Different chemical behaviors and antioxidant activity of three novel schiff bases containing hydroxyl groups. X-ray structure of CH2{cyclo-C6H10-NH=CH-(2-O-naphth)}2.H2O

The antioxidant activities of three new Schiff base compounds, 1–3, were studied through their direct scavenging ability to eliminate free radicals using DPPH and ABTS methods and also through their indirect antioxidant activity as measured using the ferric thiocyanate (FTC) method. The number of OH groups in the compounds and their positions play a role in the activity. The crystal structure of CH2{cycloC6H10NHCH-(2-O-naphth)}2.H2O (1), has been determined and proves the existence of intramolecular hydrogen-bonds and hydrogen-bonded water molecules and reveals the keto-amine (NH⋯O) tautomer of this compound. One cyclo-hexyl ring was found to be disordered, and was resolved in two orientations. Hydrogen atoms of the NHCH groups were located in difference maps and were refined freely. Compounds 2 and 3 exhibit the enol-imine form. The UV–vis spectra of the three compounds have been studied in organic solvents of different polarity, and in basic and acidic media, and were found helpful in understanding the tautomeric forms in these compounds; the polarity was modified by adding (CF3COOH) or [(C2H5)3N] to the solvent. All three compounds have been characterized by elemental analysis, UV–vis, FTIR, NMR and MS

Exposure to Methylmercury at Juvenile Stage Worsens Autism-like Symptoms in Adult BTBR T+tf/J Mice Due to Lack of Nuclear Factor Erythroid 2-Related Factor 2 Signaling Upregulation in Periphery and Brain

Autism spectrum disorder (ASD) is a multifaceted developmental condition that first appears in infancy. The condition is characterized by recurrent patterns in behavior and impairments in social and vocalization abilities. Methylmercury is a toxic environmental pollutant, and its derivatives are the major source of organic mercury to human beings. Inorganic mercury, which is released from a variety of pollutants into oceans, rivers, and streams, is transformed into methylmercury by bacteria and plankton in the water, which later builds up in fish and shellfish, and then enters humans through the consumption of fish and shellfish and increases the risk of developing ASD by disturbing the oxidant–antioxidant balance. However, there has been no prior research to determine the effect of juvenile exposure of methylmercury chloride on adult BTBR mice. Therefore, the current study evaluated the effect of methylmercury chloride administered during the juvenile stage on autism-like behavior (three-chambered sociability, marble burying, self-grooming tests) and oxidant–antioxidant balance (specifically Nrf2, HO-1, SOD-1, NF-kB, iNOS, MPO, and 3-nitrotyrosine) in the peripheral neutrophils and cortex of adult BTBR and C57BL/6 (B6) mice. Our results show that exposure to methylmercury chloride at a juvenile stage results in autism-like symptoms in adult BTBR mice which are related to a lack of upregulation of the Nrf2 signaling pathway as demonstrated by no significant changes in the expression of Nrf2, HO-1, and SOD-1 in the periphery and cortex. On the other hand, methylmercury chloride administration at a juvenile stage increased oxidative inflammation as depicted by a significant increase in the levels of NF-kB, iNOS, MPO, and 3-nitrotyrosine in the periphery and cortex of adult BTBR mice. This study suggests that juvenile exposure to methylmercury chloride contributes to the worsening of autism-like behavior in adult BTBR mice through the disruption of the oxidant–antioxidant balance in the peripheral compartment and CNS. Strategies that elevate Nrf2 signaling may be useful to counteract toxicant-mediated worsening of ASD and may improve quality of life