Amelioration of benzo (a) pyrene-induced lung carcinogenesis in strain A mice by diphenylmethyl selenocyanate

被引:16
作者
Das, Raiat K. [1 ]
Banerjee, Sarmistha [1 ]
Bhattacharya, Sudin [1 ]
机构
[1] Chittaranjan Natl Canc Inst, Dept Canc Chemoprevent, Kolkata 700026, W Bengal, India
关键词
chemoprevention; organoselenocyanate; diphenylmethyl selenocyanate; benzo (a) pyrene (BP); lung cancer prevention; non-small cell lung carcinoma;
D O I
10.1016/j.etp.2006.10.003
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Organoselenocyanates are an important class of chemopreventive agents, which possess antioxidative, antimutagenic and anticarcinogenic properties. In the present study, we used benzo (a) pyrene (BP)-induced lung carcinogenesis model for assessment of the chemopreventive efficacy of diphenylmethyl selenocyanate, a synthetic organoselenocyanate. BP was given at a dose of 0.2 mg/mouse to initiate lung carcinogenesis in strain A mouse and the Se compound was given orally at a dose of 3mg/kg b.w. Histopathological characterizations and biochemical estimation were done to determine the protective effect of Se compound during the progression of lung carcinogenesis. Hyperplasia and severe dysplasia, the precancerous stage, were evident in carcinogen control group after 8th and 22nd week, respectively. These times were selected as the targets for chemoprevention. Treatment with the Se compound effectively reduced the incidence of hyperplasia and severe dysplasia. The Se compound also significantly (p < 0.0 1) reduced microsomal lipid peroxidation and induced glutathione-S-transferase activity in liver and lung when measured after 8th and 22nd week. Lung cancer is diagnosed in majority of cases only at a later stage. These findings will further strengthen the view on organoselenocyanate as an effective cancer chemopreventive agent against lung carcinogenesis when applied at the post-initiation phase. (c) 2006 Elsevier GmbH. All rights reserved.
引用
收藏
页码:351 / 360
页数:10
相关论文
共 50 条
[1]  
[Anonymous], INT J CANC PREV
[2]   SERUM LEVELS OF SELENIUM AND RETINOL AND THE SUBSEQUENT RISK OF CANCER [J].
COATES, RJ ;
WEISS, NS ;
DALING, JR ;
MORRIS, JS ;
LABBE, RF .
AMERICAN JOURNAL OF EPIDEMIOLOGY, 1988, 128 (03) :515-523
[3]  
Comstock GW, 1997, CANCER EPIDEM BIOMAR, V6, P907
[4]   Diphenylmethyl selenocyanate inhibits DMBA-croton oil induced two-stage mouse skin carcinogenesis by inducing apoptosis and inhibiting cutaneous cell proliferation [J].
Das, RK ;
Hossain, SKU ;
Bhattacharya, S .
CANCER LETTERS, 2005, 230 (01) :90-101
[5]  
ELBAYOUMY K, 1999, NUTR ONCOLOGY, P299
[6]   Pathology of lung cancer [J].
Franklin, WA .
JOURNAL OF THORACIC IMAGING, 2000, 15 (01) :3-12
[7]  
FRED RH, 2001, CLIN CANCER RES, V7, P5
[8]   PROSPECTIVE-STUDY OF TOENAIL SELENIUM LEVELS AND CANCER AMONG WOMEN [J].
GARLAND, M ;
MORRIS, JS ;
STAMPFER, MJ ;
COLDITZ, GA ;
SPATE, VL ;
BASKETT, CK ;
ROSNER, B ;
SPEIZER, FE ;
WILLETT, WC ;
HUNTER, DJ .
JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1995, 87 (07) :497-505
[10]  
HABIG WH, 1974, J BIOL CHEM, V249, P7130