LC-MS based untargeted metabolomics studies of the metabolic response of Ginkgo biloba extract on arsenism patients.

Arsenic is an environmentally ubiquitous toxic metalloid. Chronic exposure to arsenic may lead to arsenicosis, while no specific therapeutic strategies are available for the arsenism patients. And Ginkgo biloba extract (GBE) exhibited protective effect in our previous study. However, the mechanisms by which GBE protects the arsenism patients remain poorly understood. A liquid chromatography-mass spectrometry (LC-MS) based untargeted metabolomics analysis was used to study metabolic response in arsenism patients upon GBE intervention. In total, 39 coal-burning type of arsenism patients and 50 healthy residents were enrolled from Guizhou province of China. The intervention group (n = 39) were arsenism patients orally administered with GBE (three times per day) for continuous 90 days. Plasma samples from 50 healthy controls (HC) and 39 arsenism patients before and after GBE intervention were collected and analyzed by established LC-MS method. Statistical analysis was performed by MetaboAnalyst 5.0 to identify differential metabolites. Multivariate analysis revealed a separation in arsenism patients between before (BG) and after GBE intervention (AG) group. It was observed that 35 differential metabolites were identified between BG and AG group, and 30 of them were completely or partially reversed by GBE intervention, with 14 differential metabolites significantly up-regulated and 16 differential metabolites considerably down-regulated. These metabolites were involved in promoting immune response and anti-inflammatory functions, and alleviating oxidative stress. Taken together, these findings indicate that the GBE intervention could probably exert its protective effects by reversing disordered metabolites modulating these functions in arsenism patients, and provide insights into further exploration of mechanistic studies.

Rosa roxburghii Tratt juice inhibits NF-κB and increases IL-2 to alleviates the Foxp3-mediated Tregs imbalance in the peripheral blood of arseniasis patients.

Arsenic can cause immune inflammation, which is the basis of arsenic-induced damage to multiple organs and systems. Forkhead box P3 (Foxp3)-labelled CD4+CD25+ regulatory T cells (Tregs) play an essential role in maintaining immune homeostasis. Nuclear factor-κb (NF-κB) and Interleukin-2 (IL-2) are critical regulators of Foxp3. Rosa roxburghii Tratt (RRT) is an edible medicinal plant with anti-inflammation effects. In this study, a control group (n = 41) and an arseniasis group (n = 209) were recruited, and screened subjects from the arseniasis patients for RRTJ (n = 46) or placebo (n = 43) to explore the possible mechanism by which RRT alleviates immune inflammation. The results indicated that RRTJ can inhibits NF-κB and increases IL-2, and alleviates the Foxp3-mediated Tregs imbalance in the peripheral blood of arseniasis patients. In summary, these findings suggest a novel intervention or therapeutic target for immune inflammation in arseniasis patients and provide new evidence that RRTJ inhibits immune inflammation. Supplementary Information: The online version contains supplementary material available at 10.1007/s10068-023-01384-0.

Assessing the health risks of coal-burning arsenic-induced skin damage: A 22-year follow-up study in Guizhou, China.

Risk assessment of arsenic-induced skin damage has always received significant global attention. Theories derived from arsenic exposure in drinking water may not be applicable to the coal-burning type to arsenic-exposed area. Furthermore, very few studies have successfully determined the reference value of cumulative arsenic (CA) exposure that leads to specific skin lesions. In this study, we conducted a 22-year follow-up investigation to assess the risk of skin lesions and cancer resulting from long-term, multi-channel arsenic exposure from hazard identification, dose-response assessment, exposure assessment, and risk characterization. The results show that the arsenic exposure can significantly increase the prevalence of skin lesions. For each interquartile range increase of hair arsenic (HA) and CA, the risk of skin damage increased by 1.91 and 3.90 times, respectively. The lower confidence limit of the benchmark dose of HA of arsenic-induced various skin lesions ranged from 0.07 to 0.12 µg·g-1, and 932.57 to 1368.92 mg for CA. The chronic daily intake, lifetime average daily dose in the arsenic-exposed area after the comprehensive prevention and control measures have decreased significantly, but remained higher than the daily baseline level of 3.0 µg·kg-1·d-1. Even as recently as 2020, the hazard quotients and hazard index still exceeded 1, measuring 155.33 and 55.20, and the lifetime excess risk of skin cancer (2.80 × 10-3) remains significantly higher than the acceptable level of 10-6. Our study underscores the effectiveness of comprehensive prevention and control measures in managing high arsenic exposure in coal-burning arsenic poisoning areas. However, it is crucial to acknowledge that the risk of both non-carcinogenic and carcinogenic effects on the skin remains substantially higher than the acceptable level. We recommend setting reference limits for monitoring skin damage among individuals exposed to arsenic, with a recommended upper limit of 0.07 µg·g-1 for HA and a maximum acceptable level of 935.57 mg for CA.

