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Arsenic poisoning is a geochemical disease that seriously endangers human health. The liver is one of the important target organs for arsenic poisoning, several studies have shown that oxidative stress plays an important role in arsenic-induced liver damage. However, the specific mechanism of arsenic-induced oxidative stress has not yet been fully elucidated, and currently, there are no effective intervention measures for the prevention and treatment of arsenic-induced liver damage. In this study, the effect of the Nrf2/GPX4 signaling pathway and oxidative stress in the arsenic-induced liver damage was first evaluated. The results show that arsenic can activate the Nrf2/GPX4 signaling pathway and increase the oxidative stress, which in turn promotes arsenic-induced liver damage in MIHA cells. Moreover, when we applied the Nrf2 inhibitor, the promoting effect of arsenic on liver damage was alleviated by inhibiting the activation of the Nrf2/GPX4 signaling pathway. Subsequently, the Rosa roxburghii Tratt [Rosaceae] (RRT) intervention experiments in cells and arsenic poisoning population were designed. The results revealed that RRT can inhibit Nrf2/GPX4 signaling pathway to reduce oxidative stress, thereby alleviates arsenic-induced liver damage. This study provides some limited evidence that arsenite can activate Nrf2/GPX4 signaling pathway to induce oxidative stress, which in turn promotes arsenic-induced liver damage in MIHA cells. The second major finding was that Kaji-ichigoside F1 may be a potential bioactive compound of RRT, which can inhibit Nrf2/GPX4 signaling pathway to reduce oxidative stress, thereby alleviates arsenic-induced liver damage. Our study will contribute to a deeper understanding of the mechanisms in arsenic-induced liver damage, these findings will identify a possible natural medicinal food dual-purpose fruit, RRT, as a more effective prevention and control strategies for arsenic poisoning., Competing Interests: The authors declare they have no actual or potential competing financial interests., (Copyright © 2022 Yuyan Xu et al.)

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., (© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

To evaluate the effect of coal-burning arsenic (As) exposure on lung function and the potential underlying mechanisms, a total of 217 As-exposed subjects and 75 reference subjects were recruited into this study. Hair arsenic (H-As), pulmonary function tests, and serum inflammatory markers CC16, SP-A, MMP-9, and TIMP-1 were evaluated. Residents from As-exposed areas showed higher H-As concentrations (median 0.25 μg/g) than subjects from the reference area (median 0.14 μg/g). Large reductions in lung function parameters were noted in the As-exposed group. A significant negative correlation was observed between H-As concentrations and lung function. Specifically, monotonic negative dose-response relationships were observed between H-As and FEV1(%), FEV1/FVC (%) and FEF75 (%) (all P < 0.05), while the associations between H-As and FVC (%), FEF25 (%), and FEF50 (%) were nonlinear (P for nonlinearity = 0.03, 0.001, 0.01, respectively). In addition, there was a direct positive relationship between H-As and the inflammatory response. Alterations in inflammatory biomarkers (CC16, SP-A, MMP-9, and MMP-9/TIMP-1) were significantly associated with As-induced lung function impairment. Thus, this population-based study revealed that As exposure has significant toxic effects on lung function and increased inflammation may occur during this toxic process. We provide scientific evidence for an As-induced alteration in inflammatory biomarkers and pulmonary damage in an As-exposed population. The results of this study can inform risk assessment and risk control processes in relation to human As exposure in coal-burning arsenicosis areas., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Chronic exposure to arsenic remains a major environmental public health concern worldwide, affecting hundreds of millions of people. Arsenic-induced multiorgan damage and miRNA expression changes after arsenic exposure have been determined, but their associations and risks have not been fully examined. In this study, we measured the expression levels of five miRNAs in plasma from control and arsenic poisoned populations, and we analyzed the relationship between miRNAs and multiorgan damage. The results clearly show that the upregulation of miR-155 expression can increase the risk of arsenic induced skin damage (OR = 10.55; 95% CI: 6.02, 18.47); further, there is a link between the expression of miR-21 (OR = 11.84; 95% CI: 5.34, 26.28) and miR-145 (OR = 2.39; 95% CI: 1.61, 3.55) and liver damage, and miR-191 and kidney damage (OR = 3.65; 95% CI: 1.49, 8.93). In addition, we analyzed the diagnostic value of miRNAs associated with specific organ damage in arsenic-induced multiorgan damage. It was found that the miR-155 has a certain diagnostic value in arsenic-induced skin damage (AUC = 0.83), miR-21 and miR-145 have diagnostic value for liver damage (AUC = 0.80, 0.81) and miR-191 has diagnostic value for kidney damage (AUC = 0.83). This study provides the first comprehensive assessment of the association and risk of five miRNAs with arsenic-induced multiorgan damage. The study can provide a scientific basis for further understanding the causes of arsenic-induced multiorgan damage, identification of possible biological markers, and improvement of targeted prevention and control strategies., (Copyright © 2019 Elsevier B.V. All rights reserved.)

