Arsenic in the treatment of some kinds of dermatoses

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Author:
LUAN Li(Department of Dermatology, First Affiliated Hospital of Dalian Medical University, Dalian 116011, China)
ZHANG Zhen-ying(Department of Dermatology, First Affiliated Hospital of Dalian Medical University, Dalian 116011, China)
LIU Xiao-ming(Department of Dermatology, First Affiliated Hospital of Dalian Medical University, Dalian 116011, China)
Journal Title:
International Journal of Dermatology and Venereology
Issue:
Volume 38, Issue 05, 2012
DOI:
10.3760/cma.j.issn.1673-4173.2012.05.007
Key Word:
Arsenicals; Psoriasis; Lymphoma, T cell, cutaneous; Melanoma

Abstract: Arsenic has shown some medicinal properties in psoriasis,cutaneous T cell lymphoma,melanoma,and so on.On the one hand,arsenic at certain concentrations can suppress cell growth,induce cell apoptosis and cause the regression of skin neoplasms.On the other hand,arsenic has cytotoxicity,and can be accumulated in and induce damages to yarious organs of the human body.Epidemiological studies have shown that arsenic may be carcinogenic.Therefore,more basic research and clinical trials are warranted to optimize the therapeutic dose of arsenic so as to minimize its side effects.Individualized administration of arsenic based on gene polymorphisms associated with its side effects may enable arsenic to be an effective treatment option for some kinds of skin disorders with minimal risk.

  • [1]张亭栋,李元善.癌灵1号治疗急性粒细胞白血病临床分析及实验研究.中西医结合杂志,1984,4(1):19-20.
  • [2]刘文.全反式维A酸联合三氧化二砷治疗急性早幼粒细胞性白血病并银屑病三例.白血病·淋巴瘤,2005,14(6):381.
  • [3]Tse WP,Cheng CH,Che CT,et al.Arsenic trioxide,arsenic pentoxide,and arsenic iodide inhibit human keratinocyte proliferation through the induction of apoptosis.J Pharmacol Exp Ther,2008,326(2):388-394.
  • [4]Tse WP,Cheng CH,Che CT,et al.Realgar-mediated growth inhibition on HaCaT human keratinocytes is associated with induction of apoptosis.Int J Mol Med,2009,24(2):189-196.
  • [5]Liao WT,Chang KL,Yu CL,et al.Arsenic induces human keratinocyte apoptosis by the FAS/FAS ligand pathway,which correlates with alterations in nuclear factor-kappa B and activator protein-1 activity.J Invest Dermatol,2004,122 (1):125-129.
  • [6]Bi X,Gu J,Guo Z,et al.Different pathways are involved in arsenic-trioxide-induced cell proliferation and growth inhibition in human keratinocytes.Skin Pharmacol Physiol,2010,23 (2):68-78.
  • [7]Huang HS,Liu ZM,Hong DY.Blockage of JNK pathway enhances arsenic trioxide-induced apoptosis in human keratinocytes.Toxicol Appl Pharmacol,2010,244(2):234-241.
  • [8]Michel L,Dupuy A,Jean-Louis F,et al.Arsenic trioxide induces apoptosis of cutaneous T cell lymphoma cells:evidence for a partially caspase-independent pathway and potentiation by ascorbic acid (vitamin C).J Invest Dermatol,2003,121 (4):881-893.
  • [9]Tun Kyi A,Qin JZ,Oberholzer PA,et al.Arsenic trioxide down-regulates antiapoptotic genes and induces cell death in mycosis fungoides tumors in a mouse model.Ann Oncol,2008,19 (8):1488-1494.
  • [10]Amaria RN,Lewis KD,Gonzalez R.Therapeutic options in cutaneous melanoma:latest developments.Ther Adv Med Oncol,2011,3(5):245-251.
  • [11]Hiwatashi Y,Tadokoro H,Henmi K,et al.Antiproliferative and anti-invasive effects of inorganic and organic arsenic compounds on human and murine melanoma cells in vitro.J Pharm Pharmacol,2011,63(9):1202-1210.
  • [12]Chen MJ,Yang PY,Ye YZ,et al.Arsenic trioxide induces apoptosis in uveal melanoma cells through the mitochondrial pathway.Am J Chin Med,2010,38(6):1131-1142.
  • [13]Tarhini AA,Kirkwood JM,Tawbi H,et al.Safety and efficacy of arsenic trioxide for patients with advanced metastatic melanoma.Cancer,2008,112(5):1131-1138.
  • [14]Chowdhury R,Chowdhury S,Roychoudhury P,et al.Arsenic induced apoptosis in malignant melanoma cells is enhanced by menadione through ROS generation,p38 signaling and p53 activation.Apoptosis,2009,14(1):108-123.
  • [15]Bowling BD,Doudican N,Manga P,et al.Inhibition of mitochondrial protein translation sensitizes melanoma cells to arsenic trioxide cytotoxicity via a reactive oxygen species dependent mechanism.Cancer Chemother Pharmacol,2008,63(1):37-43.
  • [16]Zhao QH,Zhang Y,Liu Y,et al.Anticancer effect of realgar nanoparticles on mouse melanoma skin cancer in vivo via transdermal drug delivery.Med Oncol,2010,27(2):203-212.
  • [17]Hughes MF,Beck BD,Chen Y,et al.Arsenic exposure and toxicology:a historical perspective.Toxicol Sci,2011,123 (2):305-332.
  • [18]Sun Y,Kojima C,Chignell C,et al.Arsenic transformation predisposes human skin keratinocytes to UV-induced DNA damage yet enhances their survival apparently by diminishing oxidant response.Toxicol Appl Pharmacol,2011,5 (3):242-250.
  • [19]Sengupta SR,Das NK,Datta PK.Pathogenesis,clinical features and pathology of chronic arsenicosis.Indian J Dermatol Venereol Leprol,2008,74(6):559-570.
  • [20]Gentry PR,McDonald TB,Sullivan DE,et al.Analysis of genomic dose-response information on arsenic to inform key events in a mode of action for carcinogenicity.Environ Mol Mutagen,2010,51(1):1-14.
  • [21]Ahsan H,Chen Y,Wang Q,et al.DNA repair gene XPD and susceptibility to arsenic-induced hyperkeratosis.Toxicol Lett,2003,143(2):123-131.
  • [22]Applebaum KM,Karagas MR,Hunter DJ,et al.Polymorphisms in nucleotide excision repair genes,arsenic exposure,and non-melanoma skin cancer in New Hampshire.Environ Health Perspect,2007,115(8):1231-1236.
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