Chemopreventive effect of sinapic acid on 1,2-dimethylhydrazine-induced experimental rat colon carcinogenesis

被引:25
作者
Balaji, C. [1 ]
Muthukumaran, J. [1 ]
Nalini, N. [1 ]
机构
[1] Annamalai Univ, Fac Sci, Dept Biochem & Biotechnol, Annamalainagar 608002, Tamil Nadu, India
关键词
Sinapic acid; colon cancer; chemoprevention; oxidative stress; xenobiotics; ABERRANT CRYPT FOCI; LIPID-PEROXIDATION; OXIDATIVE STRESS; CYTOCHROME-P450; 2E1; COLORECTAL-CANCER; LIVER MICROSOMES; GLUTATHIONE; ENZYMES; MODEL; PEROXYNITRITE;
D O I
10.1177/0960327114522501
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
Sinapic acid (SA) is a naturally occurring phenolic acid found in various herbal plants which is attributed with numerous pharmacological properties. This study was aimed to investigate the chemopreventive effect of SA on 1,2-dimethylhydrazine (DMH)-induced rat colon carcinogenesis. Rats were treated with DMH injections (20 mg kg(-1) bodyweight (b.w.) subcutaneously once a week for the first 4 consecutive weeks and SA (20, 40 and 80 mg kg(-1) b.w.) post orally for 16 weeks. At the end of the 16-week experimental period, all the rats were killed, and the tissues were evaluated biochemically. Our results reveal that DMH alone treatment decreased the levels/activities of lipid peroxidation by-products such as thiobarbituric acid reactive substances, conjugated dienes and antioxidants such as superoxide dismutase, catalase, glutathione reductase, glutathione peroxidase and reduced glutathione in the intestine and colonic tissues which were reversed on supplementation with SA. Moreover, the activities of drug-metabolizing enzymes of phase I (cytochrome P450 and P4502EI) were enhanced and those of phase II (glutathione-S-transferase, DT-diaphorase and uridine diphosphate glucuronosyl transferase) were diminished in the liver and colonic mucosa of DMH alone-treated rats and were reversed on supplementation with SA. All the above changes were supported by the histopathological observations of the rat liver and colon. These findings suggest that SA at the dose of 40 mg kg(-1) b.w. was the most effective dose against DMH-induced colon carcinogenesis, and thus, SA could be used as a potential chemopreventive agent.
引用
收藏
页码:1253 / 1268
页数:16
相关论文
共 61 条
[1]   Cytochrome P450 gene polymorphism and cancer [J].
Agúndez, JAG .
CURRENT DRUG METABOLISM, 2004, 5 (03) :211-224
[2]   Peroxynitrite and NO+ donors form colored nitrite adducts with sinapinic acid:: potential applications [J].
Akhter, S ;
Green, JR ;
Root, P ;
Thatcher, GJ ;
Mutus, B .
NITRIC OXIDE-BIOLOGY AND CHEMISTRY, 2003, 8 (04) :214-221
[3]  
[Anonymous], 2011, COL CANC FACTS FIG 2
[4]  
[Anonymous], 2011, INT J PHARM CLIN RES
[5]  
Arutyunyan A. V., 1997, Voprosy Onkologii (St. Petersburg), V43, P618
[6]   Phenobarbital and 3-methylcholanthrene treatment alters phase I and II enzymes and the sensitivity of the rat colon to the carcinogenic activity of azoxymethane [J].
Baijal, PK ;
Fitzpatrick, DW ;
Bird, RP .
FOOD AND CHEMICAL TOXICOLOGY, 1997, 35 (08) :789-798
[7]   Exocyclic DNA adducts as oxidative stress markers in colon carcinogenesis: Potential role of lipid peroxidation, dietary fat and antioxidants [J].
Bartsch, H ;
Nair, J ;
Owen, RW .
BIOLOGICAL CHEMISTRY, 2002, 383 (06) :915-921
[8]   Protein oxidation in aging, disease, and oxidative stress [J].
Berlett, BS ;
Stadtman, ER .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (33) :20313-20316
[9]   Associated changes of lipid peroxidation and transforming growth factor β1 levels in human colon cancer during tumour progression [J].
Biasi, F ;
Tessitore, L ;
Zanetti, D ;
Cutrin, JC ;
Zingaro, B ;
Chiarpotto, E ;
Zarkovic, N ;
Serviddio, G ;
Poli, G .
GUT, 2002, 50 (03) :361-367
[10]  
CARLBERG I, 1985, METHOD ENZYMOL, V113, P484