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., (Copyright © 2019 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Evidence from epidemiological studies suggests that chronic arsenic exposure may be associated with a higher incidence of hypertension in the population. However, the effect of arsenic exposure on blood pressure remains unexplored in different populations, regions, and regarding arsenic biomarkers. This study investigated 233 arsenicosis patients and 84 participants from a non-arsenic-exposed area to explore the relationship between arsenic exposure and blood pressure and the occurrence of hypertension and wide pulse pressure (WPP) in patients with coal-burning arsenicosis. The results show that arsenic exposure is related to an increased incidence of hypertension and WPP in the arsenicosis population, primarily due to an induced increase in systolic blood pressure (SBP) and pulse pressure (PP) (OR = 1.47, 1.65, all p < 0.05). The dose–effect relationships between monomethylated arsenicals (MMA), trivalent arsenic (As3+), hypertension, and WWP were characterized following trend analyses (all p-trend < 0.05) in the coal-burning arsenicosis population. After adjusting for age, gender, body mass index (BMI), smoking, and alcohol usage, compared with low-level exposure, the high level of MMA exposure increases the risk of hypertension by 1.99 times (CI: 1.04–3.80) and the WPP by 2.42 times (CI: 1.23–4.72). Similarly, the high level of As3+ exposure increases the hypertension risk by 3.68 times (CI: 1.86–7.30) and the WPP by 3.84 times (CI: 1.93–7.64). Together, the results revealed that urinary MMA and As3+ levels are mainly associated with increased SBP and induce a higher incidence of hypertension and WPP. This study provides preliminary population evidence that cardiovascular-related adverse events such as hypertension and WPP ought to be noticed in the coal-burning arsenicosis population. [ABSTRACT FROM AUTHOR]

Environmental exposure to arsenic remains a worldwide public health challenge. Oxidative stress and aberrant DNA methylation are both characteristics of arsenic toxicology; however, the relationship between these is not well understood. Ten-eleven translocation (TET1, TET2 and TET3), which is the conversion of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC), plays a central role in the DNA demethylation process. Further, it can prevent cytosine-phosphate-guanine (CpG) islands from developing abnormal hypermethylation under oxidative stress. Here, we observed that NaAsO 2 could induce oxidative stress in human bronchial epithelial (HBE) cells. This was accompanied by an inhibition of TET-mediated DNA demethylation. Subsequent results showed that TET1 and TET2 siRNA led to further inhibition of genome 5hmC and a higher level of oxidative stress in NaAsO 2 -treated HBE cells. Conversely, l -ascorbic acid enhanced TET proteins and effectively upregulated 5hmC, which antagonized the NaAsO 2 -induced oxidative stress. Additionally, the TETs positively regulated the promoter methylation of the antioxidant genes 8-oxoguanine DNA glycosylase (OGG1) and glutathione S-transferase Pi 1 (GSTP1). Taken together, the results indicate that arsenic induced the inhibition of TET-mediated DNA demethylation, which induced promoter hypermethylation, inhibiting the expression of the OGG1 and GSTP1, and increasing oxidative stress in lung cells in vitro. l -ascorbic acid effectively alleviated arsenic-induced oxidative stress by restoring TET function. • NaAsO 2 inhibits TET-mediated DNA demethylation in HBE cells. • TET-mediated DNA demethylation is involved in NaAsO 2 -induced oxidative stress. • TETs positively regulated the promoter methylation of OGG1 and GSTP1. • L-ascorbic acid alleviates NaAsO 2 -induced oxidative stress by restoring TET. [ABSTRACT FROM AUTHOR]