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Natural killer (NK) cell activity was evaluated after the initiation and promotion steps in a medium-term multi-organ bioassay for carcinogenesis. NK cell activity was assessed in vitro by Cr51 release assay at the 4th and 30th weeks of the experiment. Male Wistar rats were sequentially initiated with N-diethylnitrosamine (DEN i.p.), N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN drinking water), N-methyl-N-nitrosourea (MNU i.p.), dihydroxy-di-N-propylnitrosamine (DHPN drinking water) and N,N'-dimethylhydrazine (DMH s.c.) at subcarcinogenic doses for 4 weeks (DMBDD initiation). One group was evaluated at the 4th week and the other was maintained without any further treatment until the 30th week. Two initiated groups were exposed through the diet to 2-acetylaminofluorene (2-AAF) or phenobarbital (PB), from the 6th until the 30th week. Five additional groups were studied to evaluate the effects of each initiator on NK activity. All groups submitted to initiation only, initiation plus promotion, or promotion only, developed significantly more preneoplastic lesions than the untreated control group. The main target organs for tumor development in the initiated animals were the liver and the colon, irrespective of treatment with 2-AAF or PB. NK cell activity was not affected by exposure to genotoxic carcinogens after initiation, at the 4th week. Treatments only with PB or 2-AAF did not change NK cell activity. However, decreased NK cell activity was registered in the group only initiated with DMBDD and in the group given DMBDD+2-AAF. This late depression of NK cell activity at the 30th week could be related to the production of suppressing molecules by the tumor cells.
A L Spinardi, and
R Kaneno, and
M A Rodrigues, and
D M Salvadori, and
N S Rocha, and
L F Barbisan, and
L R Ribeiro, and
J L de Camargo
November 2011,
Toxicology,
A L Spinardi, and
R Kaneno, and
M A Rodrigues, and
D M Salvadori, and
N S Rocha, and
L F Barbisan, and
L R Ribeiro, and
J L de Camargo
March 1993,
Japanese journal of cancer research : Gann,
A L Spinardi, and
R Kaneno, and
M A Rodrigues, and
D M Salvadori, and
N S Rocha, and
L F Barbisan, and
L R Ribeiro, and
J L de Camargo
January 2010,
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association,
A L Spinardi, and
R Kaneno, and
M A Rodrigues, and
D M Salvadori, and
N S Rocha, and
L F Barbisan, and
L R Ribeiro, and
J L de Camargo
April 2008,
Journal of food science,
A L Spinardi, and
R Kaneno, and
M A Rodrigues, and
D M Salvadori, and
N S Rocha, and
L F Barbisan, and
L R Ribeiro, and
J L de Camargo
May 1993,
International journal of cancer,
A L Spinardi, and
R Kaneno, and
M A Rodrigues, and
D M Salvadori, and
N S Rocha, and
L F Barbisan, and
L R Ribeiro, and
J L de Camargo
January 2008,
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association,
A L Spinardi, and
R Kaneno, and
M A Rodrigues, and
D M Salvadori, and
N S Rocha, and
L F Barbisan, and
L R Ribeiro, and
J L de Camargo
February 1996,
Experimental and toxicologic pathology : official journal of the Gesellschaft fur Toxikologische Pathologie,
A L Spinardi, and
R Kaneno, and
M A Rodrigues, and
D M Salvadori, and
N S Rocha, and
L F Barbisan, and
L R Ribeiro, and
J L de Camargo
January 2010,
Asian Pacific journal of cancer prevention : APJCP,
A L Spinardi, and
R Kaneno, and
M A Rodrigues, and
D M Salvadori, and
N S Rocha, and
L F Barbisan, and
L R Ribeiro, and
J L de Camargo
January 1993,
Teratogenesis, carcinogenesis, and mutagenesis,
A L Spinardi, and
R Kaneno, and
M A Rodrigues, and
D M Salvadori, and
N S Rocha, and
L F Barbisan, and
L R Ribeiro, and
J L de Camargo
November 1994,
Carcinogenesis,
