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Gastrointestinal toxicity induced by microcystins. | LitMetric

Gastrointestinal toxicity induced by microcystins.

World J Clin Cases

Department of Environmental Hygiene, College of Public Health, Zhengzhou University, Zhengzhou 450001, Henan Province, China.

Published: September 2018

AI Article Synopsis

  • * Exposure to MCs has been associated with outbreaks of enterogastritis, which presents symptoms similar to food poisoning, especially in regions near lakes.
  • * The toxins disrupt gut barrier function, alter gut microbiota, inhibit digestive enzyme secretion, and impact immune gene expression, leading to significant intestinal damage that requires further study to understand the molecular mechanisms involved.

Article Abstract

Microcystins (MCs) are produced by certain bloom-forming cyanobacteria that can induce toxicity in various organs, including renal toxicity, reproductive toxicity, cardiotoxicity, and immunosuppressive effects. It has been a significant global environmental issue due to its harm to the aquatic environment and human health. Numerous investigators have demonstrated that MC exposure can induce a widespread epidemic of enterogastritis with symptoms similar to food poisoning in areas close to lakes. Both and studies have provided evidence of positive associations between MC exposure and gastrointestinal toxicity. The toxicity of MCs on the gastrointestinal tract is multidimensional. MCs can affect gastrointestinal barrier function and shift the structure of gut microbiota in different gut regions. Furthermore, MCs can inhibit the secretion of gastrointestinal digestive enzymes and the release of inflammatory cytokines, which affects the expression of immune-related genes in the intestine. The damage of the intestine is closely correlated to MC exposure because the intestine is the main site for the digestion and absorption of nutrients. The damage to the gastrointestinal tract due to MCs was summarized from different aspects, which can be used as a foundation for further exploration of molecular damage mechanisms.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6163130PMC
http://dx.doi.org/10.12998/wjcc.v6.i10.344DOI Listing

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