcium uptake and efflux ( Tari et al, 1986 ). These changes induce increased neuronal excitability and impaired glial function.…”

Section: Vinca Alkaloidsmentioning

confidence: 99%

Long-Term Effects, Pathophysiological Mechanisms, and Risk Factors of Chemotherapy-Induced Peripheral Neuropathies: A Comprehensive Literature Review

et al. 2017

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Neurotoxic anticancer drugs, such as platinum-based anticancer drugs, taxanes, vinca alkaloids, and proteasome/angiogenesis inhibitors are responsible for chemotherapy-induced peripheral neuropathy (CIPN). The health consequences of CIPN remain worrying as it is associated with several comorbidities and affects a specific population of patients already impacted by cancer, a strong driver for declines in older adults. The purpose of this review is to present a comprehensive overview of the long-term effects of CIPN in cancer patients and survivors. Pathophysiological mechanisms and risk factors are also presented. Neurotoxic mechanisms leading to CIPNs are not yet fully understood but involve neuronopathy and/or axonopathy, mainly associated with DNA damage, oxidative stress, mitochondria toxicity, and ion channel remodeling in the neurons of the peripheral nervous system. Classical symptoms of CIPNs are peripheral neuropathy with a “stocking and glove” distribution characterized by sensory loss, paresthesia, dysesthesia and numbness, sometimes associated with neuropathic pain in the most serious cases. Several risk factors can promote CIPN as a function of the anticancer drug considered, such as cumulative dose, treatment duration, history of neuropathy, combination of therapies and genetic polymorphisms. CIPNs are frequent in cancer patients with an overall incidence of approximately 38% (possibly up to 90% of patients treated with oxaliplatin). Finally, the long-term reversibility of these CIPNs remain questionable, notably in the case of platinum-based anticancer drugs and taxanes, for which CIPN may last several years after the end of anticancer chemotherapies. These long-term effects are associated with comorbidities such as depression, insomnia, falls and decreases of health-related quality of life in cancer patients and survivors. However, it is noteworthy that these long-term effects remain poorly studied, and only limited data are available such as in the case of bortezomib and thalidomide-induced peripheral neuropathy.

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“…In 2006, Siau and colleagues demonstrated that vincristine-caused neuropathic pain, an evident mechanical allodynia and mechanical hyperalgesia in rats, was significantly improved by different Ca 2+ regulators (TMB-8, Quin-2, EGTA and EGTA-AM) [ 10 ]. In fact, it was demonstrated that vincristine is able to affect Ca 2+ movement through the mitochondrial membrane, reducing both the amount and rate of Ca 2+ uptake and decreasing Ca 2+ efflux [ 112 ]. Alterations in the mitochondrial Ca 2+ uptake would affect the spatio-temporal changes of Ca 2+ concentration, alter Ca 2+ signaling, Ca 2+ signals [ 113 ], and regulate Ca 2+ -dependent processes as increased exocytosis of neurotransmitters [ 114 ].…”

Section: Vincristinementioning

confidence: 99%

Mitochondrial Dysfunction in Chemotherapy-Induced Peripheral Neuropathy (CIPN)

Canta

Pozzi

Carozzi

2015

Toxics

155

129

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The mitochondrial dysfunction has a critical role in several disorders including chemotherapy-induced peripheral neuropathies (CIPN). This is due to a related dysregulation of pathways involving calcium signalling, reactive oxygen species and apoptosis. Vincristine is able to affect calcium movement through the Dorsal Root Ganglia (DRG) neuronal mitochondrial membrane, altering its homeostasis and leading to abnormal neuronal excitability. Paclitaxel induces the opening of the mitochondrial permeability transition pore in axons followed by mitochondrial membrane potential loss, increased reactive oxygen species generation, ATP level reduction, calcium release and mitochondrial swelling. Cisplatin and oxaliplatin form adducts with mitochondrial DNA producing inhibition of replication, disruption of transcription and morphological abnormalities within mitochondria in DRG neurons, leading to a gradual energy failure. Bortezomib is able to modify mitochondrial calcium homeostasis and mitochondrial respiratory chain. Moreover, the expression of a certain number of genes, including those controlling mitochondrial functions, was altered in patients with bortezomib-induced peripheral neuropathy.

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Action of vinca alraloides on calcium movements through mitochondrial membrane

Cited by 25 publications

References 3 publications

Assessment of genotoxicity of vincristine, vinblastine and vinorelbine in human cultured lymphocytes: a comparative study

Assessment of genotoxicity of vincristine, vinblastine and vinorelbine in human cultured lymphocytes: a comparative study

Long-Term Effects, Pathophysiological Mechanisms, and Risk Factors of Chemotherapy-Induced Peripheral Neuropathies: A Comprehensive Literature Review

Mitochondrial Dysfunction in Chemotherapy-Induced Peripheral Neuropathy (CIPN)

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