Single-cell transcriptome analysis reveals cellular heterogeneity and highlights Fstl1-regulated alveolar myofibroblasts in mouse lung at birth.

The matricellular protein, follistatin-like 1 (FSTL1), regulates lung development and saccular formation. Here, we employed single-cell RNA sequencing (scRNA-seq) to construct a transcriptomic atlas of 22,774 individual cells from wild-type (WT) and Fstl1-/- lung (E18.5) samples and identified 27 cell subtypes. We observed abnormal population sizes and gene expression profiles in diverse cell subtypes in Fstl1-/- lung samples. We identified Pdgfra and Tgfbi as genetic markers specifically expressed in postnatal myofibroblasts (MyoFBs). Fstl1 deletion decreased the number of MyoFB cells and downregulated their roles in ECM organization and muscle tissue/vasculature development, partly through the TGF-ß1/BMP4 signaling pathway. Our data provide a single-cell view of the cellular heterogeneity and the molecular mechanisms underlying abnormal saccular formation and atelectatic lungs in Fstl1-/- mice.

Using bioinformatics and systems biology to discover common pathogenetic processes between sarcoidosis and COVID-19.

The coronavirus disease (COVID-19) pandemic caused by SARS-CoV-2 is ongoing. Individuals with sarcoidosis tend to develop severe COVID-19; however, the underlying pathological mechanisms remain elusive. To determine common transcriptional signatures and pathways between sarcoidosis and COVID-19, we investigated the whole-genome transcriptome of peripheral blood mononuclear cells (PBMCs) from patients with COVID-19 and sarcoidosis and conducted bioinformatic analysis, including gene ontology and pathway enrichment, protein-protein interaction (PPI) network, and gene regulatory network (GRN) construction. We identified 33 abnormally expressed genes that were common between COVID-19 and sarcoidosis. Functional enrichment analysis showed that these differentially expressed genes were associated with cytokine production involved in the immune response and T cell cytokine production. We identified several hub genes from the PPI network encoded by the common genes. These hub genes have high diagnostic potential for COVID-19 and sarcoidosis and can be potential biomarkers. Moreover, GRN analysis identified important microRNAs and transcription factors that regulate the common genes. This study provides a novel characterization of the transcriptional signatures and biological processes commonly dysregulated in sarcoidosis and COVID-19 and identified several critical regulators and biomarkers. This study highlights a potential pathological association between COVID-19 and sarcoidosis, establishing a theoretical basis for future clinical trials.

Assessing the risk of coal-burning arsenic-induced liver damage: a population-based study on hair arsenic and cumulative arsenic.

Exposure to arsenic-contaminated air and food caused by the burning of coal in unventilated indoor stoves is a major environmental public health concern in Guizhou Province, China. The liver is one of the main target organs for coal-fired arsenic exposure; however, there is little information about the risk assessment between cumulative arsenic exposure and the prevalence of liver damage. This study first evaluated the chronic daily intake (CDI) for two exposure pathways (inhalation and ingestion) and five environmental media (i.e., indoor and outdoor air, drinking water, rice, corn, and chili peppers) in 1998, 2006, 2014, and 2017. Then, the dose-effect and dose-response relationship between hair arsenic (HA) and cumulative arsenic (CA) levels and liver damage was analyzed. The results clearly show that the CDI in 1998 was 34.9 µg·kg-1·d-1, 22.9 µg·kg-1·d-1 in 2006, 11.7 µg·kg-1·d-1 in 2014, and 6.7 µg·kg-1·d-1 in 2017 in the arsenic exposure area. All of these values were higher than the daily baseline level of 3.0 µg·kg-1·d-1 as recommended by the Joint FAO/WHO Expert Committee on Food Additives (JECFA), and the increased HA and CA can increase the risk of coal-fired arsenic-induced liver damage. In addition, we analyzed the possible maximum acceptable CA exposure level for coal-fired arsenic-induced liver damage using the Bayesian benchmark dose. The recommended maximum acceptable CA exposure level for liver damage caused by coal-burning arsenic is 7120 mg. This study provides scientific insight into understanding the dose-response relationship of liver damage caused by coal-burning arsenic exposure and the monitoring and prevention of arsenic poisoning.

Assessing the potential value of Rosa Roxburghii Tratt in arsenic-induced liver damage based on elemental imbalance and oxidative damage.

