BIOCHEMICAL INTERPRETATION OF ALTERATIONS IN IRON HOMEOSTASIS AND LIVER PROTEIN-SYNTHETIC FUNCTION DURING POSTRESECTION REGENERATION FOLLOWING ACETAMINOPHEN-INDUCED LIVER INJURY
DOI:
https://doi.org/10.31861/biosystems2026.01.049Keywords:
iron, total iron-binding capacity, transferrin, total protein, albumin, acetaminophen, partial hepatectomy, liver regenerationAbstract
The present study investigated alterations in iron homeostasis and liver protein-synthesizing function during different stages of postresection regeneration following acetaminophen-induced liver injury.
Acute toxic liver injury was induced by administering acetaminophen at a dose of 1250 mg/kg body weight for two consecutive days prior to partial hepatectomy. A model of postresection liver regeneration was established by performing a 70% partial hepatectomy. The animals were divided into two groups: control rats subjected to partial hepatectomy and rats subjected to partial hepatectomy following acetaminophen-induced liver injury. Serum iron concentration, total iron-binding capacity (TIBC), transferrin saturation, total protein, and albumin levels were determined at 24, 48, 72, and 168 hours after surgery.
In control animals, the early stages of liver regeneration (24–48 h) were characterized by increased serum iron concentration and TIBC, accompanied by a transient decrease in transferrin saturation at 48 h. These changes occurred simultaneously with a temporary reduction in total protein and albumin concentrations, followed by normalization of the studied parameters at later stages of recovery.
In contrast, rats with acetaminophen-induced liver injury exhibited pronounced phase-dependent disturbances in iron homeostasis after partial hepatectomy. At 24 h after surgery, serum iron concentration and TIBC decreased markedly, whereas at 48 h a substantial increase in serum iron levels and transferrin saturation was observed against a background of reduced iron-binding capacity. During the later stages of regeneration (72–168 h), the investigated parameters showed partial recovery; however, they did not return to physiological levels. Moreover, persistent hypoproteinemia and hypoalbuminemia were detected throughout the entire observation period, indicating incomplete restoration of the liver’s protein-synthesizing function.
The findings demonstrate that acetaminophen-induced liver injury significantly impairs the course of postresection liver regeneration and is associated with disturbances in iron transport, redistribution, and utilization. The sustained suppression of protein-synthesizing function further suggests limited compensatory and regenerative capacity of the liver under conditions of prior toxic injury. These results contribute to a better understanding of the biochemical mechanisms underlying liver regeneration and may provide a basis for developing novel approaches aimed at correcting regenerative dysfunction following toxic liver damage.
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