Realgar is a mineral traditional medicine with definite efficacy. The function of realgar is detoxicating, insecticiding, eliminating dampness and phlegm, etc. It is widely applied in clinical practice by compatibility medicines. However, the safety and scientificalness of clinical application are questioned because of the toxic effect caused by arsenic compounds. At present, there are still many problems in the research of realgar, which are mainly manifested in three areas: the expression of main components and effective substances are inconsistent; the anti-tumor mechanism is difficult to explain at the molecular level; the mechanism of compatibility is not clear. As a result, realgar and realgar-containing Chinese patent medicines are frequently prohibited from entering the international market, and the reputation of traditional Chinese medicine is also damaged. This paper would analyze the research status of realgar at home and abroad as well as its problems from its main components, effective substances, anti-tumor mechanism and compatibility mechanism. In view of these difficulties, quantum chemical calculation method is proposed to solve them, so as to make up for the shortcomings and limitations of experimental technology and experimental conditions, reduce the cost of realgar research and improve research efficiency. Moreover, it provides inspiration for research of other mineral medicine.
Arsenicals ; pharmacology ; Medicine, Chinese Traditional ; Minerals ; Sulfides ; pharmacology

Arsenic is a common metal-like element. Drinking arsenic-containing water and occupational exposure to arsenic are the main ways exposure to arsenic for population. Long-term exposure to arsenic can cause various organs dysfunction and cancer. After entering the body, inorganic arsenic is mainly methylated into monomethyl arsenic and dimethyl arsenic in the liver. Only a small part of inorganic arsenic is metabolized in the kidneys and lungs, and finally the metabolites of arsenic are excreted in the urine. understanding the biological characteristics of arsenic absorption, metabolism, and distribution in the body and formulating biological indicators related to occupational exposure to arsenic and can provide a scientific basis for the prevention and treatment of arsenic-related diseases. This article will review the biological monitoring indicators of occupational exposure to arsenic and the metabolic process of arsenic in the body.
Arsenicals ; Arsenic ; Occupational Exposure ; Drinking Water ; Liver/metabolism*

This study aims to establish a method for the determination of As B,As C,DMA,As( Ⅲ),MMA and As( Ⅴ) by using HPLC-ICP-MS. A Dioncx Ion PacTMAS7( 4 mm×250 mm) column was used for the HPLC-ICP-MS method. The mobile phase was 100 mmol·L-1 ammonium carbonate-1. 5 mmol·L-1 ammonium dibasic phosphate( gradient elution) at a flow rate of 1 m L·min-1. The injection volume was 10 μL. The linear relationships of As B,As C,DMA,As( Ⅲ),MMA,As( Ⅴ) were good with the concentration of10-500 μg·L-1. The average recovery rates( n = 6) were 105. 7%,100. 5%,102. 9%,105. 7%,100. 2%,92. 69%. The RSD were0. 50%,2. 4%,0. 93%,1. 3%,0. 89%,1. 5%. The precision and repeatability of this method were good. In this study,six forms of arsenic were separated effectively by this method. With methodological validation and sample determination,this method can be used to determine the morphological valence of arsenic in content determination.
Arsenic/analysis* ; Arsenicals/analysis* ; Chromatography, High Pressure Liquid ; Mass Spectrometry

This study was aimed to investigate the change of expression and activity of protein phosphatases type 2A (PP2A) during the apoptosis of NB4 and MR2 cells induced by Arsenic trioxide (ATO). NB4 and MR2 cells were incubated with Okadaic acid (OKA) (0.5 nmol/L), ATO (0.5 - 2.0 micromol/L), and the combination of OKA and ATO at the same doses as in the single-agent treatment respectively. Then the proliferation of NB4 and MR2 cells was determined by MTT assay, the morphologic changes of cells were evaluated by Wright's staining, the apoptosis rates were detected by flow cytometry. At last, the activities of PP2A were evaluated by the serine/threonine phosphatase assay system, and the levels of PP2A subunits were detected by Western blot analysis. The results showed that ATO inhibited proliferation of NB4 and MR2 cells, and the inhibition rates of ATO on the two cells significantly increased after the addition of OKA. OKA could augment the apoptosis of NB4 and MR2 cells induced by ATO. During the apoptosis of NB4 and MR2 cells, the activity of PP2A decreased with increasing concentration of ATO, and OKA augmented the inhibitory effect of ATO on the activity. The level of PP2A structural subunit (PP2A-A) decreased during ATO-induced apoptosis of NB4 and MR2 cells, that expressions of B and C subunits of PP2A were relatively unaltered. It is concluded that the activity of PP2A decreases with increasing concentration of ATO during the apoptosis of NB4 and MR2 cells, and the decrease of the activity of PP2A maybe is related to the repression of expression of PP2A -A subunit; the inhibition of the activity of PP2A can promote the ATO induced apoptosis of NB4 and MRL cells.
Apoptosis ; drug effects ; Arsenicals ; pharmacology ; Cell Line, Tumor ; Humans ; Oxides ; pharmacology ; Protein Phosphatase 2 ; metabolism