Environmental exposure to arsenic is a major public health challenge worldwide. Growing evidence indicates that coal-burning arsenic can cause hepatic oxidative damage. However, the value of Rosa roxburghii Tratt (RRT) with antioxidant properties on arsenic-caused hepatic oxidative damage has never been elucidated yet. In this study, the animals were exposed to coal-burning arsenic (10 mg/kg bw) for 90 days and the result showed a loss of body weight, impaired liver function and liver diseases, increased hepatic oxidative damage and metabolic disorder of multiple elements including selenium, copper, zinc which were related to synthesis of antioxidant enzymes. Another finding is that RRT restored the abnormal liver function and alleviated the procedures of liver diseases of arsenic poisoning rats. In addition, it could also effectively reduce the degree of oxidative damage in serum and liver, and restore the activity of some antioxidant enzymes. Importantly, RRT reversed the content of most disordered elements caused by arsenic in liver and reduced the excretion of several essential elements in urine, including selenium, copper and zinc. Our study provides some limited evidence that RRT can alleviate coal-burning arsenic-induced liver damage induced by regulating elemental metabolic disorders and liver oxidation and antioxidant balance. The study provides a scientific basis for further studies of the causes of the arsenic-induced liver damage, and effective intervention strategies.

In-Silico Multi-Omics Analysis of the Functional Significance of Calmodulin 1 in Multiple Cancers.

Aberrant activation of calmodulin 1 (CALM1) has been reported in human cancers. However, comprehensive understanding of the role of CALM1 in most cancer types has remained unclear. We systematically analyzed the expression landscape, DNA methylation, gene alteration, immune infiltration, clinical relevance, and molecular pathway of CALM1 in multiple cancers using various online tools, including The Cancer Genome Atlas, cBioPortal and the Human Protein Atlas databases. Kaplan-Meier and receiver operating characteristic (ROC) curves were plotted to explore the prognostic and diagnostic potential of CALM1 expression. Multivariate analyses were used to evaluate whether the CALM1 expression could be an independent risk factor. A nomogram predicting the overall survival (OS) of patients was developed, evaluated, and compared with the traditional Tumor-Node-Metastasis (TNM) model using decision curve analysis. R language was employed as the main tool for analysis and visualization. Results revealed CALM1 to be highly expressed in most cancers, its expression being regulated by DNA methylation in multiple cancers. CALM1 had a low mutation frequency (within 3%) and was associated with immune infiltration. We observed a substantial positive correlation between CALM1 expression and macrophage and neutrophil infiltration levels in multiple cancers. Different mutational forms of CALM1 hampered immune cell infiltration. Additionally, CALM1 expression had high diagnostic and prognostic potential. Multivariate analyses revealed CALM1 expression to be an independent risk factor for OS. Therefore, our newly developed nomogram had a higher clinical value than the TNM model. The concordance index, calibration curve, and time-dependent ROC curves of the nomogram exhibited excellent performance in terms of predicting the survival rate of patients. Moreover, elevated CALM1 expression contributes to the activation of cancer-related pathways, such as the WNT and MAPK pathways. Overall, our findings improved our understanding of the function of CALM1 in human cancers.

miR-122-5p Mediates Fluoride-Induced Osteoblast Activation by Targeting CDK4.

Chronic intake of fluoride, existing in the environment, may cause endemic fluorosis, which is characterized by the occurrence of skeletal and dental fluorosis. However, the pathogenesis of fluorosis has not yet been elucidated. Abnormal osteoblast proliferation and activation have a pivotal role in bone turnover disorders which are linked to skeletal fluorosis. MicroRNAs are involved in fundamental cellular processes, including cell proliferation. Based on our previous study, population study and in vitro experiments were designed to understand the effect of miR-122-5p on osteoblast activation in skeletal fluorosis through targeting cyclin-dependent kinase 4 (CDK4). In human populations with coal-burning type fluoride exposure, the results showed that miR-122-5p was downregulated but CDK4 expression was upregulated and miR-122-5p was negatively correlated with CDK4 expression. Furthermore, in human osteoblasts treated with sodium fluoride, we demonstrated that miR-122-5p mediated osteoblast activation of skeletal fluorosis via upregulation of the CDK4 protein. In support of this, dual-luciferase reporter assay showed that miR-122-5p modulated CDK4 protein levels by targeting its 3'-untranslated region. These findings show, for the first time, that miR-122-5p may be involved in the cause and development of skeletal fluorosis by targeting CDK4.

Alterations of arsenic levels in arsenicosis residents and awareness of its risk factors: A population-based 20-year follow-up study in a unique coal-borne arsenicosis County in Guizhou, China.

