Experimental Hypothyroidism Inhibits δ-Aminolevulinate Dehydratase Activity in Neonatal Rat Blood and Liver

Abstract

The aim of this study was to investigate the potential relationship between hypothyroidism and δ-aminolevulinate dehydratase (δ-ALA-D) activity in rat blood and liver. Experimental hypothyroidism was induced in weanling rats by exposing their mothers to propylthiouracil (PTU) diluted in tap water (0.05% w/ v), ad libitum, during the lactational period (PTU group). Control (euthyroid) group included weanling rats whose mothers received just tap water, ad libitum, during the lactational period. Reverted-hypothyroid group (PTU + 3,3′,5-triiodo-L-thyronine [T3]) included weanling rats whose mothers were exposed to PTU similarly to those in the hypothyroid group, but pups received daily subcutaneous injections of T3(20 μg/kg, from Postnatal Days 2–20). After the treatment, serum T3levels were drastically decreased (around 70%) in the PTU group, and this phenomenon was almost reverted by exogenous T3. PTU decreased blood δ-ALA-D activity by 75%, and T3treatment prevented such phenomena. Erythrocytes and hemoglobin levels were increased by 10% in PTU-treated animals and higher increments (around 25%) were observed in these parameters when exogenous T3was coadministered. Dithiothreitol did not change blood δ-ALA-D activity of PTU-exposed animals when present in the reaction medium, suggesting no involvement of the enzyme’s essential thiol groups in PTU-induced δ-ALA-D inhibition. PTU did not affect blood δ-ALA-D activity in vitro. These results are the first to show a correlation between hypothyroidism and decreased δ-ALA-D activity and point to this enzyme as a potential molecule involved with hypothyroidism-related hematological changes.