An Overview on Arsenic Trioxide-Induced Cardiotoxicity

Vineetha, Vadavanath Prabhakaran; Raghu, Kozhiparambil Gopalan

doi:10.1007/s12012-018-09504-7

Cited by 60 publications

(36 citation statements)

References 146 publications

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“…oxidative stress is considered to be an imbalance between generation of roS and the activity of antioxidant defenses. oxidative stress is a negative consequence of the in vivo production of radicals, and it is considered to be an important factor leading to apoptosis (34). Multiple studies have reported that high a concentration of arsenic can cause oxidative stress and increase roS (53,54).…”

Section: Discussionmentioning

confidence: 99%

“…Multiple studies have reported that high a concentration of arsenic can cause oxidative stress and increase roS (53,54). excessive roS cause injury to numerous types of macromolecules, including dna, lipid and protein (34,55). roS alters cell signaling processes, such as gene expression level changes, transcription factor activation and apoptosis (56).…”

Section: Discussionmentioning

confidence: 99%

“…in addition, studies have suggested that high doses of aTo can cause oxidative stress, increased roS and inhibit enzyme and mitochondrial activity (32,33). Mitochondrial impairment leads to the release of mitochondrial-associated proteins cytochrome c, second mitochondria-derived activator of caspases (Smac) and high-temperature requirement a2 (Htra2); the release of cytochrome c can activate caspase-3 (34). Moreover, the Bcl-2 family, which serves a crucial role in the regulation of cardiomyocyte apoptosis, is a primary regulator of cytochrome c release and caspase-3 activation (34).…”

Section: Introductionmentioning

confidence: 99%

“…Mitochondrial impairment leads to the release of mitochondrial-associated proteins cytochrome c, second mitochondria-derived activator of caspases (Smac) and high-temperature requirement a2 (Htra2); the release of cytochrome c can activate caspase-3 (34). Moreover, the Bcl-2 family, which serves a crucial role in the regulation of cardiomyocyte apoptosis, is a primary regulator of cytochrome c release and caspase-3 activation (34). arsenic exposure increases the levels of pro-apoptotic proteins Bax (35) and Bad (36) and decreases the expression levels of anti-apoptotic protein Bcl-2 (37).…”

Section: Introductionmentioning

confidence: 99%

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Mechanisms underlying the protective effect of tannic acid against arsenic trioxide‑induced cardiotoxicity in rats: Potential involvement of mitochondrial apoptosis

Xue

et al. 2020

Mol Med Rep

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arsenic trioxide (aTo) is a frontline chemotherapy drug used in the therapy of acute promyelocytic leukemia. However, the clinical use of aTo is hindered by its cardiotoxicity. The present study aimed to observe the potential effects and underlying mechanisms of tannic acid (Ta) against aTo-induced cardiotoxicity. Male rats were intraperitoneally injected with aTo (5 mg/kg/day) to induce cardiotoxicity. Ta (20 and 40 mg/kg/day) was administered to evaluate its cardioprotective efficacy against ATO-induced heart injury in rats. administration of aTo resulted in pathological damage in the heart and increased oxidative stress as well as levels of serum cardiac biomarkers creatine kinase and lactate dehydrogenase and the inflammatory marker NF-κB (p65). conversely, Ta markedly reversed this phenomenon. additionally, Ta treatment caused a notable decrease in the expression levels of cleaved caspase-3/caspase-3, Bax, p53 and Bad, while increasing Bcl-2 expression levels. notably, the application of Ta decreased the expression levels of cytochrome c, second mitochondria-derived activator of caspases and high-temperature requirement a2, which are apoptosis mitochondrial-associated proteins. The present findings indicated that Ta protected against aTo-induced cardiotoxicity, which may be associated with oxidative stress, inflammation and mitochondrial apoptosis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Mechanisms underlying the protective effect of tannic acid against arsenic trioxide‑induced cardiotoxicity in rats: Potential involvement of mitochondrial apoptosis

Xue

et al. 2020

Mol Med Rep

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“…Combination therapy is frequently used in clinical studies to improve the beneficial effects and reduce the toxicity of anti-cancer agents [18,19]. Higher dose of ATO is toxic and induces side effects in hepatic, cardiovascular, and nervous systems [20,21]. Therefore, the combination treatment of ATO with other agents have been reported to inhibit cell growth and induce apoptosis in various cancer cells including lung cancer [22][23][24].…”

Section: Introductionmentioning

confidence: 99%

Combination of Arsenic Trioxide and Valproic Acid Efficiently Inhibits Growth of Lung Cancer Cells via G2/M-Phase Arrest and Apoptotic Cell Death

Park

Han

Park

2020

IJMS

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Arsenic trioxide (ATO; As2O3) has anti-cancer effects in various solid tumors as well as hematological malignancy. Valproic acid (VPA), which is known to be a histone deacetylase inhibitor, has also anti-cancer properties in several cancer cells including lung cancer cells. Combined treatment of ATO and VPA (ATO/VPA) could synergistically enhance anti-cancer effects and reduce ATO toxicity ATO. In this study, the combined anti-cancer effects of ATO and VPA (ATO/VPA) was investigated in NCI-H460 and NCI-H1299 lung cancer cells in vitro and in vivo. A combination of 3 μM ATO and 3 mM VPA (ATO/VPA) strongly inhibited the growths of both lung cancer cell types. DNA flow cytometry indicated that ATO/VPA significantly induced G2/M-phase arrest in both cell lines. In addition, ATO/VPA strongly increased the percentages of sub-G1 cells and annexin V-FITC positive cells in both cells. However, lactate dehydrogenase (LDH) release from cells was not increased in ATO/VPA-treated cells. In addition, ATO/VPA increased apoptosis in both cell types, accompanied by loss of mitochondrial membrane potential (MMP, ∆Ψm), activation of caspases, and cleavage of anti-poly ADP ribose polymerase-1. Moreover, a pan-caspase inhibitor, Z-VAD, significantly reduced apoptotic cell death induced by ATO/VPA. In the xenograft model, ATO/VPA synergistically inhibited growth of NCI-H460-derived xenograft tumors. In conclusion, the combination of ATO/VPA effectively inhibited the growth of lung cancer cells through G2/M-phase arrest and apoptotic cell death, and had a synergistic antitumor effect in vivo.

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Arsenic, Antimony, and Bismuth

Madden

Fowler²

2023

Patty's Toxicology

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Arsenic, Antimony, and Bismuth are members of Group V of the Periodic Table of Elements. These elements have been used for a variety of medicinal and pest control purposes over a number of centuries. They have also been used in metallic alloys and in the production of III–V semiconductors to increase electronic speeds of computer chips. Arsenicals are largely metabolized by methylation pathways and bismuth is known to induce the metal‐binding protein metallothionein and to form electron–dense cytoplasmic and intranuclear inclusion bodies.

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An Overview on Arsenic Trioxide-Induced Cardiotoxicity

Cited by 60 publications

References 146 publications

Mechanisms underlying the protective effect of tannic acid against arsenic trioxide‑induced cardiotoxicity in rats: Potential involvement of mitochondrial apoptosis

Mechanisms underlying the protective effect of tannic acid against arsenic trioxide‑induced cardiotoxicity in rats: Potential involvement of mitochondrial apoptosis

Combination of Arsenic Trioxide and Valproic Acid Efficiently Inhibits Growth of Lung Cancer Cells via G2/M-Phase Arrest and Apoptotic Cell Death

Arsenic, Antimony, and Bismuth

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