Hibiscus protocatechuic acid protects against oxidative damage induced by tert-butylhydroperoxide in rat primary hepatocytes

被引:130
作者
Tseng, TH
Wang, CJ
Kao, ES
Chu, HY
机构
[1] Institute of Biochemistry, Chung Shan Med. and Dental College, Taichung 402, No. 113, Section 2, Ta-Ching Street
关键词
protocatechuic acid; oxidative damage; tert-butylhydroperoxide; hepatocyte;
D O I
10.1016/0009-2797(96)03721-0
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Hibiscus protocatechuic acid (PCA), a simple phenolic compound isolated from Hibiscus sabdariffa L., was studied for its protective effects against oxidative damage induced by tert-butylhydroperoxide (t-BHP) in a primary culture of rat hepatocytes. It had been reported that exposure of isolated hepatocytes to t-BHP results in leakage of lactate dehydrogenase (LDH) and alanine transaminase (ALT), peroxidation of cellular lipids, and depolarization of mitochondria. The present investigations showed that PCA at concentrations of 0.05 mg/ml and 0.10 mg/ml significantly decreased the leakage of LDH (P < 0.01) and ALT (P < 0.05 and P < 0.01) and the formation of malondialdehyde (MDA; P < 0.05 and P < 0.01) induced by 30-min treatment with t-BHP (1.5 mM) in primary cultured rat hepatocytes. PCA also attenuated t-BHP (0.10 mM) induced mitochondrial depolarization as determined by a retention test of rhodamine 123 and DNA repair synthesis as evidenced by unscheduled DNA synthesis (UDS). In addition, PCA exhibited an effective ability to quench 1,1-diphenyl-2-picrylhydrazyl radicals (DPPH). In conclusion, PCA demonstrated protective effects against cytotoxicity and genotoxicity of hepatocytes induced by t-BHP. One of mechanisms of PCA's protective effect may be associated with its property of scavenging free radicals.
引用
收藏
页码:137 / 148
页数:12
相关论文
共 38 条
[1]  
ALLEY MC, 1988, CANCER RES, V48, P589
[2]   TERT-BUTYL HYDROPEROXIDE-MEDIATED DNA-BASE DAMAGE IN CULTURED-MAMMALIAN-CELLS [J].
ALTMAN, SA ;
ZASTAWNY, TH ;
RANDERS, L ;
LIN, ZL ;
LUMPKIN, JA ;
REMACLE, J ;
DIZDAROGLU, M ;
RAO, G .
MUTATION RESEARCH, 1994, 306 (01) :35-44
[3]   DIETARY CARCINOGENS AND ANTICARCINOGENS - OXYGEN RADICALS AND DEGENERATIVE DISEASES [J].
AMES, BN .
SCIENCE, 1983, 221 (4617) :1256-1264
[4]  
BELLOMO G, 1991, CELL CALCIUM, V12, P355
[5]  
BONNEY RJ, 1974, IN VITRO CELL DEV B, V9, P399
[6]  
BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1016/0003-2697(76)90527-3
[7]   MOLECULAR MECHANISMS OF OXYGEN RADICAL CARCINOGENESIS AND MUTAGENESIS - THE ROLE OF DNA-BASE DAMAGE [J].
BREIMER, LH .
MOLECULAR CARCINOGENESIS, 1990, 3 (04) :188-197
[8]   PROOXIDANT STATES AND TUMOR PROMOTION [J].
CERUTTI, PA .
SCIENCE, 1985, 227 (4685) :375-381
[10]   RHODAMINE-123 AS A PROBE OF TRANSMEMBRANE POTENTIAL IN ISOLATED RAT-LIVER MITOCHONDRIA - SPECTRAL AND METABOLIC PROPERTIES [J].
EMAUS, RK ;
GRUNWALD, R ;
LEMASTERS, JJ .
BIOCHIMICA ET BIOPHYSICA ACTA, 1986, 850 (03) :436-448