NDLI: Trivalent methylated arsenic metabolites induce apoptosis in human myeloid leukemic HL-60 cells through generation of reactive oxygen species

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Metallomics Vol - 6 Issue - 7

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Metallomics Vol - 6 Issue - 2

Trivalent methylated arsenic metabolites induce apoptosis in human myeloid leukemic HL-60 cells through generation of reactive oxygen species

Content Provider	Royal Society of Chemistry (RSC)
Author	Zhou, Xin Yi Wang, Qian Qian Fu, Yu Jie Wu, Bin Sun, Wu Hui Rehman, Kanwal Zhang, Yan Fang Wu, Yuan Sun, Tian Fu Naranmandura, Hua
Copyright Year	2014
Abstract	Arsenic trioxide (As2O3) has remarkable therapeutic efficacy against leukemia. However, after As2O3 biotransformation, the role of arsenic metabolites in the clinical efficacy against leukemia still needs to be elucidated. Therefore, to explore the contribution of trivalent methylated arsenicals in the therapeutic effects, we investigated and compared the effects of arsenite (iAsIII), monomethylarsonous acid (MMAIII) and dimethylarsinous acid (DMAIII) on HL-60 cells. Methylated arsenic species MMAIII and DMAIII showed potentially reduced cell survival with IC50 values of 3 and 2 μM, respectively. We found that methylated metabolites caused apoptosis through oxidative stress and loss of mitochondrial membrane potential. Furthermore, we found that the caspase-9 and -3 were markedly activated by exposure to methylated metabolites, with cleavage of poly-ADP ribose polymerase (PARP). Conversely, cellular apoptosis, generation of ROS, activation of caspase-3, -9 as well as PARP cleavage were significantly attenuated by pretreatment with an antioxidant, N-acetylcysteine (NAC). DNA damage was also markedly observed in HL-60 cells exposed to either MMAIII or DMAIII, while iAsIII did not show any relevant effects in HL-60 cells. Likewise, phosphorylation of the histone H2A variant (γ-H2AX), a biomarker of DNA damage, significantly occurred in cellular nuclei following exposure to two methylated species, which was reduced in the presence of NAC, suggesting that the induction of DNA damage was predominantly caused by the two metabolites via oxidative stress. In conclusion, we suggest that arsenic intermediate metabolites; MMAIII and DMAIII might prove to be of clinical relevance in future as such approaches may help in the treatment of leukemia and other types of cancers.
Starting Page	1502
Ending Page	1512
Page Count	11
File Format	HTM / HTML PDF
ISSN	17565901
Volume Number	6
Issue Number	8
Journal	Metallomics
DOI	10.1039/c4mt00119b
Language	English
Publisher	Royal Society of Chemistry
Access Restriction	Open
Subject Keyword	Oxidative stress Reactive oxygen species Phosphorylation Biomarker Arsenic Caspase Acetylcysteine Arsenic trioxide Antioxidant Polymerase NAC Ribose Biotransformation DNA IC50 Antimony trioxide Membrane potential Histone Arsenite Apoptosis
Content Type	Text
Resource Type	Article
Subject	Chemistry Medicine Metals and Alloys Biochemistry Biomaterials Biophysics

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