Exposure to cigarette smoke during prenatal period alters the brain energy metabolism of rats subjected to an animal model of schizophrenia.

Schizophrenia (SZ) has a neurodevelopmental component and animal studies show that cigarette smoke exposure may affect dopamine pathways and induce hyperactivity in offspring. Cigarette smoke releases particles that cause hypoxia and cytotoxicity, impairing brain cell development, survival, and differentiation. The electron transport chain (ETC) is a significant source of reactive oxygen species, and mitochondrial dysfunction is associated with SZ. This study aimed to evaluate alterations in the ETC in brain structures of rats exposed to cigarette smoke during pregnancy and submitted to the SZ model in adult life. Pregnant Wistar rats were divided into two groups: a control group exposed to cigarette smoke and a group exposed to cigarette smoke throughout pregnancy. After reaching 60 days, the offspring were submitted to the SZ model with ketamine for seven days. They were divided into four groups: control/saline, control/ketamine, exposure to cigarette smoke/saline, and exposure to cigarette smoke/ketamine. Exposure to cigarette smoke increased the activity of complex I, II in the olfactory bulb of the offspring. In the prefrontal cortex, the activity of complex I, II, and IV increased in the cigarette-ketamine and cigarette/saline groups. Evaluating the cigarette/ketamine group in the striatum, there was an increase in the activity of complexes I and IV, and an increase in sulfhydryl in the olfactory bulb and hippocampus. In conclusion, the increased activity of complexes I, II, and IV in the brain structures analyzed suggests that maternal exposure to cigarette smoke may be associated with metabolic imbalance in an SZ model.