scholarly journals The mechanism of directed Ni(ii)-catalyzed C–H iodination with molecular iodine

2018 ◽  
Vol 9 (5) ◽  
pp. 1144-1154 ◽  
Author(s):  
Brandon E. Haines ◽  
Jin-Quan Yu ◽  
Djamaladdin G. Musaev
Keyword(s):  
Computational Study ◽  
Molecular Iodine

This computational study reveals electrophilic cleavage pathways for substrates with N,N-bidentate directing centers in Ni(ii)-catalyzed C–H iodination with molecular iodine.

A computational study of cobalt-catalyzed C–H iodination reactions using a bidentate directing group with molecular iodine

2019 ◽  
Vol 6 (4) ◽  
pp. 537-543 ◽  
Author(s):  
Ken Yamazaki ◽  
Yadagiri Kommagalla ◽  
Yusuke Ano ◽  
Naoto Chatani
Keyword(s):  
Computational Study ◽  
Molecular Iodine ◽  
Directing Group ◽  
Computational Methodology

A computational methodology was used to collect detailed mechanistic information on the cobalt-catalyzed C–H iodination of aromatic amides with molecular iodine using an N,N′-bidentate directing group.

Molecular iodine synergized and sensitized neuroblastoma cells to the antineoplastic effect of ATRA

2020 ◽  
Vol 27 (12) ◽  
pp. 699-710
Author(s):  
Irasema Mendieta ◽  
Gabriel Rodríguez-Gómez ◽  
Bertha Rueda-Zarazúa ◽  
Julia Rodríguez-Castelán ◽  
Winniberg Álvarez-León ◽  
...  
Keyword(s):  
Residual Disease ◽  
Neuroblastoma Cells ◽  
Survivin Expression ◽  
Body Weight Loss ◽  
Immunohistochemical Analysis ◽  
Molecular Iodine ◽  
Tyrosine Kinase Receptor ◽  
Adjuvant Effect

Neuroblastoma (NB) is the most common solid childhood tumor, and all-trans retinoic acid (ATRA) is used as a treatment to decrease minimal residual disease. Molecular iodine (I2) induces differentiation and/or apoptosis in several neoplastic cells through activation of PPARγ nuclear receptors. Here, we analyzed whether the coadministration of I2 and ATRA increases the efficacy of NB treatment. ATRA-sensitive (SH-SY5Y), partially-sensitive (SK-N-BE(2)), and non-sensitive (SK-N-AS) NB cells were used to analyze the effect of I2 and ATRA in vitro and in xenografts (Foxn1 nu/nu mice), exploring actions on cellular viability, differentiation, and molecular responses. In the SH-SY5Y cells, 200 μM I2 caused a 100-fold (0.01 µM) reduction in the antiproliferative dose of ATRA and promoted neurite extension and neural marker expression (tyrosine hydroxylase (TH) and tyrosine kinase receptor alpha (Trk-A)). In SK-N-AS, the I2 supplement sensitized these cells to 0.1 μM ATRA, increasing the ATRA-receptor (RARα) and PPARγ expression, and decreasing the Survivin expression. The I2 supplement increased the mitochondrial membrane potential in SK-N-AS suggesting the participation of mitochondrial-mediated mechanisms involved in the sensibilization to ATRA. In vivo, oral I2 supplementation (0.025%) synergized the antitumor effect of ATRA (1.5 mg/kg BW) and prevented side effects (body weight loss and diarrhea episodes). The immunohistochemical analysis showed that I2 supplementation decreased the intratumoral vasculature (CD34). We suggest that the I2 + ATRA combination should be studied in preclinical and clinical trials to evaluate its potential adjuvant effect in addition to conventional treatments.

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