Arsenic is a non-metallic element, and the International Agency for Research on Cancer has identified arsenic and its compounds as carcinogens. Arsenic and its compounds can be absorbed through the respiratory tract, skin and digestive tract, distributed in the liver, kidney, lung and skin, and cause damage. Non-coding RNAs are closely related to arsenic-induced nervous system disorders, cell necrosis, reproductive toxicity, and carcinogenesis. In recent years, the network regulation of microRNAs (miRNAs) , long non-coding RNAs (lncRNAs) , and circular RNAs (circRNAs) among non-coding RNAs in various diseases induced by arsenic has become a new research field. This paper summarizes the existing scientific research results, and expounds the mechanism of miRNAs, lncRNAs and circRNAs in arsenic toxicity, and provides basic data and theoretical basis for the prevention and treatment of arsenic poisoning.
Arsenic/toxicity* ; Arsenic Poisoning ; Humans ; MicroRNAs/genetics* ; RNA, Circular ; RNA, Long Noncoding/genetics*

A 29-year-old male with eleven-year history of hyperkeratotic papules and speckled pigmentation developed cutaneous squamous cell carcinoma. Arsenicosis was confirmed by elevated hair arsenic level, and histopathologic findings of arsenical keratosis and one lesion showing carcinoma-in-situ. Chronic arsenic exposure has been found to activate inflammatory and carcinogenic pathways leading to development of pre-malignant and malignant lesions. A multi-disciplinary approach involving healthcare specialists and environmentalists is crucial in source control and management of long-term complications.
Arsenic ; Arsenic Poisoning ; Carcinoma, Squamous Cell ; Carcinoma In Situ

BACKGROUND: Non-melanoma skin cancers (NMSCs, basal cell carcinoma [BCC], and squamous cell carcinoma, [SCC]) are skin conditions, and the propensity of NMSCs to develop multiple tumors may be associated with some genodermatoses, arsenic poisoning, and chronic exposure to radiation or coal tar. OBJECTIVE: To report our experience of treating multiple NMSCs and to investigate the clinical characteristics of NMSCs. METHODS: We retrospectively evaluated 16 patients who had been diagnosed with NMSCs from May 2010 to December 2014. RESULTS: The male-female sex ratio was 0.6:1 in the patients with multiple BCCs and SCCs. The most frequent age group was the seventh decade (75%). The mean patient age was 76.36 years. The most common involved site was the face, particularly the cheek (54.3%). Nodular BCCs were the most frequent (61.9%), followed by infiltrate BCCs (28.6%) and superficial BCCs (9.5%). Among the SCCs, the moderately differentiated SCCs were the most frequent (50%). More NMSCs were found on the left than on the right side of the head and neck areas in both sexes. Development of BCC (68.8%) was more frequent than that of SCC in sun-exposed areas. CONCLUSION: In our study, differences in the demographic variables, such as age, sex, or residence were found between the patients with multiple BCCs and SCCs. The incidence of BCC has markedly increased, which is mainly because of the increment of aged people in their residence, along with environmental factors. Further cohort studies that include cumulative lifetime sun exposure and a large sample size are needed.
Arsenic Poisoning ; Carcinoma, Basal Cell ; Carcinoma, Squamous Cell ; Cheek ; Clinical Study* ; Coal Tar ; Cohort Studies ; Head ; Humans ; Incidence ; Neck ; Retrospective Studies ; Sample Size ; Sex Ratio ; Skin Neoplasms* ; Skin* ; Solar System

Arsenic is a known human carcinogen and skin manifestations are the earliest and most specific markers of chronic arsenic poisoning. A 43-year-old man from Luzon presented at the Section of Dermatology with a one-year history of hyperkeratotic papules and plaques on the palms and soles. Numerous round hypopigmented macules were scattered on the upper back. Initial 24-hour urine arsenic level was elevated at 288mcg/liter. The patient underwent successful chelation with N-acetylpenicillamine and the palmoplantar keratoses were treated with cryotherapy and topical 20% salicylic acid in white petrolatum. In cooperation with the Department of Health, a comprehensive health and environmental assessment was conducted in the affected communities. This case highlights the role of dermatologists in the diagnosis and management of this public health problem.

