PUBLICATION
The probiotic SLAB51 as agent to counteract BPA toxicity on zebrafish gut microbiota -liver-brain axis
- Authors
- Giommi, C., Lombo, M., Habibi, H.R., Rossi, G., Basili, D., Mangiaterra, S., Ladisa, C., Giulia, C., Carnevali, O., Maradonna, F.
- ID
- ZDB-PUB-231224-4
- Date
- 2023
- Source
- The Science of the total environment 912: 169303 (Journal)
- Registered Authors
- Carnevali, Oliana
- Keywords
- Endocrine disruptors, metabolomics, Histology, Immune system, Immunohistochemistry, Probiotics
- MeSH Terms
-
- Animals
- Benzhydryl Compounds/toxicity
- Brain
- Endocrine Disruptors*/toxicity
- Fatty Liver*
- Female
- Gastrointestinal Microbiome*
- Glycogen
- Male
- Phenols*
- Probiotics*
- Zebrafish/microbiology
- PubMed
- 38135076 Full text @ Sci. Total Environ.
Citation
Giommi, C., Lombo, M., Habibi, H.R., Rossi, G., Basili, D., Mangiaterra, S., Ladisa, C., Giulia, C., Carnevali, O., Maradonna, F. (2023) The probiotic SLAB51 as agent to counteract BPA toxicity on zebrafish gut microbiota -liver-brain axis. The Science of the total environment. 912:169303.
Abstract
A plethora of studies have so far described the toxic effects of bisphenol A (BPA) on organism health highlighting the urgent need to find new strategies not only to reduce the presence of this toxicant but also to counteract its adverse effects. In this context, probiotics emerged as a potential tool since they promote organism welfare. Using a multidisciplinary approach, this study explores the effects of SLAB51 dietary administration to counteract BPA toxicity using zebrafish as a model. Adult males and females were maintained under standard conditions (control group; C), exposed for 28 days via the water to an environmental relevant dose of BPA (10 μg/L; BPA), dietary treated with SLAB51 (109 CFU/g of body weight; P) and co-treated with BPA plus SLAB51 (BPA + P). In the gut, exposure to BPA resulted in altered architecture in both males and females, with females also experiencing an increase of pathogenic bacterial species. Co-administration of BPA + P led to the restoration of normal gut architecture, favored beneficial bacteria colonization, and decreased the abundance of pathogenic species. In the liver, male BPA exposure led to steatosis and glycogen depletion, which was partially mitigated by SLAB51 co-administration. In contrast, in females exposed to BPA, the lack of steatosis along with the greater glycogen depletion, suggested an increase in energy demand as supported by the metabolomic phenotype. The analysis of liver metabolites in BPA + P males revealed increased levels of anserine and reduced levels of glutamine, which could lie behind the counteraction of the brain histopathological damage caused by BPA. In BPA + P females, a reduction of retinoic acid was found in the liver, suggesting an increase in retinoids responsible for BPA detoxification. Overall, these results demonstrate that SLAB51 exerts its beneficial effects on the gut microbiota-brain-liver axis through distinct molecular pathways, effectively mitigating the pleiotropic toxicity of BPA.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping