Effects of varied‑intensity endurance exercise training on oxidative and antioxidant factors in the liver of rats with valproic acid‑induced autism

Abstract

Autism spectrum disorders are complex behavioral disorders that can be caused by exposure to valproic acid (VPA) during pregnancy. A therapeutic role for exercise training has been reported in many neurological diseases and problems, including autism. We aimed to evaluate various intensities of endurance exercise training and investigate its effects on oxidative and antioxidant factors in the liver of young males in a rat model of autism. Female rats were divided into a treatment (autism) and a control group. The autism group received VPA intraperitoneally on day 12.5 of pregnancy and the control pregnant females received saline. On the 30th day post‑birth, a social interaction test was performed on the offspring to confirm autistic‑like behavior. Offspring were divided into three subgroups: no exercise, mild exercise training, and moderate exercise training. Then the oxidative index of malondialdehyde (MDA) and the antioxidant indices of superoxide dismutase (SOD), total antioxidant capacity (TAC), and catalase in liver tissue were examined. The results of this study showed that both indices of sociability and social novelty decreased in the autism group. MDA levels in the liver of the autistic group increased, and moderate exercise training was shown to reduce the levels. Catalase and SOD activity as well as TAC levels decreased in the autism group, and moderate‑intensity exercise training was shown to increase the values. Parameters of hepatic oxidative stress were altered in VPA‑induced autism, and moderate‑intensity endurance exercise training was demonstrated to have beneficial effects on hepatic oxidative stress factors by modul ating the antioxidant/oxidant ratio.

Hepatic Alterations in a BTBR T + Itpr3tf/J Mouse Model of Autism and Improvement Using Melatonin via Mitigation Oxidative Stress, Inflammation and Ferroptosis

“…The etiology of ASD is not well understood [2,5], but it is likely that both biological and environmental factors are involved [6]. Biologically, genetic and nongenetic factors play a role, such as immunological and mitochondrial malfunction associated with oxidative stress, neurotrophic dysregulation and inflammation [7][8][9][10]. There is increasing evidence that ASD patients show excessive reactive oxygen species (ROS) production [8,11,12].…”

“…This animal model is considered a translational tool to evaluate potential therapies for ASD [18,19]. Recently, liver disorders have become a significant health concern and are an issue commonly found in autistic children [9,20]. Moreover, Trinchese et al [8] showed that inflammation and oxidative stress in these mice induce mitochondrial dysfunction and mitochondrial fission in the liver.…”