Evidence suggests that maternal immune activation (MIA) during pregnancy is a risk factor for neurodevelopmental disturbances including autism spectrum disorders (ASDs). Animal models support this linkage and demonstrate that MIA in rodents leads to behavioral alterations in offspring that are characteristic of autism. However, the mechanism by which MIA causes long‑term behavioral deficits is unknown. Investigation of the links between maternal infection during pregnancy, mitochondrial dysfunction, and behavioral alterations in offspring. To induce MIA, pregnant Wistar rats were injected with lipopolysaccharide (LPS; 0.1mg/kg, intraperitoneally) on gestational day 9.5, a time point analogous to the first trimester of human gestation. Brains from adolescent offspring were evaluated for mitochondrial outcomes. Prenatal exposure to MIA led to anxiety and repetitive behavior. Adolescent offspring of MIA dams exhibited up-regulation of pro-inflammatory cytokines, oxidative stress, and disturbances in redox homoeostasis. Moreover, substantial mitochondrial abnormalities were observed. A significant decrease in mitochondrial membrane potential and changes in ATP production could be attributed to a downregulation of complex I and IV. Deregulated bioenergetics of mitochondria were accompanied by impaired mitochondrial dynamics, altered expression of fusion/fission machinery proteins including mitofusin 1 and 2 (Mfn1, Mfn2), Opa1, dynamin related protein‑1 (Drp1), and fission protein 1 (Fis1). We also demonstrated lower expression of the genes coding for PGC1α and TFAM (PPARGC1A and TFAM, respectively) that are responsible for mitochondrial biogenesis. MIA at early gestation leads to long-lasting effects on the mitochondrial bioenergetics, dynamics, and biogenesis in the offspring which can lead to synaptic dysfunction and behavioral abnormalities similar to ASD. FINANCIAL SUPPORT: Supported by the NSC grant 2016/23/D/NZ4/03572.