Disrupted intestinal mucosal barrier mediated by alcohol consumption aggravates systemic microplastic accumulation

Area of Science:

• Environmental Health
• Toxicology
• Gastroenterology

Background:

• Microplastics (MPs) accumulate in the human body via the food chain and digestive tract.
• Alcohol consumption can compromise intestinal barrier integrity.
• The combined effects of alcohol and MPs on organ distribution and toxicity are not well understood.

Purpose of the Study:

• To investigate the relationship between alcohol consumption and the organ distribution of microplastics.
• To examine how alcohol-induced disruption of the intestinal barrier affects microplastic accumulation.
• To explore the impact of microplastic accumulation on alcohol-related pathologies, such as hepatic steatosis.

Main Methods:

• A mouse model (C57BL/6) was used, divided into control, control + MP, ethanol (EtOH), and EtOH + MP groups.
• Mice were administered a Lieber-DeCarli diet with or without EtOH, and microplastics (polystyrene MPs) via oral gavage.
• MP accumulation in the liver, intestines, spleen, and brain was quantified, along with intestinal damage and hepatic steatosis.

Main Results:

• The EtOH + MP group exhibited significantly higher microplastic accumulation in the liver, intestines, spleen, and brain compared to the control + MP group.
• Intestinal damage was most severe in the EtOH + MP group.
• Hepatic steatosis was more pronounced in the EtOH + MP group than in the EtOH group.

Conclusions:

• Alcohol consumption exacerbates microplastic accumulation in organs by disrupting the intestinal mucosa.
• Microplastic accumulation may contribute to secondary health issues, such as worsening hepatic steatosis.
• This study highlights the critical role of the gut-liver axis in understanding alcohol-induced gut permeability and microplastic toxicity.