Deoxyadenosine family: improved synthesis, DNA damage and repair, analogs as drugs

Abstract

Improved synthesis of 2 ′ -deoxyadenosine using Escherichia coli overexpressing some enzymes and gram-scale chemical synthesis of 2 ′ -deoxynucleoside 5 ′ -triphosphates reported recently are described in this review. Other topics include DNA damage induced by chromium(VI), Fenton chemistry, photoinduction with lumazine, or by ultrasound in neutral solution; 8,5 ′ -cyclo-2 ′ -deoxyadenosine isomers as potential biomarkers; and a recapitulation of purine 5 ′ ,8-cyclonucleoside studies. The mutagenicities of some products generated by oxidizing 2 ′ -deoxyadenosine 5 ′ -triphosphate, nucleotide pool sanitization, and translesion synthesis are also reviewed. Characterizing cross-linking between nucleosides in opposite strands of DNA and endonuclease V-mediated deoxyinosine excision repair are discussed. The use of purine nucleoside analogs in the treatment of rarer chronic lymphoid leukemias is reviewed. Some analogs at the C8 position induced delayed polymerization arrest during HIV-1 reverse transcription. The susceptibility of clinically metronidazole-resistant Trichomonas vaginalis to two analogs, toyocamycin and 2-fluoro-2 ′ -deoxyadenosine, were tested in vitro . GS-9148, a dAMP analog, was translocated to the priming site in a complex with reverse transcriptase and double-stranded DNA to gain insight into the mechanism of reverse transcriptase inhibition.

Plausible Mechanisms of the Fenton-Like Reactions, M = Fe(II) and Co(II), in the Presence of RCO2– Substrates: Are OH• Radicals Formed in the Process?

“…Since then the reaction of Fe­(H 2 O) 6 2+ with H 2 O 2 , which initiates this catalytic process is called “the Fenton reaction” and the reactions of low valent transition-metal complexes M n L m , where M = Fe II or other low valent transition metal cations, with H 2 O 2 or other peroxides are called “Fenton-like reactions”. These reactions are of major importance as it is commonly accepted that they cause aging and a large variety of diseases, − what is called oxidative stress (note: refs – are some recent reviews and clearly do not represent a full literature survey.) Furthermore, these reactions are involved in a variety of advanced oxidation processes, AOPs, − and synthetic catalytic processes …”

Integrated analysis of transcriptomics, proteomics and metabolomics data reveals the role of SLC39A1 in renal cell carcinoma

“…Downregulated DPYD and DCK increased the consumption of uracil and then diminished the production of dCMP, thereby reducing UTP, GTP and dCTP production. Deoxyinosine was also declined with augmented SLC39A1 and was reported to participate in DNA damage repair (Biswas et al, 2013). Amino acid Metabolism was also altered: SLC39A1 decreased methionine, spermidine in renal cancer Frontiers in Cell and Developmental Biology frontiersin.org cell.…”

“…Downregulated DPYD and DCK increased the consumption of uracil and then diminished the production of dCMP, thereby reducing UTP, GTP and dCTP production. Deoxyinosine was also declined with augmented SLC39A1 and was reported to participate in DNA damage repair ( Biswas et al, 2013 ).…”