OBJECTIVE: To compare inhibition of cell growth and apoptosis in human cervical cancer cell lines (CaSki) by paclitaxel, cisplatin, arsenic trioxide and tetraarsenic oxide. METHODS: Inhibition of cell growth was determined by the water-soluble tetrazolium salts (WSTs) -1 assay. For apoptosis analysis in CaSki cell line treated with single or combination of two agents, CaSki cell line treated with each agent was stained with annexin-V/PI and flow cytometry was performed. RESULTS: Progression of apoptosis in CaSki cell line treated with paclitaxel, cisplatin, arsenic trioxide, and tetraarsenic oxide was time dependent. Inhibition of cell growth in CaSki cell line by paclitaxel, cisplatin, arsenic trioxide, and tetraarsenic oxide was dose and time dependent. Especially, tetraarsenic oxide was more effective in inhibition of CaSki cell growth compared to arsenic trioxide. Group treated with combination of cisplatin and tetraarsenic oxide showed more progressive apoptosis compared to other combination group. CONCLUSION: Tetraarsenic oxide has more potent anti-tumor effects than other agents on CaSki cell line. We need to consider further study about antitumor effect of tetraarsenic oxide through clinical study.
Apoptosis ; Arsenic ; Arsenicals ; Cell Line ; Cisplatin ; Flow Cytometry ; Humans ; Oxides ; Paclitaxel ; Tetrazolium Salts ; Uterine Cervical Neoplasms

OBJECTIVES: This study was conducted to evaluate the cytotoxicity of gallium arsenide(GaAs), indium phosphide(InP) and indium arsenide(InAs) all of which are used as the semiconductor eletments in semiconductor industry. METHODS: Cytotoxicity in the alveolar macrophage was evaluated by the measurement of in vitro magnetometry, LDH release assay and histological examination. RESULTS: The relaxation curves by the in vitro magnetometry showed that GaAs has the cytotoxicity for the alveolar macrophage which is more significant in the higher dosages, while this cytotoxicity is not appeared in the groups added with InP or InAs or PBS. In the decay constant for two minutes after magnetization, GaAs-added groups showed a significant decrease with increasing doses, but both InP- and InAs-added groups did not show any significance. The LDH release assay showed a dose-dependent increasing tendency in the GaAs-, InP- and InAs-added groups. In terms of cellular morphological changes, GaAs-added groups revealed such severe cellular damages as prominent destructions in cell membranes and their morphological changes of nucleus, while InP- and InAs-added groups remained intact in intracellular structures, except for cytoplasmic degenerations. CONCLUSIONS: It is suggested that GaAs is more influential to cytotoxicity of alveolar macrophages than InP and InAs.
Arsenic* ; Arsenicals* ; Cell Membrane ; Cytoplasm ; Gallium ; Indium ; Macrophages* ; Macrophages, Alveolar ; Magnetometry ; Relaxation ; Semiconductors

BACKGROUND: Bowen's disease(BD) is an in situ squamous cell carcinoma(SCC) of the skin, which clinically presents as a scaly slightly elevated erythematous plaque. Approximately two thirds of patients with BD have solitary lesions, whereas the remaining patients have multiple lesions. Lesions of BD have a wide distribution covering both sun-exposed and covered skin. Chronic sunlight exposure is an important etiological factor in many patients, and inorganic arsenicals can cause lesions on unexposed skin. If untreated, 3-5% of BD cases evolve into invasive carcinoma including SCC, basal cell carcinoma(BCC), and sebaceous carcinoma(SC), although the precise mechanism is not yet clear. OBJECTIVE: The purpose of this study was to investigate the factors which may be involved in the development of BD and progression to invasive carcinoma. METHODS: We performed immunohistochemical analysis using monoclonal antibodies for p53, mdm-2, and bcl-2 in 7 cases of multiple BD with invasive carcinoma. RESULTS: In four of 6 cases of SCC immunopositive for p53, at least one lesion of each BD was positive for p53. Among them, two cases showed the consistency of p53 staining between BD and its SCC and the localization of the lesions on sun-exposed areas. On the other hand, two cases of SCC and the associated BD were immunonegative for p53 and positive for mdm-2 and all the lesions developed on the UV-nonexposed areas. In one particular case which had a history of arsenic ingestion, SC was immunopositive for p53, whereas the associated SCC and BD were immunonegative for p53. In one case associated adenoid BCC, BD was immunopositive for p53 and negative for bcl-2, whereas BCC was immunonegative for p53 and strongly positive for bcl-2. CONCLUSION: These results suggest that UV light may play a role in the development of BD and its progression to SCC and in addition to p53, some additional factor or conditions are required in the progression towards these invasive carcinomas from BD.
Adenoids ; Antibodies, Monoclonal ; Arsenic ; Arsenicals ; Bowen's Disease* ; Eating ; Hand ; Humans ; Skin ; Sunlight ; Ultraviolet Rays

Arsenic ; urine ; Arsenicals ; analysis ; Environmental Monitoring ; methods ; Humans ; Sensitivity and Specificity ; Spectrometry, Fluorescence ; methods

Apoptosis ; drug effects ; Arsenicals ; pharmacology ; Cell Line, Tumor ; Humans ; Oxides ; pharmacology

OBJECTIVETo investigate the proliferation effects of arsenic trioxide (As2O3) on salivary adenoid cystic carcinoma-2 (ACC-2) cells in vitro and to study the role of Survivin on the apoptosis of ACC-2 induced by As2O3.

METHODSACC-2 cells were treated with different concentration of As2O3 for different time. The inhibitory effects on cell's viability were assayed with methyl thiazolyl tetrazolium (MTT) test. Apoptosis was determined by flow cytometry. The expression of Survivin mRNA and protein were investigated by reverse transcription-polymerase chain raction (RT-PCR) and Western blot analysis respectively.

RESULTSCell viability after As2O3 treatment was markedly suppressed and exhibited as a dose- and time-dependent pattern. The apoptotic index showed the similar trend. The results of RT-PCR revealed gene expression of Survivin was suppressed significantly. Through Western blot analysis, a negative correlation between concentration and amount of protein product of Survivin was determined.

CONCLUSIONAs2O3 might markedly suppressed ACC-2 cell's viability in vitro. The inhibition of Survivin gene expression may play a critical role on ACC-2 cell apoptosis induced by As2O3.