Arsenic Trioxide Triggers Mitochondrial Dysfunction, Oxidative Stress, and Apoptosis via Nrf 2/Caspase 3 Signaling Pathway in Heart of Ducks

Rao, G. Srinivasa; Zhong, Gaolong; Hu, Ting; Wu, Shaofeng; Tan, Jiajia; Zhang, Xiaoyong; Huang, Riming; Tang, Zhaoxin; Hu, Lianmei

doi:10.1007/s12011-022-03219-1

Cited by 4 publications

(2 citation statements)

References 43 publications

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“…Renton et al ( 25 ) demonstrated different effects of DFO on the proliferation of neural tumor cell lines depending on the drug concentration and exposure time. Scientific data have demonstrated that ATO-induced apoptosis is associated with up-regulation of the expression of the proenzymes of caspase 3 and activation of caspase 3 ( 26 , 27 ). Moreover, Wang et al reported that DFO induces apoptosis of HL-60 cells by activating caspase 3 ( 28 ).…”

Section: Discussionmentioning

confidence: 99%

Combination Effect of Deferoxamine and Arsenic Trioxide on Viability and Vitality of APL Like Cell Line

Kazem Ghaffari,

Ali Bayat,

Ali Ghasemi

2023

Ethiop J Health Sci

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BACKGROUND: Arsenic trioxide is an activist agent in the treatment of acute promyelocytic leukemia (APL), which acts alone, but has an adverse effect on patients. Moreover, deferoxamine has antiproliferative activity and induces leukopenia. In order to enhance antileukemic effectiveness and to reduce the dosage of arsenic trioxide, the combination effect of it with deferoxamine (DFO) was evaluated on the APL cell line (NB4). METHODS: In this experimental study, to investigate the cytotoxic effects of ATO/DFO in acute promyelocytic leukemia, the NB4 cell line (provided by Pasteur Institute of Iran) was treated with different doses and then at 24, 48, and 72 hrs intervals, the percentage of survival, cell count, metabolic activity and apoptosis induction were investigated respectively. Also, hTERT gene expression was analyzed by the RT-PCR method. RESULTS: We found that DFO alone and in combination with ATO has cytotoxic and antiproliferative effects, and reduces viability and cell metabolic activity in the NB4 cell line in a dose and time-dependent manner. In addition, this combination causes an increase in apoptosis, up-regulation of Caspase-3, and down-regulation of hTERT genes in cells. CONCLUSION: Combined ATO/ DFO treatment cooperatively decreased the mRNA levels of the hTERT and increased the mRNA levels of Caspase-3 in a time-dependent manner compared to DFO alone.

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Section: Discussionmentioning

confidence: 99%

Combination Effect of Deferoxamine and Arsenic Trioxide on Viability and Vitality of APL Like Cell Line

Kazem Ghaffari,

Ali Bayat,

Ali Ghasemi

2023

Ethiop J Health Sci

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“…The ultrastructure of cardiomyocytes was observed utilizing a transmission electron microscope (TEM) as has been described (34)(35)(36). Briefly, the heart tissues were sectioned into small granules less than 1 mm 3 , fixed in 2.5% glutaraldehyde (P1126, Solarbio, CHN) for 24 h, and then washed in PBS.…”

Section: Transmission Electron Microscopymentioning

confidence: 99%

Modified Linggui Zhugan Decoction protects against ventricular remodeling through ameliorating mitochondrial damage in post-myocardial infarction rats

Xiang

Zhao

et al. 2023

Front. Cardiovasc. Med.

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IntroductionModified Linggui Zhugan Decoction (MLZD) is a Traditional Chinese Medicine prescription developed from Linggui Zhugan Decoction (LZD) that has been used for the clinical treatment of ischemic cardiovascular diseases. However, the cardioprotective mechanism of MLZD against post-myocardial infarction (MI) ventricular remodeling remains unclear.MethodsWe explored the effects of MLZD on ventricular remodeling and their underlying mechanisms, respectively, in SD rats with MI models and in H9c2 cardiomyocytes with oxygen-glucose deprivation (OGD) models. The cardiac structure and function of rats were measured by echocardiography, HE staining, and Masson staining. Apoptosis, inflammation, mitochondrial structure and function, and sirtuin 3 (SIRT3) expression were additionally examined.ResultsMLZD treatment significantly ameliorated cardiac structure and function, and thus reversed ventricular remodeling, compared with the control. Further research showed that MLZD ameliorated mitochondrial structural disruption, protected against mitochondrial dynamics disorder, restored impaired mitochondrial function, inhibited inflammation, and thus inhibited apoptosis. Moreover, the decreased expression level of SIRT3 was enhanced after MLZD treatment. The protective effects of MLZD on SIRT3 and mitochondria, nevertheless, were blocked by 3-TYP, a selective inhibitor of SIRT3.DiscussionThese findings together revealed that MLZD could improve the ventricular remodeling of MI rats by ameliorating mitochondrial damage and its associated apoptosis, which might exert protective effects by targeting SIRT3.

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Exposure to copper induces endoplasmic reticulum (ER) stress-mediated apoptosis in chicken (Gallus gallus) myocardium

Yang

et al. 2023

Vet Res Commun

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Arsenic Trioxide Triggers Mitochondrial Dysfunction, Oxidative Stress, and Apoptosis via Nrf 2/Caspase 3 Signaling Pathway in Heart of Ducks

Cited by 4 publications

References 43 publications

Combination Effect of Deferoxamine and Arsenic Trioxide on Viability and Vitality of APL Like Cell Line

Combination Effect of Deferoxamine and Arsenic Trioxide on Viability and Vitality of APL Like Cell Line

Modified Linggui Zhugan Decoction protects against ventricular remodeling through ameliorating mitochondrial damage in post-myocardial infarction rats

Exposure to copper induces endoplasmic reticulum (ER) stress-mediated apoptosis in chicken (Gallus gallus) myocardium

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