Affiliations: Department of Medical Laboratory Science and
Biotechnology, Central Taiwan University of Science and Technology,
Taiwan | Department of Food and Nutrition, Providence
University, Taiwan | Graduate Institute of Veterinary Pathology, National
Chung Hsing University, Taiwan | Department of Physical Education, Central Taiwan
University of Science and Technology, Taiwan | Department of Food Science and Biotechnology, National
Chung Hsing University, Taiwan
Note: [] Address for correspondence: Professor M.-L. Hu, Department of
Food Science and Biotechnology, National Chung Hsing University, 250 Kuo-Kuang
Road, Taichung, 402, Taiwan. Tel./Fax: +886 4 22812363; E-mail:
mlhuhu@dragon.nchu.edu.tw
Abstract: The deleterious effects of ethanol in senescence-accelerated prone 8
mice (SAMP8) and the protective role of nicotinamide (NAM) against
ethanol-induced liver injury were examined. The mice were orally administered
2 g ethanol/kg BW and 200 mg or 500 mg NAM/kg BW three times/week for 10 weeks.
Results showed that ethanol elevated activity of alanine aminotransferase (ALT)
significantly. Ethanol also enhanced the formation of malondialdehyde (MDA) and
protein carbonyls in the liver, whereas ethanol treatment resulted in
significantly lower activity of hepatic glutathione peroxidase (GPx), catalase
and superoxide dismutase (SOD). Hematoxylin and eosin staining indicated
moderate to severe fatty infiltration but not fibrosis. Administration of high
NAM (500 mg/kg BW) led to markedly decreased levels of hepatic MDA, protein
carbonyls, fatty infiltration and the activity of ALT, and increased activity
of GPx, catalase and SOD in the ethanol-fed group. Thus, using SAMP8 as animal
model for ethanol-induced liver injury in the aged mice, this study
demonstrates that NAM is effective in protecting such damage.
