Abstract

Arsenic is considered a worldwide pollutant that can be present in drinking water. Arsenic exposure is associated with various diseases, including cancer. Antioxidants as selenite and α-tocopherol-succinate have been shown to modulate arsenic toxic effects. Since changes in STAT3 and PSMD10 gene expression have been associated with carcinogenesis, the aim of this study was to evaluate the effect of arsenic exposure and co-treatments with selenite or α-tocopherol-succinate on the expression of these genes, in the livers of chronically exposed Syrian golden hamsters. Animals were divided into six groups: (i) control, (ii) chronically treated with 100 ppm arsenic, (iii) treated with 6 ppm α-tocopherol-succinate (α-TOS), (iv) treated with 8.5 ppm selenite, (v) treated with arsenic + α-TOS, and (vi) treated with arsenic + selenite. Urine samples and livers were collected after 20 weeks of continuous exposure. The urine samples were analyzed for arsenic species by atomic absorption spectrophotometry, and real-time RT-qPCR analysis was performed for gene expression evaluation. A reduction in STAT3 expression was observed in the selenite-treated group. No differences in PSMD10 expression were found among groups. Histopathological analysis revealed hepatic lymphocytosis in selenite-treated animals. As a conclusion, long-term exposure to arsenic does not significantly alter the expression of STAT3 and PSMD10 oncogenes in the livers of hamsters; however, selenite down-regulates STAT3 expression and provokes lymphocytosis.

Highlights

  • The toxic properties of arsenic have been known since the 13th century, and the use of arsenic as a poison has played a role in domestic and dynastic intrigues throughout history [1]

  • Hamsters in each group were monitored every week for 20 weeks to evaluate weight gain and survival, in animals exposed chronically to arsenic and/or the selected antioxidants

  • For α-TOS and selenite doses, they were chosen on previous studies in animal models where not toxicity was observed by these two antioxidants [14,21,27,28]

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Summary

Introduction

The toxic properties of arsenic have been known since the 13th century, and the use of arsenic as a poison has played a role in domestic and dynastic intrigues throughout history [1]. Depending on the level of exposure, inorganic arsenic can cause liver diseases, neurological disorders, cardiovascular lesions, cancer, among others [2]. Chronic arsenic exposure has been associated with non-cirrhotic portal fibrosis, with or without the development of portal hypertension [3]. Since the introduction of arsenic to industrial processes, and due to anthropogenic activities, such as mining, the prevalence of several types of cancer has increased in workers in specific environments [2,4,5]. Arsenic is a well-known water pollutant that generates worldwide public health concerns. There is an association of skin cancer and diabetes mellitus prevalence in this arsenic chronically exposed areas [7]. The World Health Organization (WHO) has established a limit of 10 μg/L in drinking water and a provisional tolerable daily intake for inorganic arsenic (2.14 μg/kg/day) [8]

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