The impact of insulin-like growth factor-1, growth hormone, and oxidative stress in the experimental model of juvenile and adult hypothyroid retinal degeneration

Abstract

Background: The pathophysiological mechanisms involved in hypothyroid retinal damage are still being debated. Materials and methods: Ninety-six pups of albino rats were equally divided into control, hypothyroid model and thyroid supplement groups. Each group was separated into juvenile and adult subgroups that were sacrificed at day 20 and 60 postnatally, respectively. Pups in the hypothyroid group were born to mothers who received 0.05 mg Carbimazole/day/pregnant female orally during gestation and at 20 days of lactation in juvenile subgroup. The adult subgroup received the hypothyroid agent until day 60 postnatally. The thyroid supplement group received antithyroid agent, then were treated with L-thyroxine orally (10 ug/kg body weight) for one month. Results: A significant reduction in body weight, temperature, heart rate, levels of Triiodothyronine (T3), Tetra-iodothyronine T4), growth hormone (GH) and Insulin-like growth factor (1GF-1), and antioxidant enzymes and an increase in systolic pressure and lipid peroxidation (LP) products were evident in hypothyroid subgroups associated with a decreasing thickness and degeneration of retina l layers. Thyroid supplementation group showed a partial normalization of the measured mediators accompanied by recovery of structural changes especially in the juvenile subgroup. Conclusions: Thyroid hormone has a vital role in normal retinal growth. GH, IGF-1 and oxidative stress are also significant mediators of retinal degeneration.