Effect of S-adenosylmethionine on age-induced hepatocyte damage in old Wistar rats

被引:16
作者
Castillo, C
Salazar, V
Ariznavarreta, C
Fossati, M
Tresguerres, JAF
Vara, E
机构
[1] Univ Complutense, Lab Exp Endocrinol, Dept Physiol, Sch Med, E-28040 Madrid, Spain
[2] Univ Buenos Aires, Sch Nat & Exact Sci, Lab Cellular Biol, RA-1053 Buenos Aires, DF, Argentina
[3] Univ Complutense, Dept Biochem & Mol Biol, Sch Med, E-28040 Madrid, Spain
关键词
aging; free radicals; glutathione; liver; oxidative stress; S-adenosylmethionine;
D O I
10.1007/s10522-005-4806-2
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
Aging is accompanied by changes in the morphology and physiology of organs and tissues, such as the liver. This process might be due to the accumulation of oxidative damage induced by reactive oxygen (ROS) and reactive nitrogen species (RNS). Hepatocytes are very rich in mitochondria and have a high respiratory rate, so they are exposed to large amounts of ROS and permanent oxidative stress. S-Adenosylmethionine (SAMe) is an endogenous metabolite that has shown to exert protective effects on different experimental pathological models in which free radicals are involved. The aim of this study was to investigate the effect of SAMe on age-induced damage in hepatocytes. For this purpose, male and female Wistar rats of 18 and 2 months of age were used. Cells were isolated and, after incubation in the presence or in the absence of SAMe, different parameters were measured. Aging induced a significant increase in nitric oxide, carbon monoxide and cGMP, and a reduction in reduced glutathione, ATP and phosphatidylcholine synthesis, as well as in methionine-adenosyl-transferase and methyl-transferase activities. Incubation of old cells with SAMe prevented all these age-related changes, reaching values in some of the parameters similar to those found in young animals. In conclusion, SAMe seems to have beneficial effects against age-induced damage in hepatocytes.
引用
收藏
页码:313 / 323
页数:11
相关论文
共 60 条
[51]   Mechanisms of aging: An appraisal of the oxidative stress hypothesis [J].
Sohal, RS ;
Mockett, RJ ;
Orr, WC .
FREE RADICAL BIOLOGY AND MEDICINE, 2002, 33 (05) :575-586
[52]   THE FREE-RADICAL HYPOTHESIS OF AGING - AN APPRAISAL OF THE CURRENT STATUS [J].
SOHAL, RS .
AGING-CLINICAL AND EXPERIMENTAL RESEARCH, 1993, 5 (01) :3-17
[53]  
STRAMENTINOLI G, 1986, 1 C BIOCH PHARM CLIN
[54]   Multiple pathways of peroxynitrite cytotoxicity [J].
Szabó, C .
TOXICOLOGY LETTERS, 2003, 140 :105-112
[55]  
Troen BR, 2003, MT SINAI J MED, V70, P3
[56]  
Van Remmen H, 2001, EXP GERONTOL, V36, P957
[57]   TNF-alpha-induced inhibition of PC synthesis by human type II pneumocytes is sequentially mediated by PGE(2) and NO [J].
Vara, E ;
AriasDiaz, J ;
Garcia, C ;
Hernandez, J ;
Balibrea, JL .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 1996, 271 (03) :L359-L365
[58]   EFFECT OF DIFFERENT SEPSIS-RELATED CYTOKINES ON LIPID-SYNTHESIS BY ISOLATED HEPATOCYTES [J].
VARA, E ;
ARIASDIAZ, J ;
TORRESMELERO, J ;
GARCIA, C ;
RODRIGUEZ, JM ;
BALIBREA, JL .
HEPATOLOGY, 1994, 20 (04) :924-931
[59]  
VARELA I, 1986, 1 C BIOCH PHARM CLIN, P25
[60]   EFFECTS OF ORAL S-ADENOSYL-L-METHIONINE ON HEPATIC GLUTATHIONE IN PATIENTS WITH LIVER-DISEASE [J].
VENDEMIALE, G ;
ALTOMARE, E ;
TRIZIO, T ;
LEGRAZIE, C ;
DIPADOVA, C ;
SALERNO, MT ;
CARRIERI, V ;
ALBANO, O .
SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY, 1989, 24 (04) :407-415