Mechanism of N-acetylcysteine (NAC) and other thiols as both positive and negative modifiers of MNNG-induced mutagenicity in V79 Chinese hamster cells.

@article{Romert1987MechanismON,
  title={Mechanism of N-acetylcysteine (NAC) and other thiols as both positive and negative modifiers of MNNG-induced mutagenicity in V79 Chinese hamster cells.},
  author={L Romert and Dag Jenssen},
  journal={Carcinogenesis},
  year={1987},
  volume={8 10},
  pages={1531-5}
}
Carcinogenic xenobiotics can be detoxified by nucleophilic thiols, which interact directly or through enzyme catalyzed reactions with electrophilic metabolites/compounds or metabolically produced oxidants. Formation of such conjugates is assumed to be a dominating competitive pathway reducing the mutagenic and carcinogenic effects of several known carcinogens. In the case of the potent carcinogen N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) the situation is different since this carcinogen is… CONTINUE READING

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In the case of the potent carcinogen N - methyl - N'-nitro - N - nitrosoguanidine ( MNNG ) the situation is different since this carcinogen is transformed to reactive intermediates by nucleophilic agents such as thiols .
In the case of the potent carcinogen N - methyl - N'-nitro - N - nitrosoguanidine ( MNNG ) the situation is different since this carcinogen is transformed to reactive intermediates by nucleophilic agents such as thiols .
In the case of the potent carcinogen N - methyl - N'-nitro - N - nitrosoguanidine ( MNNG ) the situation is different since this carcinogen is transformed to reactive intermediates by nucleophilic agents such as thiols .
In the case of the potent carcinogen N - methyl - N'-nitro - N - nitrosoguanidine ( MNNG ) the situation is different since this carcinogen is transformed to reactive intermediates by nucleophilic agents such as thiols .
As demonstrated with MNU , intracellular thiol concentrations ( in milli / molar range ) , which is high enough to bring about the activation of MNNG , are not sufficiently high to protect DNA from damage by the alkylating intermediate .
No effect of the thiols could be detected on the mutagenicity of MNU , indicating that the intermediates of MNU and MNNG react , in agreement with the reaction kinetics , in favour of water and thiols become less important .
No effect of the thiols could be detected on the mutagenicity of MNU , indicating that the intermediates of MNU and MNNG react , in agreement with the reaction kinetics , in favour of water and thiols become less important .
The modification of MNNG - mutagenicity was compared to the effect of thiols on the mutagenicity of N - methyl - N'-nitrosourea ( MNU ) in V79 Chinese hamster cells .
No effect of the thiols could be detected on the mutagenicity of MNU , indicating that the intermediates of MNU and MNNG react , in agreement with the reaction kinetics , in favour of water and thiols become less important .
As demonstrated with MNU , intracellular thiol concentrations ( in milli / molar range ) , which is high enough to bring about the activation of MNNG , are not sufficiently high to protect DNA from damage by the alkylating intermediate .
The modification of MNNG - mutagenicity was compared to the effect of thiols on the mutagenicity of N - methyl - N'-nitrosourea ( MNU ) in V79 Chinese hamster cells .
No effect of the thiols could be detected on the mutagenicity of MNU , indicating that the intermediates of MNU and MNNG react , in agreement with the reaction kinetics , in favour of water and thiols become less important .
In the case of the potent carcinogen N - methyl - N'-nitro - N - nitrosoguanidine ( MNNG ) the situation is different since this carcinogen is transformed to reactive intermediates by nucleophilic agents such as thiols .
In the case of the potent carcinogen N - methyl - N'-nitro - N - nitrosoguanidine ( MNNG ) the situation is different since this carcinogen is transformed to reactive intermediates by nucleophilic agents such as thiols .
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