Aim To explore the role of prenatal exposure to lipopolysaccharides (LPS) on blood lipids in offspring rats. Methods Eight pregnant rats were randomly divided into control group and LPS group. The rats in these groups were intraperitoneally administered with vehicle or LPS 0.79 mg/ kg on the 8 th, 10 th and 12 th days, respectively. Liver histopathological alteration was observed by hematoxylin-eosin staining and transmission electron microscopy, 8-OHdG expression was determined by confocal laser-scanning microscope and mitochondrial potential was detected by microplate reader in 8-week-old offsprings. Simultaneously, the body weight was measured in offsprings weekly and at day 1. Results By comparison of those offsprings in control group, body weight of offspring rats in 1 day and 1 week were both significantly decreased (P＜0.01). Whereafter, the body weight of offsprings in LPS group were increased obviously from 2 nd week to 8 th week (P＜0.01). Compared with offsprings from control group, there were dramatic increases in the serum level of TG, TC, LDL and AST (P＜0.05 or P＜0.01). In 8-week-old LPS offsprings, the liver exhibited significant lesions, in particular mitochondrial pathological alterations. The functional analysis of mitochondria suggested the expression of 8-OHdG increased obviously, and the mitochondrial potential decreased significantly in offsprings of LPS group (P＜0.01). Furthermore, the thoracic aortas exhibited lesions, including impaired endothelial cells, and migration and proliferation of vascular smooth muscle cells. Conclusion Our results indicate that maternal LPS exposure during pregnancy leads to mitochondrial dysfunction in offspring that predispose to disorder of blood lipids and even atherosclerosis in adult.