Arsenic Poisoning ; Philippines ; Keratoderma, Palmoplantar

Animals ; Arsenic Poisoning ; pathology ; Imaging, Three-Dimensional ; Liver ; blood supply ; ultrastructure ; Mice

OBJECTIVETo investigate the changes of genetic damage in patients with arsenism caused by coal-burning in 9 years. To analyze the relationship between the changes of genetic damage and disease progression and provide a basis for condition monitoring.

METHODSOf 206 arsenism patients from the area with endemic arsenism in Guizhou province were tracking surveyed in February 1998 and divided into 4 groups, including suspicious, mild, moderate and severe poisoning group. Another 67 healthy residents from a neighbour township 12 km away where arsenic was not prevalent were surveyed. Over a 9-year follow-up, 131 arsenism patients and 45 controls with the complete biochemical indexes among them were selected as subjects in December 2006. Arsenic (As) concentration of urine and hair were detected by silver diethyldithiocarbamate spectrophotometry (Ag-DDC). Micronucleis (MN) and chromosome aberrations (CA) were analyzed by conventional methods. DNA single-strand breaks of peripheral blood were measured by single cell gel electrophoresis (SCGE), and the tail lengths of comet were used to measure DNA damage.

RESULTSAmong the control, suspicious, mild, moderate and severe arsenic poisoning group, the As contents of urine and hair were respectively (34.16 ± 10.25), (52.35 ± 22.41), (62.26 ± 31.13), (71.43 ± 49.92), (78.45 ± 50.64) µg/L and (1.37 ± 0.56), (3.69 ± 1.78), (4.88 ± 3.49), (5.21 ± 3.10), (6.25 ± 4.04) µg/g in 2006, which were lower than that 9 years before (urine as contents were (36.07 ± 20.70), (73.65 ± 41.33) , (90.92 ± 82.14) , (126.55 ± 107.31) and (139.44 ± 90.90) µg/L, and hair As contents were (1.41 ± 1.18), (4.85 ± 4.20), (5.72 ± 4.07) , (6.43 ± 4.32) and (7.19 ± 4.68) µg/g, respectively, F value was 10.63, 7.72, 14.66, 11.00 respectively, all P values were < 0.05). Except for suspicious poisoning group, the differences of urine As contents in the other groups all showed significance (P < 0.05). The incidences of MN were (0.238 ± 0.130) %, (0.268 ± 0.192) %, (0.283 ± 0.157) % and (0.391 ± 0.233)%; the incidences of CA were (14.36 ± 5.44) %, (18.09 ± 6.49) %, (19.38 ± 5.63)% and (19.83 ± 5.84) %; the tail lengths of comet were (29.88 ± 13.81) , (29.84 ± 12.80) , (34.50 ± 9.88) and (41.58 ± 12.98) µm respectively in 2006 for all poisoning groups; which were higher than that 9 years before(the incidences of MN were (0.163 ± 0.051) %, (0.186 ± 0.117) %, (0.196 ± 0.104) % and (0.273 ± 0.142) %; the incidences of CA were (13.18 ± 5.17)%, (14.48 ± 6.61)%, (15.67 ± 8.49) % and (16.90 ± 8.38) %; the tail lengths of comet were (15.07 ± 12.93) , (19.57 ± 8.80) , (27.03 ± 10.77) and (34.71 ± 14.95) µm) , except for the incidences of MN and CA in suspicious poisoning group and of MN in mild poisoning group , the differences of the three indexes in the other groups were significant (P < 0.05) . The state of illness of arsenic poisoning patients aggravated 9 years later. With the increase of urine and hair As contents and the development of arsenism, the incidences of MN, CA and the tail lengths of comet of all poisoning groups increased. There were positive correlations among them (r values were respectively 0.212, 0.316, 0.232, 0.263, 0.321, 0.654 and 0.760) (P < 0.05).

