The antitumor drug, 1,3-bis(2-chloroethyl)-1-nitroso-urea, inactivates human nicotinamide mononucleotide adenylyltransferase

Biochem Pharmacol. 1995 Feb 14;49(4):575-9. doi: 10.1016/0006-2952(94)00478-5.

Abstract

Nicotinamide mononucleotide (NMN) adenylyltransferase (EC 2.7.7.1) from human placenta is rapidly inactivated by 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU). A similar inactivation is observed with other C- and N-nitroso compounds. The inactivation by BCNU is dependent on incubation time, temperature and BCNU concentration. Protective reagents for -SH groups, dithiothreitol and beta-mercaptoethanol, and the substrate NMN are very effective in protecting NMN adenylyltransferase from BCNU inactivation and in preserving its catalytic properties, while ATP is less efficient. Incubation of BCNU-inactivated and dialysed NMN adenylyltransferase with dithiothreitol results in a partial recovery of the enzymatic activity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Triphosphate / pharmacology
  • Carmustine / antagonists & inhibitors
  • Carmustine / pharmacology*
  • Dithiothreitol
  • Humans
  • Nicotinamide Mononucleotide / pharmacology
  • Nicotinamide-Nucleotide Adenylyltransferase / antagonists & inhibitors*
  • Placenta / enzymology
  • Temperature
  • Time Factors

Substances

  • Nicotinamide Mononucleotide
  • Adenosine Triphosphate
  • Nicotinamide-Nucleotide Adenylyltransferase
  • Dithiothreitol
  • Carmustine