Probiotic Bifidobacterium longum Subsp. longum 51A Protects Mice from Genotoxic and Metabolic Alterations Induced by Subchronic Exposure to a Low-Dose Pesticide Cocktail

长双歧杆菌 益生菌 杀虫剂 食品科学 生物 双歧杆菌 毒理 化学 细菌 发酵 乳酸菌 生态学 遗传学
作者
Mirna Maciel d’Auriol Souza,Viviani Mendes de Almeida,Clênio Silva Cruz,Victor Gabriel Santos Rocha,Paola Caroline Lacerda Leocárdio,Sumaia Araújo Pires,Maysa do Vale Oliveira,Tainá Brumate,Maria José Nunes de Paiva,Jacqueline I. Alvarez‐Leite,Geovanni Dantas Cassali,Flaviano S. Martins,Angélica T. Vieira,Leiliane Coelho André
出处
期刊:ACS omega [American Chemical Society]
卷期号:10 (32): 36238-36251
标识
DOI:10.1021/acsomega.5c04121
摘要

Environmental exposure to low levels of pesticide mixtures through food and domestic settings raises significant public health concerns due to their potential link to metabolic diseases, including obesity, type 2 diabetes, and cancer. As the intestinal microbiota and gastrointestinal tract serve as primary contact points for these contaminants, potentially eliminating residues or suffering direct damage leading to dysbiosis, probiotic interventions have emerged as promising therapeutic strategies for metabolic disorders. This study aimed to evaluate, in mice, the consequences of subchronic exposure to low doses of a mixture of three pesticides: glyphosate (15 mg/kg body weight/day), imidacloprid (5 mg/kg body weight/day), and tebuconazole (4 mg/kg body weight/day). Mice were exposed for 6 weeks. The probiotic Bifidobacterium longum subsp. longum strain 51A was employed as a therapeutic strategy for gut microbiota modulation. Exposed animals experienced adverse metabolic and genotoxic effects including increased cholesterol and reduced insulin sensitivity, oxidative stress, and intestinal dysbiosis. B. longum 51A reversed these effects, improving metabolism and reducing prediabetes markers. As the first study examining this specific pesticide combination, imidacloprid, tebuconazole, and glyphosate highlight the distinct impact of pesticide mixtures on health, suggesting that intestinal dysbiosis may drive the observed metabolic changes, with microbiota modulation aiding recovery.
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