This study showed that betaine may protect liver from fibrogenesis by maintaining cellular antioxidant capacity.
Male rats were supplemented with betaine (1%, w/v) in drinking water from 2 weeks prior to the initiation of dimethylnitrosamine (DMN) treatment (10mg/(kg day), i.p., 3 days/week, for 1, 2, or 4 weeks). Induction of liver injury was determined by quantifying serum alanine aminotransferase, aspartate aminotransferase activities, bilirubin levels, hepatic xenobiotic-metabolizing capacity, histopathological changes and 4-hydroxyproline levels. Development of oxidative injury was estimated by malondialdehyde (MDA) levels and total oxyradical scavenging capacity (TOSC) of liver and serum toward hydroxyl, peroxyl radicals, and peroxynitrite.
Betaine supplementation markedly attenuated the DMN-induced hepatotoxicity, fibrosis and oxidative injury (e.g. elevation of MDA and the reduction of TOSC were depressed significantly).
Kim et al (2009). "Alleviation of dimethylnitrosamine-induced liver injury and fibrosis by betaine supplementation in rats." Chem Biol Interact 177(3): 204-11.