Authors:F. Könczöl, D. Lőrinczy, Zs. Vértes, G. Hegyi and J. Belagyi
Chemical cross-links which covalently connected the Cys-374 and Glu-41 residues of adjacent monomers in the same strand of
F-actin were used to follow the consequences of the modification for the motional and structural properties of the actin filaments.
DSC measurements reported that the inter-monomer cross-links shifted the thermal transition temperature and affected strongly
the cooperativity of the transition in comparison with uncross-linked F-actin. Addition of HMM to F-actin induced significant
decrease of the transition temperature to lower value from 69.4 to 67. 5 °C.
Authors:B Raposa, R Pónusz, G Gerencsér, F Budán, Z Gyöngyi, A Tibold, D Hegyi, I Kiss, Á Koller and T Varjas
It has been reported that some of the food additives may cause sensitization, inflammation of tissues, and potentially risk factors in the development of several chronic diseases. Thus, we hypothesized that expressions of common inflammatory molecules – known to be involved in the development of various inflammatory conditions and cancers – are affected by these food additives. We investigated the effects of commonly used food preservatives and artificial food colorants based on the expressions of NFκB, GADD45α, and MAPK8 (JNK1) from the tissues of liver. RNA was isolated based on Trizol protocol and the activation levels were compared between the treated and the control groups. Tartrazine alone could elicit effects on the expressions of NFκB (p = 0.013) and MAPK8 (p = 0.022). Azorubine also resulted in apoptosis according to MAPK8 expression (p = 0.009). Preservatives were anti-apoptotic in high dose. Sodium benzoate (from low to high doses) dose-dependently silenced MAPK8 expression (p = 0.004 to p = 0.002). Addition of the two preservatives together elicited significantly greater expression of MAPK8 at half-fold dose (p = 0.002) and at fivefold dose (p = 0.008). This study suggests that some of the food preservatives and colorants can contribute to the activation of inflammatory pathways.