BACKGROUND: Currently, most arsenic (As) studies in populations are concerned with water-borne arsenicosis. However, residents in Xingren County of Guizhou Province, Southwest of China, represent a unique case of arsenicosis which is related to indoor combustion of high As-containing coal. This study aimed to assess the alterations of As levels and its risk factors in coal-borne arsenicosis residents during the past 20 years. METHODS: Four follow-up investigations in Xingren County were selected from the year 1998 to 2017, a total of 245, 272, 584, and 309 residents were involved in the four investigations, respectively. Local external environmental medium (coal, soil, water, air, rice, corn and chili peppers) and biological samples (urine, hair) were collected at each time of investigation for total As analysis. Sociodemographics and lifestyles variables were extracted from the questionnaire investigation. Both univariate and multivariate unconditional logistic regression models were performed to analyze the variation of risk factors for coal-borne arsenicosis. RESULTS: A substantial reduction of total As levels was observed both in external environmental medium and biological samples in the unique coal-borne arsenicosis region, especially since the year 2006. In addition, age, duration of consuming high As-containing coal and smoking status were found to be the most significant risk factors for coal-borne arsenicosis during the past 20 years by both two different logistic regression models. Room ventilation and grain drying modes were no longer to be risk factors since 1998 survey. Annual household income had always been an important protective factor for coal-borne arsenicosis in recent 20 years by both two different logistic regression models. Grain storage modes had become significant protective factor in 2014 and 2017 survey. A certain correlation between sex, education and coal-borne arsenicosis was observed by univariate logistic regression model but no clear links were found by multivariate logistic regression model. CONCLUSIONS: Considerable efforts to blocking As exposure from burning coal and As contaminated foods in this region are observed over the study period. Further practical health education programs may need to target individuals with long-term of As exposure, lower socioeconomic status and smoking in order to better prevent and control the occurrence and development of coal-borne arsenicosis.

The PKCδ-Nrf2-ARE signalling pathway may be involved in oxidative stress in arsenic-induced liver damage in rats.

Arsenic poisoning is a worldwide endemic disease that affects thousands of people. Growing evidence from animal, cell, and human studies indicates that arsenic has deleterious effects on the liver. Oxidative stress is considered the primary mechanism for arsenic toxicity in liver damage. However, the mechanisms remain unclear. In light of this fact, the main objective of this study was to investigate the effects of the protein kinase C delta-nuclear factor E2-related factor 2-antioxidant response element (PKCδ-Nrf2-ARE) signalling pathway on oxidative stress in liver damage. In the present study, we used a model of liver damage induced by coal-burning arsenic in rats, which was set up by our research group. The oxidative stress index and the transcription and protein expression levels of PKCδ, Nrf2, Keap1, SOD1, and GPx1 were detected, and then their correlation analyses were carried out. The results demonstrated that coal-burning arsenic can cause oxidative stress liver damage in rats, which may be related to the PKCδ-Nrf2-ARE signalling pathway. This study may provide a new pathway for studies of the mechanisms of arsenism.

The effect of elemental content on the risk of dental fluorosis and the exposure of the environment and population to fluoride produced by coal-burning.

Endemic fluorosis is a geochemical disease that affects thousands of people. Growing evidence from domestic and foreign studies indicate that fluorosis is associated with an abnormal level of the elements (such as F, Ca, Fe, Mg, Cu, Zn, P) in the environment and a population exposed to fluoride. To study the effect of the elemental content on the risk of dental fluorosis, the content of 25 elements in the environment produced by coal-burning and a population exposed to fluoride was determined. The results show that an abnormal level of various elements (including F, Al, Se, Zn, Cu, Fe, Mo, Mn, B, V, Ca, Mg, and P) in the population exposed to fluoride, which is related to the increasing or decreasing of the corresponding elements in the environment. Subsequent univariate and multivariate regression analyses show that high levels of F, Al, As, Pb and Cr were a risk factor for dental fluorosis, but not Se, Zn, Cu, B, Ca and P which were a protective factor for dental fluorosis. This study can provide a scientific basis for a further understanding of the causes of health damage caused by fluoride and the improvement of targeted prevention strategies.

A possible new mechanism and drug intervention for kidney damage due to arsenic poisoning in rats.

