Mizoguchi Y, Kodama C, Sakai M, Sakagami Y, Kobayashi K, Morisawa S, Yamamoto S, Yamada J
Third Department of Internal Medicine, Osaka City University Medical School, Japan.
Gastroenterol Jpn. 1988 Oct;23(5):534-7. doi: 10.1007/BF02779485.
We have reported that in rats with D-galactosamine-induced liver injury, the serum level of indoleacetic acid (IAA), a metabolite of tryptophan (TRP), increases before the increase in serum transaminase activity. To determine whether this IAA is derived from hepatocytes, isolated hepatocytes were treated with D-galactosamine and loaded with TRP, and the changes in TRP and IAA levels in the culture supernatant of the isolated hepatocytes were measured at various time intervals. As a result, IAA level in the culture supernatant of hepatocytes treated with D-galactosamine and loaded with TRP significantly increased in a time-dependent manner. This indicates that in D-galactosamine-induced liver injury, a metabolic pathway which produces IAA from TRP through tryptamine is present in hepatocytes.