Metabolic Response To Subacute And Subchronic Iron Overload In A Rat Model.
One of the common causes of iron overload is excessive iron intake in cases of iron-poor anemia, where
iron saccharate complex (ISC) is routinely used to optimize erythropoiesis. However, non-standardized
ISC administration could entail the risk of iron overload. To induce iron overload, Wistar rats were intraperitoneally
injected with subacute (0.2 mg kg–1) and subchronic (0.1 mg kg–1) overdoses of ISC for 2
and 4 weeks, respectively. Iron status was displayed by an increase in transferrin saturation (up to 332%)
and serum and liver iron burden (up to 19.3 μmol L–1 and 13.2 μmol g–1 wet tissue, respectively) together
with a drop in total and unsaturated iron binding capacities “TIBC, UIBC” as surrogate markers of
transferrin activity. Iron-induced leukocytosis (up to 140%), along with the decline in serum transferrin
markers (up to 43%), respectively, mark positive and negative acute phase reactions. Chemical stress was
demonstrated by a significant rise (p > 0.05) in indices of the hemogram (erythrocytes, hemoglobin,
hematocrit, leukocytes) and stress metabolites [corticosterone (CORT) and lactate]. Yet, potential causes
of the unexpected decline in serum activities of ALT, AST and LDH (p > 0.05) might include decreased
hepatocellular enzyme production and/or inhibition or reduction of the enzyme activities. The current
findings highlight the toxic role of elevated serum and liver iron in initiating erythropoiesis and acute
phase reactions, modifying iron status and animal organ function, changing energy metabolism and bringing
about accelerated glycolysis and impaired lactate clearance supposedly by decreasing anaerobic
threshold and causing premature entering to the anaerobic system.
Keywords: Iron overload – iron status – acute phase reactions – organ function enzymes – chemical stress
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