AI Article Synopsis
- Atrazine (ATZ), a common herbicide, negatively impacts mitochondrial function and lipid metabolism in the liver, leading to potential health risks.
- Melatonin (MLT), a natural hormone, shows promise in protecting against the harmful effects of ATZ by improving mitochondrial function and lipid metabolism.
- In laboratory studies, MLT helped restore important proteins and improve fatty acid utilization, suggesting it may counteract ATZ-induced disruptions in liver cells without directly affecting overall mitochondrial function.
Article Abstract
Atrazine (ATZ), a widely used herbicide, disrupts mitochondrial function and lipid metabolism in the liver. Melatonin (MLT), a naturally synthesized hormone, combats mitochondrial dysfunction and alleviates lipid toxicity. However, the mechanisms behind ATZ-induced lipid metabolism toxicity and the protective effects of MLT remain unexplored. Mice were randomly assigned to four groups: control (Con), 5 mg/kg MLT, 170 mg/kg ATZ, and a cotreatment group receiving 170 mg/kg ATZ with 5 mg/kg MLT (ATZ+MLT). Additionally, we analyzed the effects of MLT and Rab8a on mRNA and proteins related to mitochondrial function and lipid metabolism disrupted by ATZ in AML12 cells. In conclusion, ATZ induced mitochondrial stress and disrupted fatty acid metabolism in mouse hepatocytes and AML12 cells. Exogenous MLT restores Rab8a levels, regulating fatty acid utilization in mitochondria and mitochondrial function. Notably, targeting Rab8a does not significantly affect mitochondrial function but prevents ATZ-induced lipid metabolism disorders in hepatocytes.
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| http://dx.doi.org/10.1021/acs.jafc.4c07006 | DOI Listing |
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