PM_2.5 exposure induces age-dependent hepatic lipid metabolism disorder in female mice

Particulate matter exposure has been described to elevate the risk of lung and cardiovascular diseases. An increasing number of recent studies have indicated positive correlations between PM_2.5 (the fraction of airborne particles with an aerodynamic diameter less than 2.5 μm) exposure and the risk of liver diseases. However, research on the effects of PM_2.5 exposure on liver fat synthesis, secretion, and clearance mechanisms under normal diet conditions is limited, and whether these effects are age-dependent is largely unknown. Female C57BL/6 mice at different ages (4 weeks (4 w), 4 months (4 m), and 10 months (10 m)) were treated with 3 mg/kg body weight of PM_2.5 every other day for 4 weeks. Subsequently, the ultrastructural changes of liver, the expression of genes involved in oxidative damage and lipid metabolism in the liver were examined. Observation of hepatic ultrastructure showed more and larger lipid droplets in the livers of 4-week-old and 10-month-old mice exposed to PM_2.5. Further analysis showed that PM_2.5 exposure increased the expression of genes related to lipid synthesis, but decreased the expression of genes involved in lipid transport and catabolism in the livers of 10-month-old mice. Our findings suggest that exposure to PM_2.5 disrupts the normal metabolism of liver lipids and induces lipid accumulation in the liver of female mice in an age-dependent manner, with older mice being more susceptible to PM_2.5.