Oxidative stress response induced by chemotherapy in leukemia treatment (Review)

Zhang, Jin; Lei, Wen; Chen, Xiaohui; Wang, Shibing; Qian, W.

doi:10.3892/mco.2018.1549

Cited by 45 publications

(45 citation statements)

References 82 publications

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“…Also, other examinations showed that both drugs induce lipid peroxidation and decrease GSH in isolated neurons. Our results are consistent with previously published data examining Ara-C, and IFOS-induced oxidative stress in several systems [29,30].…”

Section: Discussionsupporting

confidence: 93%

“…Our measured toxicity parameters showed that Ara-C, and IFOS significantly induce ROS formation. Previous studies showed that Ara-C, and IFOS increase the ROS formation and oxidative stress in normal and tumor cells [29,30]. Also, other examinations showed that both drugs induce lipid peroxidation and decrease GSH in isolated neurons.…”

Section: Discussionmentioning

confidence: 94%

“…Antioxidants may reduce the effectiveness of chemotherapies, which are based on increasing oxidative stress in tumor cells [37]. For example, Ara-C was toxic to MLH1 and MLH2 deficient tumor cells, but this cytotoxicity was reduced by antioxidants [30]. Also, certain researchers revealed mitochondrial dysfunction and mitotoxicity contribute to amplified oxidative stress [38].…”

Section: Discussionmentioning

confidence: 99%

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Trifluoperazine an Antipsychotic Drug and Inhibitor of Mitochondrial Permeability Transition Protects Cytarabine and Ifosfamide-Induced Neurotoxicity

et al. 2020

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The link between Ca2+ dysregulation, mitochondria damages, oxidative stress and cellular derangement is particularly evident in neurotoxicity induced by chemotherapeutic agents. In the current study, we investigated effects of trifluoperazine (TFP) as an inhibitor of calmodulin against the cytotoxicity induced by cytarabine (Ara-C) and Ifosfamide (IFOS) on isolated rat neurons and also the mechanisms involved in this toxicity. Isolated rat neurons were pretreated with TFP (100 µM) for 5 min at 37°C, then Ara-C (226 µM) and IFOS (290 µM) were added in separate experiments. After 3 h, the cytotoxicity, reactive oxygen species (ROS), lysosomal membrane destabilization, mitochondrial membrane potential (MMP), lipid peroxidation (LP), glutathione (GSH) and glutathione disulfide (GSSG) levels were measured. Ara-C and IFOS treatments caused a significant decrease in cellular viability, which was accompanied by ROS generation, GSSG/GSH ratio, lipid peroxidation and lysosomal and mitochondrial damages. On the other hand, TFP (100 µM) pre-treatment attenuated Ara-C and IFOS -induced decrease in cell viability. In addition, TFP (100 µM) pre-treatment significantly protected against Ara-C and IFOS -induced increase in ROS generation, lysosomal and mitochondrial damages, lipid peroxidation levels and decrease in GSH/GSSG ratio. Our data provided insights into the mechanism of protection by TFP against Ara-C and IFOS neurotoxicity, which is related, to neuronal ROS formation and mitochondrial damages.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

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Trifluoperazine an Antipsychotic Drug and Inhibitor of Mitochondrial Permeability Transition Protects Cytarabine and Ifosfamide-Induced Neurotoxicity

et al. 2020

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“…Установлено, что универсальным механизмом действия цитостатической терапии является индукция окислительного стресса [12]. Повышенное образование свободных радикалов вносит существенный вклад в большинство побочных эффектов цитостатиков, а также в их генотоксическое действие на созревающие половые клетки.…”

