Alterations in the indexes of apoptosis and necrosis induced by galactosamine in the liver of Wistar rats treated with fructose-1,6-bisphosphate.

Galactosamine (GalN) is a hepatotoxic agent, which under determined situations provokes metabolic and energetic depletion as well as alterations in permeability, leading to cellular death. At the same time, it is known that fructose-1,6-bisphosphate (FBP) helps maintain cell energy levels and protects the cell against this lesive agent. We submitted two groups of male Wistar rats to the harmful intraperitoneal doses of GalN (400 mg/kg), one of which simultaneously received FBP (2 g/kg). Techniques were used in the analysis of the cellular components, adenosine triphosphate (ATP) and hepatic calcium and a close relationship between the types of cellular death unchained by these agents was established. The liver of the rats treated with GalN showed energy depletion and concomitant increase calcium in the hepatic tissue, which provoked higher levels of necrosis leading to reduce cellular viability. On the other hand, the group which had received GalN+FBP maintained calcium levels close to the control values and the energy rate did not decrease as much as in the GalN only group, but recovered the control values, within a period of 48 h. At the same time, the degree of apoptosis was greater than in the GalN group. This fact suggests that the FBP maintains cellular levels of ATP, thus protecting the cell from the toxic action of GalN, reducing the percentage of dead cells and causing an alteration in the pattern of the cell death, whereby there is an increase in the rate of apoptosis and a decrease in that of necrosis.