PMID- 11162776
OWN - NLM
STAT- MEDLINE
DCOM- 20010315
LR  - 20131121
IS  - 0041-008X (Print)
IS  - 0041-008X (Linking)
VI  - 170
IP  - 2
DP  - 2001 Jan 15
TI  - Developmental ontogeny of NAD+ kinase in the rat conceptus.
PG  - 124-9
AB  - The ubiquitous NAD+ kinase (NADK) is the only known enzyme to catalyze formation 
      of NADP+ from NAD+. The capacity to maintain an adequate supply of NADP(H) has 
      important implications for development because of its requirement as a cofactor 
      and electron donor in biosynthesis and detoxication reactions. Modulation of NADK 
      may directly influence NADP(H) concentrations and cell sensitivity to 
      embryotoxicants. Measurable activities of NADK were not detected in gestational 
      day (GD) 10 rat conceptuses. By GD 11, specific activities of 1.8 and 7.0 pmol 
      NADP+/min/microg protein were measured in embryos and visceral yolk sacs (VYSs), 
      respectively. The VYS specific activities decreased thereafter to 0.5 pmol 
      NADP+/min/microg protein by GD 18. Specific activities of NADK in placenta 
      increased from 1.3 pmol NADP+/min/microg protein on GD 11 to 32.7 pmol 
      NADP+/min/microg protein on GD 15. Specific activities in the liver increased 
      from 1.7 pmol NADP+/min/microg protein on GD 15 to 51.1 pmol NADP+/min/microg 
      protein on GD 21. NADK specific activities were also determined in other 
      developmentally relevant tissues such as the heart and the brain. In the heart, 
      NADK activity was at its lowest just before birth while in the brain it peaked at 
      5.4 pmol NADP+/min/microg protein just prior to birth. In the lung, activity 
      increased from 0.9 pmol NADP+/min/microg protein on GD 17 to 5.9 pmol 
      NADP+/min/microg protein on GD 21. However, activities dropped in the kidney from 
      2.0 pmol NADP+/min/microg protein on GD 17 to 1.1 pmol NADP+/min/microg protein 
      on GD 21. These results demonstrate dramatic temporal and spatial variations in 
      NADK activity. Tissue variations in NADK activities may reflect alterations in 
      functional needs for cofactors during differentiation and a cooperation between 
      tissues to optimize detoxification capacity. This is particularly important when 
      chemical exposure during pregnancy disrupts pyridine nucleotide redox status and 
      the conceptus must rely on NADK to provide additional NADP(H).
CI  - Copyright 2001 Academic Press.
FAU - Akella, S S
AU  - Akella SS
AD  - Toxicology Program, The University of Michigan, Ann Arbor, Michigan 48109, USA.
FAU - Harris, C
AU  - Harris C
LA  - eng
GR  - ES05235/ES/NIEHS NIH HHS/United States
GR  - ES07062/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Toxicol Appl Pharmacol
JT  - Toxicology and applied pharmacology
JID - 0416575
RN  - 0 (Pyridines)
RN  - 0U46U6E8UK (NAD)
RN  - 53-59-8 (NADP)
RN  - EC 2.7.1.- (Phosphotransferases (Alcohol Group Acceptor))
RN  - EC 2.7.1.23 (NAD kinase)
SB  - IM
MH  - Animals
MH  - Embryo, Mammalian/*enzymology
MH  - Female
MH  - Heart/embryology
MH  - Kidney/embryology/enzymology
MH  - Lung/embryology/enzymology
MH  - Male
MH  - Myocardium/enzymology
MH  - NAD/metabolism
MH  - NADP/metabolism
MH  - Phosphotransferases (Alcohol Group Acceptor)/*metabolism
MH  - Pregnancy
MH  - Pyridines/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
EDAT- 2001/02/13 11:00
MHDA- 2001/03/17 10:01
CRDT- 2001/02/13 11:00
PHST- 2001/02/13 11:00 [pubmed]
PHST- 2001/03/17 10:01 [medline]
PHST- 2001/02/13 11:00 [entrez]
AID - S0041-008X(00)99093-8 [pii]
AID - 10.1006/taap.2000.9093 [doi]
PST - ppublish
SO  - Toxicol Appl Pharmacol. 2001 Jan 15;170(2):124-9. doi: 10.1006/taap.2000.9093.