In collaboration with Dr. Gallo, Dr. Tian's laboratory has also found that Ah receptor pathway interacts with the cholesterol biosynthesis pathway in that the Ah receptor ligands suppresses the cholesterol levels in mouse serum as well as in the cell membrane of mouse hepatoma cell lines. Their previous study suggested that iron supplementation enhanced inflammation and the production of reactive nitrogen species in the esophageal epithelium, which could contribute to esophageal adenocarcinogenesis. They have further characterized oxidative damage in this model. CLE cells were believed to be the target cells of oxidative damages because they overexpressed heme oxygenase-1 and metallothionein, both known to be responsive to oxidative damage. They propose that oxidative damage plays an important role in the formation of EAC in the EDA model, and a similar situation may occur in humans with gastroesophageal reflux and iron over-nutrition.
Tea is a popular beverage consumed worldwide.
The metabolic fate of its major constituents, catechins, however, is not well known. They described in a recent study, detection of two catechin metabolites in the urine and plasma of human volunteers after ingestion of green tea. Repeated ingestion of green tea produced a slight accumulative effect of the metabolites. They were also detected in the plasma, showing similar kinetics as the urinary metabolites, and in the feces. Study on these metabolites may help us to further understand the cancer chemopreventive actions and other beneficial effects of tea.