4.7 Article

Food-grade titanium dioxide (E171) induces anxiety, adenomas in colon and goblet cells hyperplasia in a regular diet model and microvesicular steatosis in a high fat diet model

Journal

FOOD AND CHEMICAL TOXICOLOGY
Volume 146, Issue -, Pages -

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.fct.2020.111786

Keywords

Microvesicular steatosis; Mucin expression; Testicular damage; Food additives

Funding

  1. Direccion General de Asuntos del Personal Academico (DGAPA), Universidad Nacional Autonoma de Mexico (UNAM)
  2. Programa de Apoyo a Proyectos de Investigacion e Innovacion Tecnologica (PAPIIT) from DGAPA, UNAM [IN202219, IN224520, IN224119]
  3. Consejo Nacional de Ciencia y Tecnologia (CONACyT) [A1-S-28619]
  4. CONACyT [268769, 582547, 626239]

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Food-grade titanium dioxide (E171) is a white additive widely used in solid and liquid food products. There is still debate about E171 toxic effects after oral consumption since this additive is deposited in colon, liver, spleen, testis and brain. The consumption of E171 commonly occurs with Western diets that are characterized by a high fat content. Thus, E171 could worsen adverse effects associated with a high fat diet (HFD) such as anxiety, colon diseases and testicular damage. We aimed to evaluate the effects of E171 on anxiety-like behavior, colon, liver and testis and to analyze if the administration of a HFD could exacerbate adverse effects. E171 was administered at similar to 5 mg/kg(bw) by drinking water for 16 weeks and mice were fed with a Regular Diet or a HFD. E171 promoted anxiety, induced adenomas in colon, goblet cells hypertrophy and hyperplasia and mucins overexpression, but had no toxic effects on testicular tissue or spermatozoa in regular diet fed-mice. Additionally, E171 promoted microvesicular steatosis in liver in HFD fed-mice and the only HFD administration decreased the spermatozoa concentration and motility. In conclusion, E171 administration increases the number of adenomas in colon, induces hypertrophy and hyperplasia in goblet cells and microvesicular steatosis.

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