Section: Introductionunclassified

Pharmacological correction of pathological changes in the viable offspring of rats, caused by cytostatic impact at the stage of progenesis

et al. 2019

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Background. The number of reproductive-aged women with cancer, who desire child bearing, has increased with improvements in cancer detection and treatment. Cancer treatments have the potential to cause germline mutations that might increase the risk of cancer in the progeny of cancer patients. the aim of the study was to assess the feasibility of reducing the long-term side effects of Etoposide on the progeny of rats using Glutaxim. material and methods. Forty-five white outbred female Wistar rats, 2.5-month-old, were divided into 3 groups. Group I consisted of 15 intact rats. Group II comprised 15 rats treated with cytostatic drug (the control group). Group III consisted of 15 rats treated with Glutoxim® (Glutayil-Cysteinyl-Glycine, Pharma Vam Ltd., Russia) at a dose of 50 μg/kg 5 days before and 5 days after receiving cytostatic drug. results. An increase in the number of fetuses with external hemorrhages and pathological changes in internal organs was found in the progeny of female rats receiving Etoposide 3 months before mating. The progeny experienced a decrease in the rate of formation of sensory-motor reflexes, ability to learn and adaptive behavior. All studied parameters did not differ from background values in the progeny of female rats treated with combination of Etoposide and Glutoxim. conclusion. Glutaxim is the effective drug for correction of pathological changes in the progeny of female rats receiving cytostatic drugs.

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“…The ions then act as free radicals and pick other ions from the surrounding normal cells causing oxidative stresses (OS) which leads to cell lysis and inflammation of the surrounding tissues (13). Literature has reported of necrosis causing leukemia as a result of OS development from chemotherapy (14). In contrast to necrosis, apoptosis (programmed cell death) occurs routinely in normal cells during growth and aging in homeostatic mechanism to retain cell population in tissues (15).…”

Section: Introductionmentioning

confidence: 99%

Electrochemical Evaluation of Ion Substituted-Hydroxyapatite on HeLa Cells Plasma Membrane Potential

Asimeng¹,

Tiburu²,

Kuafmann³

et al. 2018

Preprint

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This study reports the electrochemical activities of a novel ion substituted-Hydroxyapatite material in contact with HeLa cells. The work was performed to evaluate the inhibitory effects of various concentrations of the material on the ion transfer mechanisms in HeLa cells. The materials (n=2: HAp1 and HAp3) were prepared at different stirring times from Achatina achatina snail shells and phosphate-containing solution. The structure of the materials and the trace elements concentration were evaluated using x-ray diffractometry and infrared spectrometry as well as atomic absorption spectroscopy. Electrochemical studies conducted on the cells, after 30 min of exposure to the materials, demonstrated differential responses as elucidated by cyclic voltammetry. The voltammograms revealed HAp1 to be non-redox whereas HAp3 was redox active. Minimal concentrations of HAp1 showed high anodic peak current when compared to the HeLa cells alone, indicating a hyperpolarization of the cells. The peak current gradually reduced as the concentration of HAp1 was increased, and then a sudden rise suggesting inhibition of the cell action potential. HAp3 showed a wavy pattern of the anodic peak current when the material concentration was varied. Peak currents of 0.92 and 0.57 nA were recorded for HAp1 and HAp3, respectively at the highest concentration of 5 µL. The results suggest that different inhibitory mechanisms are at play on the voltage-gated ion channels of the cells, indicating the possibility of using the materials to achieve different cancer proliferation inhibition.

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Oxidative stress response induced by chemotherapy in leukemia treatment (Review)

Cited by 45 publications

References 82 publications

Trifluoperazine an Antipsychotic Drug and Inhibitor of Mitochondrial Permeability Transition Protects Cytarabine and Ifosfamide-Induced Neurotoxicity

Trifluoperazine an Antipsychotic Drug and Inhibitor of Mitochondrial Permeability Transition Protects Cytarabine and Ifosfamide-Induced Neurotoxicity

Pharmacological correction of pathological changes in the viable offspring of rats, caused by cytostatic impact at the stage of progenesis

Electrochemical Evaluation of Ion Substituted-Hydroxyapatite on HeLa Cells Plasma Membrane Potential

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