Poster Topical Area: Energy and Macronutrient Metabolism
Location: Hall D
Poster Board Number: 533
Objectives: Liver cancer is the 6th most frequently diagnosed cancer worldwide, but the 2nd most frequent cause of cancer death. Prohibitin 1 (PHB1), a protein in the mitochondrial inner membrane, is a chaperone protein for proper mitochondrial functions. Liver injury, fibrosis and hepatocellular carcinoma (HCC) occurred in liver specific Phb1-/- mice spontaneously starting from 3 weeks after birth. Sulfur-containing amino acid (SCAA) metabolites, S-adenosylmethionine (SAMe) and taurine, and betaine have hepato-protective effect, via regulation of glutathione (GSH) metabolism. This research examines the relationships among Phb1 expression, treatments of SAMe and its combination with taurine and/or betaine (SCTB) and hepatic GSH level.
Methods: AML 12 cell line, originated from mouse normal hepatocyte, was used in this experiment. Cell viability was measured for confirming each material toxicity. mRNA expression of Phb1, GSH synthesizing and decomposing enzymes were performed in this recent study.
Results: All materials had no toxicity, however Phb1 deficiency lowered cell proliferation compared to control group. GSH concentration was increased in SCTB treatments groups compared to control group. Whereas there was no difference on GSH level in spite of SCTB treatments in Phb1 knockdown(KD) groups. Gclc expression had no significant difference in all groups. Gclm and Ggt expression was decreased both SCTB treatments and Phb1 depletion. Gss expression was decreased in only SCTB treatments groups.
Conclusions: SAMe and it combination with taurine and/or betaine treatments have hepato-protective effects by increasing GSH level via regulating GSH synthesizing and decomposing enzyme expression. However, this liver protective effect of SAMe and it combination with taurine and/or betaine treatments through cellular GSH regulation was limited probibitin 1 was diluted in mouse liver. Therefore, Phb1 expression has important effects on GSH metabolism.
Ewha Womans University
Seoul, Seoul-t'ukpyolsi, Republic of Korea