Effect of metal in Schiff bases of chitosan adsorbed on glassy carbon electrode in the inhibition of sphingomyelinase C toxin.

This study was conducted to assess the catalytic electrode surface adsorption and capture properties of different metal chitosan derivatives in aqueous phosphate buffer solution (pH = 7.3). Early, recent work showed that the response of Iron chitosan complex with R = -CH3 on the periphery, over blood red cells in presence of sphingomyelinase C was protected. The effect of others substituent (R = -Br, -Cl, -F, NO2, -OCH3, -H) on the periphery of the Schiff base ligand did not show correlation with the oxidation of sphingomyelinase C and its biological response. For this reason, various adsorbed metal (M = Fe of recent work, Cu, Ni and Co) complexes of chitosan and Schiff bases on glassy carbon electrode for the oxidation of sphingomyelinase C were investigated and compared, each one with -CH3 group on the periphery of the Schiff base. UV-Vis and IR-TF spectroscopies, electrochemistry and microscopy assay were performed; then, the metal effect underlying. For the Schiff base, cobalt and copper complexes did not proved to be a remarkable cellular protector in presence of the enzyme, but the nickel complex showed to be a cellular protector at short time, this conclusion help to proposal a reaction mechanism for the electrochemical and biological studies.

Potential Crosstalk between Fructose and Melatonin: A New Role of Melatonin-Inhibiting the Metabolic Effects of Fructose.

Increased consumption of energy-dense foods such as fructose-rich syrups represents one of the significant, growing concerns related to the alarming trend of overweight, obesity, and metabolic disorders worldwide. Metabolic pathways affected by fructose involve genes related to lipogenesis/lipolysis, beta-oxidation, mitochondrial biogenesis, gluconeogenesis, oxidative phosphorylation pathways, or altering of circadian production of insulin and leptin. Moreover, fructose can be a risk factor during pregnancy elevating the risk of preterm delivery, hypertension, and metabolic impairment of the mother and fetus. Melatonin is a chronobiotic and homeostatic hormone that can modulate the harmful effects of fructose via clock gene expression and metabolic pathways, modulating the expression of PPARγ, SREBF-1 (SREBP-1), hormone-sensitive lipase, C/EBP-α genes, NRF-1, PGC1α, and uncoupling protein-1. Moreover, this hormone has the capacity in the rat of reverting the harmful effects of fructose, increasing the body weight and weight ratio of the liver, and increasing the body weight and restoring the glycemia from mothers exposed to fructose. The aim of this review is to show the potential crosstalk between fructose and melatonin and their potential role during pregnancy.