CONCLUSIONThe exacerbation of genetic damage was related to constantly high arsenic loads. The accumulation of genetic damage and its irreversibility might be one of the important reasons of the development of arsenism and cancer.

Arsenic ; Arsenic Poisoning ; Coal ; DNA Damage ; Follow-Up Studies ; Humans

OBJECTIVETo study the effect of arsenic on neuronal cell apoptosis and the mRNA and protein expression of calpain 1, calpain 2, and cyclin-dependent kinases 5 (cdk5)/p25 and to provide a scientific basis for the research on neurotoxic mechanism of arsenic trioxide (As2O3).

METHODSPrimary cultured rat neurons were divided into untreated control group, dimethyl sulfoxide (DMSO) solvent control group, and 1, 5, and 10 µmol/L As2O3 treated groups. Eight hours after being treated with As2O3, cell apoptosis rate was determined by flow cytometry, the mRNA expression of calpain 1, calpain 2, cdk5, and p35 was measured by real-time fluorescence quantitative PCR, and the protein expression of calpain 1, calpain 2, cdk5, p35, and p25 was measured by Western blot.

RESULTSCompared with those in the untreated control group and DMSO solvent control group, the cell apoptosis rates in the 5 and 10 µmol/L As2O3 treated groups were significantly increased (P < 0.05). The mRNA expression levels of calpain 1 were 6.36±3.26, 7.11±5.13, and 7.47±2.59 in the 1, 5, and 10 µmol/L As2O3 treated groups, respectively, and the mRNA expression levels of cdk5 were 1.27±0.19, 1.54±0.04, and 1.79±0.21 in the 1, 5, and 10 µmol/L As2O3 treated groups, respectively, which were significantly higher than those in the untreated group (0.72±0.15 and 1.77±0.87) and those in the DMSO solvent control group (0.96±1.23 and 1.18±0.09) (P < 0.05). The mRNA expression levels of p35 in the 1 and 5 µmol/L As2O3 treated groups were 2.17±0.59 and 2.51±0.51, respectively, which were significantly higher than that in the untreated control group (1.26±0.37) (P < 0.05). The protein expression levels of calpain 1 were 0.37±0.10, 0.42±0.13, and 0.51±0.18 in the 1, 5, and 10 µmol/L As2O3 treated groups, respectively, which were significantly higher than those in the untreated control group (0.11±0.08) and DMSO solvent control group (0.13±0.07) (P < 0.05). In the 5 and 10 µmol/L As2O3 treated groups, the protein expression levels of cdk5 were 0.34±0.12 and 0.37±0.21, while the protein expression levels of p25 were 0.31±0.23 and 0.55±0.16, all of which were significantly higher than those in the untreated control group and DMSO solvent control group (P < 0.05). The protein expression levels of p35 were reduced in the 5 µmol/L As2O3 treated group (0.31±0.23) and 10 µmol/L As2O3 treated group (0.26±0.16), as compared with those in the untreated control group and DMSO solvent control group (P < 0.05). The mRNA and protein expression of calpain 2 showed no significant differences between all groups (P > 0.05).

CONCLUSIONThe calpain 1-cdk5/p25 pathway may be involved in the process of As2O3-induced neuronal cell apoptosis.

Animals ; Apoptosis ; drug effects ; Arsenic Poisoning ; Arsenicals ; Calpain ; metabolism ; Cells, Cultured ; Cyclin-Dependent Kinase 5 ; metabolism ; Neurons ; drug effects ; metabolism ; Oxides ; toxicity ; Rats

Adult ; Arsenic Poisoning ; etiology ; Arsenicals ; Humans ; Male ; Skin ; injuries ; Skin Absorption ; Wounds and Injuries

Acute Disease ; Adult ; Arsenic Poisoning ; Female ; Humans ; Male ; Middle Aged ; Young Adult

OBJECTIVETo establish coal arsenic poisoning rat model by feeding the rats with the corn powder baked by high arsenic coal as the main raw material.

