Therapeutic Effects of Magnesium Biotinate on Propionic Acid‐Induced Autistic Features in Rats

Abstract

ObjectiveThis study investigated the therapeutic effects of magnesium biotinate (MgB) on propionic acid (PPA)‐induced autistic features in rats.BackgroundBiotin is involved in energy metabolism and various immune and nerve functions. MgB is a novel biotin complex that has enhanced absorption. Compared to D‐Biotin, MgB has superior tissue uptake and anti‐inflammatory effects. Biotin deficiency can result in neurological abnormalities. Low levels of biotin have been found in individuals with neurodevelopmental disorders such as autism spectrum disorder.Design/MethodsThirty‐five male Wistar rats (3 weeks old) were randomized into the following five groups; 1: Control (received saline), 2: PPA alone, 3: PPA + 10 mg human equivalent dose (HED) MgB, 4: PPA + 100 mg HED MgB, 5: PPA + 500 mg HED MgB. PPA treated rats were administered 500 mg/kg BW/day of PPA by subcutaneous injection for 5 days to induce autistic features. Treatment groups then received MgB for two weeks via oral gavage following PPA treatment. Neurobehavioral tests were performed on the seventh and eighth days. Serum and tissue samples were then collected for analysis.ResultsThe neuronal loss and degeneration observed in the hippocampal CA1 region and cerebellum of PPA‐exposed rats were improved by treatment with MgB. Brain levels of oxidative stress and inflammatory markers were lower in all MgB groups compared to PPA alone (p<0.05). Brain levels of antioxidant markers were higher in the 100 and 500 mg HED MgB groups compared to PPA alone (p<0.05). These effects were most significant in the 500 mg HED MgB group. Sociability and social preference scores were greater in the 100 and 500 mg HED MgB treatment groups compared to PPA alone (p<0.05). The 500 mg HED MgB dose improved social preference score to the extent that it did not differ from normal controls.ConclusionsTreatment with MgB significantly reduced brain toxicity and improved autistic features induced by PPA.Support or Funding InformationThis study was conducted at Firat University and funded by JDS Therapeutics, LLC.