The hepatotoxicity of altrazine exposure in mice involves the intestinal microbiota.

Abstract:

:Atrazine (ATR), a bio accumulative herbicide is frequently used in agriculture to control unwanted weeds. Due to continuous application, atrazine persists in the environment and causes deleterious impacts including neurotoxicity, hepatotoxicity, and gut microbiota disorders. Therefore, this study for the first time reports the variation in the gut microbiota, induction of process of apoptosis and autophagy in mice induced by ATR. Results indicated that TUNEL-positive hepatocytes suggestive of apoptosis were increased in livers of different experimental mice. Results on metabolic analysis in liver tissues indicated an overall change in seventy-six metabolites particularly Uridine 5'-diphosphate, Propenoylcarnitine and Chinenoside V resulting in generation of energy-related metabolic disorders and imbalance of oxidation/autoxidation status. Results on gut microbiome inquisition showed that ATR changed the richness and diversity of gut microbiota of mice and number of Firmicutes. Moreover, results also revealed that ATR induced apoptosis via disruption of apoptotic (Bax, Bcl2, and Casp3) and autophagy (LC3/Map1lc3a, Beclin 1/Becn1 and P62/Sqstm1) genes. Results of our experimental study confirmed that changes in gut microbiota play a significant role in process of gut immune regulation and inflammation via different metabolites. In conclusion, the findings of our study provide a new idea for the involvement of mechanisms of detoxification in liver and inquisition of gut microbiota plays crucial role in regulation of physiological activities through liver-gut axis to mitigate toxic effects in animals.

journal_name

Chemosphere

journal_title

Chemosphere

authors

Liu B,Zeng Q,Chen H,Liao J,Bai Y,Han Q,Qiao N,Wang S,Mehmood K,Hussain R,Ahmed BZ,Tang Z,Zhang H,Li Y

doi

10.1016/j.chemosphere.2021.129572

subject

Has Abstract

pub_date

2021-01-11 00:00:00

pages

129572

eissn

0045-6535

issn

1879-1298

pii

S0045-6535(21)00042-4

journal_volume

272

pub_type

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