Polypropylene microplastics triggered mouse kidney lipidome reprogramming combined with ROS stress as revealed by lipidomics and Raman biospectra.

Abstract

Microplastics intrigue kidney toxicity such as mitochondrial dysfunction and inflammation promotion. However, as an organ relying heavily on fatty acid oxidation, how microplastics influence kidney lipidomes remain unclear. Hence, we performed Raman spectra and multidimensional mass spectrometry-based shotgun lipidomics to decode kidney lipidomics landscape under polypropylene microplastics exposure. Kidney functions and cellular redox homeostasis were remarkably disturbed as revealed by levels of biochemical renal function markers, malonaldehyde, hydrogen peroxide and antioxidants. Ultrastructure alterations including the foot process fusion implied the kidney injury associated with lipidomic changes. Raman spectra successfully further confirmed the cellular change of reactive oxygen species and lipid disorders. Lipidomics showed that polypropylene microplastics caused abnormal lipidome and irregular exchange by remodeling triglycerides and phospholipids. Genes involved in lipid metabolism such as Fads1 and Elovl5 exhibited highly diversified expression profiles responding to polypropylene microplastics stress and possessed significant correlations with ROS indicators. These results explained ultrastructure alterations and aggravation of kidney injuries. Our work revealed polypropylene microplastics inducing lipidomic detriment in mouse kidney by Raman spectra and lipidomics firstly, elucidating the significances of lipidomic remodeling coupled with ROS stress in the kidney damages. The findings provided reliable evidence on the health risks of polypropylene microplastics in kidney.