ADPRT-MEDIATED DECREASE OF CELLULAR NAD CONTENT AND THE DETECTION OF CHEMICALLY INDUCED DNA DAMAGE DEVELOPMENT OF A NEW SHORT-TERM SCREENING TEST FOR MUTAGENS

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ADPRT-MEDIATED DECREASE OF CELLULAR NAD CONTENT AND THE DETECTION OF CHEMICALLY INDUCED DNA DAMAGE DEVELOPMENT OF A NEW SHORT-TERM SCREENING TEST FOR MUTAGENS

Chinese Medical Sciences Journal Issue 1, Pages: 19-24(1990)

Updated：2024-04-10

- ADPRT-MEDIATED DECREASE OF CELLULAR NAD CONTENT AND THE DETECTION OF CHEMICALLY INDUCED DNA DAMAGE DEVELOPMENT OF A NEW SHORT-TERM SCREENING TEST FOR MUTAGENS
- Affiliations：
  
  1. Zhejiang Medical University,Hangzhou
  2. ,China
  3. Genetic Institute
  4. Fudan University
  5. Zhejiang Medical University
- Author bio：
- Funds：
- DOI：
  CLC：
- Published：1990
- Accepted：
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[1]余应年,戴一凡,方明,陈星若.ADPRT-MEDIATED DECREASE OF CELLULAR NAD CONTENT AND THE DETECTION OF CHEMICALLY INDUCED DNA DAMAGE DEVELOPMENT OF A NEW SHORT-TERM SCREENING TEST FOR MUTAGENS[J].Chinese Medical Sciences Journal,1990(01):19-24.

ADPRT-MEDIATED DECREASE OF CELLULAR NAD CONTENT AND THE DETECTION OF CHEMICALLY INDUCED DNA DAMAGE DEVELOPMENT OF A NEW SHORT-TERM SCREENING TEST FOR MUTAGENS[J]. Chinese medical sciences journal, 1990, (1): 19-24.
[1]余应年,戴一凡,方明,陈星若.ADPRT-MEDIATED DECREASE OF CELLULAR NAD CONTENT AND THE DETECTION OF CHEMICALLY INDUCED DNA DAMAGE DEVELOPMENT OF A NEW SHORT-TERM SCREENING TEST FOR MUTAGENS[J].Chinese Medical Sciences Journal,1990(01):19-24. DOI：

ADPRT-MEDIATED DECREASE OF CELLULAR NAD CONTENT AND THE DETECTION OF CHEMICALLY INDUCED DNA DAMAGE DEVELOPMENT OF A NEW SHORT-TERM SCREENING TEST FOR MUTAGENS[J]. Chinese medical sciences journal, 1990, (1): 19-24. DOI：

摘要

正

It was found that the DNA-damaging agents N-methyl-N’-nitro-N-nitrosoguanidine（MNNG）

methyl-methanesulphonate（MMS）and 4-nitroquinoline-N-oxide（4NQO）could stimulate ADP-ribosyl transferase（ADPRT）activity and reduce the cellular NAD content in a dose-dependent way.The reduction of NAD after DNA damage could be partially or completelyprevented by ADPRT inhibitors

3-aminobenzamide or nicotinamide

which showed noinfluence on reduction of NAD induced by metabolic blocking agents.Therefore

a simpleand specific method to detect DNA-damaging mutagens by measuring ADPRT-mediateddecrease of cellular NAD content was explored.Using β-naphthofiavone

a mixed functionoxygenase inducer

together with induced or uninduced human amnion FL cells

it was foundthat aflatoxin B

benzo（a）pyrene

2-acetylaminofluorene

10-dimethylanthracene andethylcarbamate could induce the ADPRT-mediated decrease of cellular NAD content

while4-acetylaminofluorene

anthracene

isopropyl-N-（3-chlorophenyl）-carbamate

β-propiolactone

γ-butyrolactone

cyclophosphamide and safrol could not.The results indicate that this isa cheap and specific method to detect DNA damage caused by chemical carcinogens/mutagenswith a spccificity approaching that of the unscheduled DNA synthesis assay.

Abstract

It was found that the DNA-damaging agents N-methyl-N’-nitro-N-nitrosoguanidine（MNNG）

methyl-methanesulphonate（MMS）and 4-nitroquinoline-N-oxide（4NQO）could stimulate ADP- ribosyl transferase（ADPRT）activity and reduce the cellular NAD content in a dose- dependent way.The reduction of NAD after DNA damage could be partially or completely prevented by ADPRT inhibitors

3-aminobenzamide or nicotinamide

which showed no influence on reduction of NAD induced by metabolic blocking agents.Therefore

a simple and specific method to detect DNA-damaging mutagens by measuring ADPRT-mediated decrease of cellular NAD content was explored.Using β-naphthofiavone

a mixed function oxygenase inducer

together with induced or uninduced human amnion FL cells

it was found that aflatoxin B

benzo（a）pyrene

2-acetylaminofluorene

10-dimethylanthracene and ethylcarbamate could induce the ADPRT-mediated decrease of cellular NAD content

while 4-acetylaminofluorene

anthracene

isopropyl-N-（3-chlorophenyl）-carbamate

β-propiolactone

γ-butyrolactone

cyclophosphamide and safrol could not.The results indicate that this is a cheap and specific method to detect DNA damage caused by chemical carcinogens/mutagens with a spccificity approaching that of the unscheduled DNA synthesis assay.

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