Background: The pathophysiological mechanisms involved in hypothyroid retinal
damage are still debate. Materials and methods: To study these mechanisms, ninety
six pubs of albino rats were equally divided into three groups, control, hypothyroid
model and thyroid supplement. Each group was separated into two juvenile and adult
subgroups that were sacrificed at day 20 and 60 postnatally respectively. Pubs in
hypothyroid group their mother received 0.05mg carbimazole/day/pregnant female
orally during gestation and 20 days of lactation in juvenile subgroup while adult
subgroup received the hypothyroid agent until day 60 postnatally. Thyroid
supplement group received antithyroid agent then treated with L-thyroxine (TH)
orally (10 ug/ kg body weight) for one month. Results: A significant reduction in body
weight, temperature, heart rate, levels of T3, T4, GH, IGF-1, and antioxidant enzymes
while increased systolic pressure and LP products were evident in hypothyroid
subgroups associated with decreased in the thickness and degeneration of retinal
layers. Thyroid supplementation group showed a partial normalization of the
measured mediators accompanied with recovery of structural changes especially in
juvenile subgroup. Conclusions: Thyroid H has a vital role in normal retinal growth.
Also, GH, IGF-1, oxidative stress are significant mediators of retinal degeneration.