Asian Science Citation Index is committed to provide an authoritative, trusted and significant information by the
coverage of the most important and influential journals
to meet the needs of the global scientific community.
Background: Thyroid hormone has profound effects on the cardiovascular
system and a regulatory effect on the rate of heme oxidation in the liver. Inducible
isoform of heme oxygenase (HO-1) protects the heart and vasculature
in pathological conditions. The present study aimed to identify the role of
heme oxygenase in cardiac changes in thyroidectomized rats. Materials and
Methods: Sixty male Wistar rats were equally divided into seven groups;
the first and second groups were the control and sham operated groups, respectively
while the 3rd and 4th groups were subjected to sham operation then treated with
hemin (G3) and KTZ (G4). The 5th group (G5)
was thyroidectomized group. The 6th and 7th groups were subjected to thyroidectomy
then treated with hemin (G5) and KTZ (G6), respectively.
Results: Hypothyroidism is documented by significant decrease in T3
accompanied with significant increase in serum TSH levels in thyroidectomized
rats. The results obtained revealed that oxidative stress due to hypothyroidism
has a detriment effect on cardiac tissue by depending on the result of cardiac
Protein Carbonyl Content (PCC) as a marker of tissue damage and a negative significant
correlation between cardiac PCC and serum Ferric Reducing Antioxidant Power
(FRAP) as marker of Total Antioxidant Capacity (TAC). The Inducible Nitric Oxide
Synthase (iNOS) activity in cardiac tissue showed significant decrease in thyroidectomized
rats and its value was increased significantly upon treatment with hemin or
ketoconazole (KTZ) as compared with sham operated rats. Treatment of thyroidectomized
rats with hemin improves the intensity of iNOS immunoreactive cells demonstrating
the recovery of some injury. Conclusion: There is a positive significant
correlation between hepatic HO and iNOS in cardiac tissue. The paradoxical effect
of both inducer and inhibitor of HO-1 on iNOS needs further studies.
Also, to address this inquiry we need further investigation on time and dose-dependent
effect of both inducer and inhibitor on cardiac tissue.
