This review covers current knowledge of selenium in the dietary intake, its bioavailability, metabolism, functions, biomarkers, supplementation and toxicity, as well as its relationship with diseases and gut microbiota specifically on the symbiotic relationship between gut microflora and selenium status. Selenium is essential for the maintenance of the immune system, conversion of thyroid hormones, protection against the harmful action of heavy metals and xenobiotics as well as for the reduction of the risk of chronic diseases. Selenium is able to balance the microbial flora avoiding health damage associated with dysbiosis. Experimental studies have shown that inorganic and organic selenocompounds are metabolized to selenomethionine and incorporated by bacteria from the gut microflora, therefore highlighting their role in improving the bioavailability of selenocompounds. Dietary selenium can affect the gut microbial colonization, which in turn influences the host's selenium status and expression of selenoproteoma. Selenium deficiency may result in a phenotype of gut microbiota that is more susceptible to cancer, thyroid dysfunctions, inflammatory bowel disease, and cardiovascular disorders. Although the host and gut microbiota benefit each other from their symbiotic relationship, they may become competitors if the supply of micronutrients is limited. Intestinal bacteria can remove selenium from the host resulting in two to three times lower levels of host's selenoproteins under selenium-limiting conditions. There are still gaps in whether these consequences are unfavorable to humans and animals or whether the daily intake of selenium is also adapted to meet the needs of the bacteria.

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Selenium in Human Health and Gut Microflora: Bioavailability of Selenocompounds and Relationship With Diseases.

The Impact of Environmental Chemicals on the Gut Microbiome.

Acute oral methylmercury exposure perturbs the gut microbiome and alters gut-brain axis related metabolites in rats.

Methylmercury (MeHg) toxicity is a major environmental concern. In the aquatic reservoir, MeHg bioaccumulates along the food chain until it is consumed by riverine populations. There has been much interest in the neurotoxicity of MeHg due to recent environmental disasters. Studies have also addressed the implications of long-term MeHg exposure for humans. The central nervous system is particularly susceptible to the deleterious effects of MeHg, as evidenced by clinical symptoms and histopathological changes in poisoned humans. In vitro and in vivo studies have been crucial in deciphering the molecular mechanisms underlying MeHg-induced neurotoxicity. A collection of cellular and molecular alterations including cytokine release, oxidative stress, mitochondrial dysfunction, Ca2+ and glutamate dyshomeostasis, and cell death mechanisms are important consequences of brain cells exposure to MeHg. The purpose of this review is to organize an overview of the mercury cycle and MeHg poisoning events and to summarize data from cellular, animal, and human studies focusing on MeHg effects in neurons and glial cells. This review proposes an up-to-date compendium that will serve as a starting point for further studies and a consultation reference of published studies.

Cellular and Molecular Mechanisms Mediating Methylmercury Neurotoxicity and Neuroinflammation.

Food contaminants represent food constituents that are accidentally introduced during food preparation cycle. In addition to their direct toxic effects on human health at different levels, they influence both gut microbiota composition and function. This often leads to metabolic disorders linked to many aspects of the human body. Foods are poisoned with physical, chemical, or biological factors either in agriculture or during processing steps. These include naturally occurring compounds such as mycotoxins, agricultural chemicals such as pesticides and antibiotics, persistent organic pollutants, thermal process contaminants (e.g., furans, aromatic compounds, and nitrosamines), or heavy metals. These xenobiotics cause a wide range of toxicities. They also disturb gut homeostasis by inducing intestinal damage and inflammation and gut microbiota dysbiosis. We present herein the first comprehensive review of how food contaminants can specifically influence gut microbiota and intestinal homeostasis, and likewise via gut microbiota-mediated contaminants metabolism. The first part summarizes the different classes of food contaminants and their impact on gut microbiota and its homeostasis, while, the second part discusses the promising role of the gut microbiota in the biodegradation of these xenobiotics and the possible unfortunate exaggerated toxicities in some cases. Finally, we summarize the novel strategies to minimize toxic effects of food contaminants and future directions needed to explore the interactions between food contaminants and the gut microbiota.

Gut homeostasis and microbiota under attack: impact of the different types of food contaminants on gut health.

Selenium modulated gut flora and promoted decomposition of methylmercury in methylmercury-poisoned rats

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Selenium modulated gut flora and promoted decomposition of methylmercury in methylmercury-poisoned rats