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6-PPD Quinone Inhibits Phosphatidic Acid Synthesis Associated with an Increase in Intestinal Barrier Permeability in C. elegans

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Jingwei Wu, Jingwei Wu, Jingwei Wu, Jingwei Wu, Dayong Wang Dayong Wang Dayong Wang Dayong Wang Qian Bian, Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Dayong Wang Qian Bian, Dayong Wang Dayong Wang Dayong Wang Qian Bian, Dayong Wang

Summary

Scientists found that 6-PPDQ, a toxic chemical from tire wear that ends up in our environment, damages the gut barrier in laboratory worms by disrupting the production of important fats needed for healthy intestinal walls. When the gut barrier becomes more permeable (or "leaky"), it allows more toxins to enter the body and can lead to health problems. This research helps explain how tire pollution might harm human digestive health, though more studies are needed to confirm these effects in people.

6-PPD quinine (6-PPDQ) affects intestinal barrier function; however, its underlying mechanisms remain largely unknown. In the current study, we examined the role of reduction in phosphatidic acid synthesis in mediating the toxicity of 6-PPDQ in affecting intestinal barrier function. In Caenorhabditis elegans, 6-PPDQ exposure reduced the phosphatidic acid content, which was accompanied by the decreased expression of acl-5 and acl-6 encoding glycerol-3-phosphate acyltransferase. The RNAi of acl-5 and acl-6 lowered the phosphatidic acid content, enhanced intestinal permeability, and resulted in the increased accumulation of 6-PPDQ. Meanwhile, acl-5 and acl-6 RNAi caused susceptibility to 6-PPDQ toxicity by upregulating the expressions of insulin ligands and receptor genes and downregulating the expressions of daf-16 and its target genes. Moreover, the RNAi of acl-5 and acl-6 elevated the expression of let-363, and the RNAi of let-363 could reduce the expressions of insulin ligand genes and confer resistance to 6-PPDQ toxicity. The double RNAi of acl-5 and acl-6 caused more severe enhanced intestinal permeability and 6-PPDQ toxicity. Therefore, 6-PPDQ exposure potentially disrupts phosphatidic acid synthesis to affect intestinal barrier function by downregulating acl-5 and acl-6 expressions.

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