Arsenic poisoning is a worldwide endemic disease that affects thousands of people. Currently, the aetiology of the disease is known, but its pathogenesis is uncharacterized and there is no specific treatment. We established a rat model of coal-burning arsenic poisoning by feeding the animals corn powder baked with high arsenic coal. By observing subsequent changes in kidney and immune function, we found that arsenic induces both kidney and immune damage. Furthermore, there is a significant correlation between kidney and immune damage. Moreover, Ginkgo biloba, a known immune enhancer, was used as an intervention agent in arsenic poisoned rats to validate the relationship between kidney and immune damage. Meanwhile, we also explored the mechanism of Ginkgo biloba treatment of kidney damage in burning-coal arsenic poisoned rats. We found that Ginkgo biloba enhanced immune function in rats with arsenic poisoning and ameliorated arsenic-induced kidney damage. These results suggest that immune suppression may be one of the mechanisms underlying arsenic-induced kidney damage and that Ginkgo biloba might relieve kidney damage by enhancing immune function.

Correction: A possible new mechanism and drug intervention for kidney damage due to arsenic poisoning in rats.

[This corrects the article DOI: 10.1039/C5TX00165J.].

[The regulation mechanism of protein kinase Cδ on arsenic liver injury caused by coal-burning].

OBJECTIVE: To investigate the effects of mRNA transcriptional and protein expressions of protein kinase Cδ (PKCδ) on the development of arsenic liver injury caused by coal-burning. METHODS: Population study:133 arsenic exposures were selected as arsenic exposure groups including the ward non-patient group (25 cases) , no obvious hepatopathy group (38 cases) , mild (43 cases) and moderate to severe hepatopathy group (27 cases) from the area with endemic arsenism in Guizhou province. Another 34 healthy residents were selected as the control group in non-arsenic pollution village. The urine and peripheral blood were collected from the subjects. The arsenic contents in urine and mRNA expressions of PKCδ in peripheral blood were detected. Animal experiment study:thirty wistar rats were randomly by random number table divided into control group, drinking water arsenic poisoning group and coal-burning arsenic poisoning group (i.e., low, medium and high arsenic contaminated grain group) by random number table method, including 6 rats in each group. The control group was fed normally for 3 months, drinking water arsenic poisoning group and coal-burning arsenic poisoning groups were fed respectively with 10 mg/kg As2O3 solution and different concentrations (25, 50 and 100 mg/kg) of arsenic-containing feed which was persisted 3 months. The arsenic contents in urine, mRNA expression levels of PKCδ in peripheral blood and liver tissue and the protein expression levels of phosphorylated protein kinase Cδ(pPKCδ) in liver tissue were detected. RESULTS: The median(quartile) of arsenic contents in urine were 25.58 (18.62-40.73), 56.66 (38.93-76.77), 64.90 (39.55- 98.37) and 75.47 (41.30-109.70) µg/g Cr respectively for the non-patient group, no obvious hepatopathy group, mild and moderate to severe hepatopathy group. The levels were higher than that in the control group (23.34 (17.84-37.45) µg/g Cr) (P < 0.05), except for the ward non-patient group. The arsenic contents in rat urine were 2223.61 (472.98-3976.73), 701.16 (194.01-1300.27), 1060.94 (246.33-2585.47) and 3101.11 (1919.97-5407.07) µg/g Cr, respectively for the drinking water arsenic poisoning group, the low, medium and high dosage arsenic grain contamination groups, all higher than that in the control group (94.32 (22.65-195.25) µg/g Cr) (P < 0.05) . The protein expressions of pPKCδ in liver tissue were 324.83 ± 25.06, 278.50 ± 30.57, 308.83 ± 34.67 and 326.33 ± 35.09, which were significantly higher than that in the control group (240.17 ± 28.07) (P < 0.05) . The protein expression levels of pPKCδ in liver cell membrane were 0.49 ± 0.06,0.33 ± 0.05,0.37 ± 0.06 and 0.50 ± 0.08, which were significantly higher than that in the control group (0.28 ± 0.04) (P < 0.05) . The protein expression levels of pPKCδ in liver cell cytoplasm were 0.38 ± 0.06,0.31 ± 0.05, 0.35 ± 0.05 and 0.36 ± 0.05, which were significantly higher than that in the control group (0.24 ± 0.05) (P < 0.05). CONCLUSION: The arsenic may regulate protein expressions of pPKCδ and induce its membrane translocation, and cause the development of arsenic liver injury caused by coal-burning.

[The establishment of the arsenic poisoning rats model caused by corn flour baked by high-arsenic coal].

OBJECTIVE: To establish coal arsenic poisoning rat model by feeding the rats with the corn powder baked by high arsenic coal as the main raw material. METHODS: Fifty 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. RESULTS: The 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). CONCLUSION: The results showed the arsenic poisoning rat model produced by coal-burning were successfully established.