Inhibitory effect of oral administration of Lactobacillus casei on 3-methylcholanthrene-induced carcinogenesis in mice

被引:42
作者
Takagi, A [1 ]
Matsuzaki, T [1 ]
Sato, M [1 ]
Nomoto, K [1 ]
Morotomi, M [1 ]
Yokokura, T [1 ]
机构
[1] Yakult Cent Inst Microbiol Res, Tokyo 1868650, Japan
关键词
cancer prevention; Lactobacillus casei; oral administration; chemically induced tumor; 3-methylcholanthrene;
D O I
10.1007/s004300050112
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The present study was designed to determine whether tumor induction by 3-methylcholanthrene (MC), a carcinogenic hydrocarbon, can be inhibited by oral administration of Lactobacillus casei strain Shirota (LC). C3H/HeN mice were divided into four groups and assigned to the following treatments: treated with MC and given control or LC-containing diet; treated with vehicle only and given control or LC-containing diet. MC (1 mg) was injected intradermally at 7 weeks of age and the tumor incidence was monitored; LC was mixed into a diet at a concentration of 0.05% (w/w) and the diet was fed from the day of MC injection throughout the study. Spleen cells were analyzed for the immune parameters at 12 and 16 weeks after the MC injection. Oral feeding of mice with LC reduced tumor incidence (P < 0.05). MC treatment lowered the in vitro response to concanavalin A (Con A) of spleen cells, the secretion of interleukin-2 in spleen cell culture after stimulation of the cells with Con A and the proportions of CD3(+) CD4(+) and CD8(+) splenic cells. However, the analysis of the spleen cells obtained from the mice treated with MC and given the LC-containing diet revealed that these disrupted host immune parameters were maintained at the level of normal controls. These results suggest that oral feeding of mice with LC inhibits MC-induced tumorigenesis by modulating the disrupted host immune responses during MC carcinogenesis.
引用
收藏
页码:111 / 116
页数:6
相关论文
共 47 条
[21]  
2-P
[22]   DIETARY RESTRICTION REDUCES THE INCIDENCE OF 3-METHYLCHOLANTHRENE-INDUCED TUMORS IN MICE - CLOSE CORRELATION WITH ITS POTENTIATING EFFECT ON HOST T-CELL FUNCTIONS [J].
KONNO, A ;
HISHINUMA, K ;
HASHIMOTO, Y ;
KIMURA, S ;
NISHIMURA, T .
CANCER IMMUNOLOGY IMMUNOTHERAPY, 1991, 33 (05) :293-298
[23]   ABSENCE OF P53 MUTATIONS IN RAT COLON TUMORS INDUCED BY 2-AMINO-6-METHYLDIPYRIDO[1,2-ALPHA-3',2'-D]IMIDAZOLE, 2-AMINO-3-METHYLIMIDAZO[4,5-F]QUINOLINE, OR 2-AMINO-1-METHYL-6-PHENYLIMIDAZO[4,5-B]PYRIDINE [J].
MAKINO, H ;
USHIJIMA, T ;
KAKIUCHI, H ;
ONDA, M ;
ITO, N ;
SUGIMURA, T ;
NAGAO, M .
JAPANESE JOURNAL OF CANCER RESEARCH, 1994, 85 (05) :510-514
[24]   RAT P53 GENE-MUTATIONS IN PRIMARY ZYMBAL GLAND TUMORS INDUCED BY 2-AMINO-3-METHYLIMIDAZO[4,5-F]QUINOLINE, A FOOD MUTAGEN [J].
MAKINO, H ;
ISHIZAKA, Y ;
TSUJIMOTO, A ;
NAKAMURA, T ;
ONDA, M ;
SUGIMURA, T ;
NAGAO, M .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1992, 89 (11) :4850-4854
[25]   The effect of oral feeding of Lactobacillus casei strain Shirota on immunoglobulin E production in mice [J].
Matsuzaki, T ;
Yamazaki, R ;
Hashimoto, S ;
Yokokura, T .
JOURNAL OF DAIRY SCIENCE, 1998, 81 (01) :48-53
[26]   Effect of oral administration of Lactobacillus casei on alloxan-induced diabetes in mice [J].
Matsuzaki, T ;
Nagata, Y ;
Kado, S ;
Uchida, K ;
Hashimoto, S ;
Yokokura, T .
APMIS, 1997, 105 (08) :637-642
[27]  
MATSUZAKI T, 1988, CANCER IMMUNOL IMMUN, V26, P209
[28]   Prevention of onset in an insulin-dependent diabetes mellitus model, NOD mice, by oral feeding of Lactobacillus casei [J].
Matsuzaki, T ;
Nagata, Y ;
Kado, S ;
Uchida, K ;
Kato, I ;
Hashimoto, S ;
Yokokura, T .
APMIS, 1997, 105 (08) :643-649
[29]   Antidiabetic effects of an oral administration of Lactobacillus casei in a non-insulin-dependent diabetes mellitus (NIDDM) model using KK-A(y) mice [J].
Matsuzaki, T ;
Yamazaki, R ;
Hashimoto, S ;
Yokokura, T .
ENDOCRINE JOURNAL, 1997, 44 (03) :357-365
[30]   CANCER CHEMOPREVENTION - PRINCIPLES AND PROSPECTS [J].
MORSE, MA ;
STONER, GD .
CARCINOGENESIS, 1993, 14 (09) :1737-1746