Metabolomics reveals the metabolic disturbance caused by arsenic in the mouse model of inflammatory bowel disease.

Abstract

Arsenic exposure has long been a significant global health concern due to its association with various human diseases. The adverse health effects of arsenic can be influenced by multiple factors, resulting in considerable individual variability. Individuals with inflammatory bowel disease (IBD) are particularly vulnerable to the effects of toxin exposure, yet the specific impact of arsenic in the context of IBD remains unclear. In this study, we employed a non-targeted metabolomics approach to investigate how arsenic exposure affects metabolic homeostasis in an IBD model using Helicobacter trogontum-infected interleukin-10 deficient mice. Our results demonstrated that arsenic exposure disrupted the balance of various metabolites, including tryptophan, polyunsaturated fatty acids, purine and pyrimidine metabolites, and branched-chain amino acids, in mice with colitis but not in those without colitis. Notably, several crucial metabolites involved in anti-inflammatory responses, oxidative stress, and energy metabolism were significantly altered in mice with colitis. These results indicate that arsenic exposure in an IBD context can lead to extensive metabolic disturbances, potentially exacerbating disease severity and impacting overall health. This study underscores the necessity of evaluating arsenic toxicity in relation to IBD to better understand and mitigate associated health risks.