These results suggest a-smooth muscle actin-expressing cells are responsible for liver fibrosis, and the elimination of factors stimulating matrix synthesis (e.g., hepatitis virus) may decrease liver fibrosis.

These results indicate that the protective effect of DFO against APAP-induced liver injury may be attributable not to changes in APAP metabolism but to the chelation of iron, which can catalyze the generation of active oxygen species, in hepatocytes.

These results suggest a-smooth muscle actin-expressing cells are responsible for liver fibrosis, and the elimination of factors stimulating matrix synthesis (e.g., hepatitis virus) may decrease liver fibrosis.

The killing of cultured hepatocytes by cyanide accelerated phospholipid metabolism, with a reduction in cytoplasmic pH, but did not accelerate proteolysis. Alkalinization of the cytoplasm by monensin, a protonsodium exchange ionophore, enhanced the loss of viability and acceleration of phospholipid metabolism caused by cyanide. Thus, acidification of the cytoplasm appears to protect against the toxic effects of cyanide. Glycine reduced the killing of hepatocytes, concomitant with reduced phospholipid metabolism. The protective effect of glycine neither enhanced the reduction in cytoplasmic pH nor prevented the depletion of adenosine triphosphate (ATP) by cyanide. The mechanism of the protection exerted by glycine against chemical ischemia can be attributed neither to changes in cytoplasmic pH nor to the prevention of ATP depletion, but appears to be due to other mechanisms that have yet to be identified.

The aim of this study was to investigate the mechanism of cytoprotection by glycine against hypoxia-induced hepatocellular injury. Incubation under hypoxic conditions (95% N2 and 5% C02) for 5 h induced about 50% cell death, but administration of glycine remarkably reduced hepatocellular death without preventing a loss in ATP content. Anaerobic glycolysis generated lactic acid, reducing extracellular pH, but glycine had no effect on changes in extracellular pH. Chloride-channel inhibitors [anthracene-9-carboxylic acid (A9C), furosemide, and strychnine] also significantly reduced hepatocellular death induced by hypoxia. These results suggest that the mechanism of protection by glycine against hypoxic injury is not related to the prevention of ATP depletion or to changes in extracellular pH, but may be due to inhibition of chloride ion influx into the hepatocyte.