METHODSFifty Wistar rats, healthy, were randomly divided into 5 groups according to the figures of their weights, including control group, drinking arsenic poisoning water group, low, medium and high arsenic contaminated grain group, 10 rats for each.Rats in control group and drinking arsenic poisoning water group were fed with standard feed without any arsenic containing. Rats in water group would drink 100 mg/L As2O3 solution and the rats in arsenic grain groups would be fed with the arsenic contaminated grain at the dose of 25, 50 and 100 mg/kg, respectively. The duration would last for 3 months.General situation and weight were observed. At the same time, the arsenic contents of urine, hair, liver and kidney of the rats in each group were detected, as well as the histopathology changes of liver and kidney, and the ultra structure of liver was observed.

RESULTSThe arsenic contents of urine (median(min-max)) of the rats in the arsenic water group, low, medium and high arsenic grain groups were separately 3055.59 (722.43-6389.05), 635.96(367.85-1551.31), 1453.84 (593.27-5302.94) and 3101.11 (666.64-6858.61) µg/g Cr; while the arsenic contents of hair of the rats in the above groups were separately (23.07 ± 10.38), (8.87 ± 3.31), (12.43 ± 6.65) and (25.68 ± 7.16) µg/g; the arsenic contents of liver of the rats in the above groups were separately (5.68 ± 3.13), (2.64 ± 1.52), (3.89 ± 1.76) and (5.34 ± 2.78) µg/g; and the arsenic contents of kidney were separately (6.90 ± 1.94), (3.48 ± 1.96), (5.03 ± 2.08) and (7.02 ± 1.62) µg/g; which were all significantly higher than those in the control group (86.70 (49.71-106.104) µg/g Cr,(1.28 ± 0.37) µg/g, (1.01 ± 0.34) µg/g and (1.82 ± 1.09) µg/g, respectively). The difference showed significance (P < 0.05). Under electron microscope detection, we observed the reduction of mitochondrial, the blurred mitochondrial cristae, some disappeared ridges, the reduced rough endoplasmic reticulum, and irregular uneven nuclear in the liver cells of rats in arsenic contaminated grain group. The contents of aspartate transaminase (AST) and total bile acid (TBA) in medium and high arsenic contaminated grain group were respectively (196.17 ± 46.18), (212.40 ± 35.14) U/L and (11.74 ± 4.07), (19.19 ± 4.68)µmol/L, which were higher than it in the control group (separately (143.10 ± 29.13) U/L and (6.23 ± 2.95)µmol/L). The contents of glutathione-S-transferases(GST), γ-glutamyltranspeptidase (GGT)and blood urea nitrogen (BUN)in high arsenic contaminated grain group were separately (196.21 ± 47.38)U/L, (1.71 ± 0.66)U/L, (9.54 ± 1.95)mmol/L, which were higher than that in the control group ((134.93 ± 24.80 )U/L, (0.75 ± 0.36)U/L, (7.67 ± 1.02)mmol/L, respectively). The contents of cholinesterase (CHE) in low, medium and high arsenic contaminated grain group were separately (259.90 ± 52.71)U/L, (263.44 ± 66.06)U/L and (244.90 ± 36.14)U/L, the contents of total protein(TP) in rats of high arsenic contaminated grain group were (62.64 ± 5.50)g/L, which was all lower than that in the control group ((448.33 ± 59.67)U/L, (69.38 ± 4.24)g/L, respectively). The contents of TBA in high arsenic contaminated grain group ( (19.19 ± 4.68) µmol/L) was higher than that in drinking water arsenic poisoning group ((15.15 ± 2.64)µmol/L). The differences of the above indexes were all significant (P < 0.05).

CONCLUSIONThe results showed the arsenic poisoning rat model produced by coal-burning were successfully established.

Animals ; Animals, Newborn ; Arsenic Poisoning ; etiology ; Coal ; Disease Models, Animal ; Environmental Exposure ; Female ; Flour ; Food Contamination ; Food Handling ; Male ; Rats ; Rats, Wistar ; Zea mays