Oral nanosilica exposure in mice accumulated most in the liver and was linked to , liver , lipid deposition, and fibrosis that probiotics partly mitigated.
Evidence
This preclinical mouse gavage study tracked SiONP tissue distribution after 12 weeks and assessed microbiome, barrier, metabolic, liver injury, and probiotic-intervention endpoints.
Caveat
The work is limited to a mouse exposure model with mechanistic pathway signals, so human exposure risk and probiotic protection remain unproven.
Simplified
BACKGROUND: The increased use of nanosilica (SiONPs) poses a safety risk to public health. Current research on the tissue distribution and microbiota-gut-liver crosstalk toxicity of orally ingested SiONPs remains poorly understood. In this study, we examined the distribution of SiONPs by gavage in major organs as well as liver and fibrotic injury induced by microbiota-gut-liver crosstalk following the sub-chronic oral ingestion thereof. In addition, probiotics were administered to investigate their protective potential against SiONPs-induced hepatotoxicity. 2 2 2 2
RESULTS: Our results showed that C57BL/6J mice that received orally administered SiONPs for 12 w exhibited , imbalance of metabolites (short-chain fatty acids and lactate), intestinal barrier damage, and disruption of gut homeostasis. Furthermore, ICP-OES revealed the silicon accumulation in the Liver, with 165% increase compared to the control, higher than that in other tissue. Liver exhibited functional abnormalities and underwent Lipid deposition, autophagy, senescence and fibrosis. 16S rRNA sequencing analysis demonstrated that SiONPs reduced the abundance of probiotic Muribaculum and Ligilactobacillus, while increasing that of pathogenic Helicobacter. Notably, supplementation with probiotics remodelled the gut microbiome, particularly corrected the microbial communities disrupted by SiONPs, increased the proliferation of other probiotics, and reduced harmful bacteria. Moreover, the results of Masson staining, Nile red staining, and immunofluorescence showed that probiotic supplementation ameliorated liver lipid deposition, senescence, and fibrosis induced by the oral ingestion of SiONPs. Mechanistically, the TLR4/NF-κB and caspase-3-cytochrome C pathways may be involved in SiONPs-induced hepatotoxicity and probiotic regulation. 2 2 2 2 2
CONCLUSIONS: Continuous oral ingestion of SiONPs induced liver-specific accumulation, and caused abnormal deposition of liver lipids, senescence and fibrosis via microbiota-gut-liver crosstalk. Microbial therapy involving probiotic supplementation mitigated SiONPs-induced hepatotoxicity and exerted protective effects. This study provides a scientific reference for the rational application, risk management, and prevention of the harmful effects caused by SiONPs. 2 2 2
Key numbers
165%
Silicon Accumulation Increase
Silicon content in the liver compared to control group after 12 weeks.
Significant reduction
Probiotic Impact on Lipid Droplets
Comparison of lipid droplet percentage in liver tissue between and + probiotics groups.
p21CIP1 and p16INK4a levels decreased
Marker Reduction
Comparison of marker levels in liver tissue after exposure with and without probiotics.
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