The probiotic SLAB51 as agent to counteract BPA toxicity on zebrafish gut microbiota -liver-brain axis

• Published in: The Science of the total environment 2024-02, Vol.912, p.169303-169303, Article 169303
• Main Authors: Giommi, Christian, Lombó, Marta, Habibi, Hamid R., Rossi, Giacomo, Basili, Danilo, Mangiaterra, Sara, Ladisa, Claudia, Chemello, Giulia, Carnevali, Oliana, Maradonna, Francesca
• Format: Article
• Language: English
• Subjects: Endocrine disruptors, metabolomics; Histology; Immune system; Immunohistochemistry; Probiotics
• ISSN: 0048-9697; 1879-1026
• DOI: 10.1016/j.scitotenv.2023.169303

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. [Display omitted] •SLAB51 mitigates BPA-induced toxicity at gut, brain, liver and spleen levels.•SLAB51 counteracts the alterations triggered by BPA on gut architecture.•SLAB51alleviates BPA-induced gut dysbiosis, enhancing the immune response.•SLAB51 mitigates BPA hepatotoxicity by restoring glycogen and lipids levels.•SLAB51 mitigates BPA neurotoxicity.