RESUMO
Nervous system growth and differentiation are closely correlated with the presence of thyroid hormones in initial development stages. Hypothyroidism during the fetal and postnatal life results in an irreversible mental retardation syndrome. At the cellular level, T3 is known to act on neuronal, neuroretinogenesis, and glial lineages. In this study, we aimed to study the influence of hypothyroidism on retinal development in juvenile and adult rats and the effects of thyroid hormone supplementation on both periods of development. This study was conducted using 56 male albino rats. They were divided into three groups: group 1 [control group] included 24 animals, group 2 [juvenile group] included 16 animals whose mother received carbimazole [NeoMercazol] antithyroid drug at a dose of 0.02 mg/day/pregnant female during gestation and lactation, this group was further subdivided into subgroup 2a [hypothyroid juvenile animals] and subgroup 2b [thyroid hormone-supplemented juvenile animals], and group 3 [adult group] included 16 animals, this group was also further subdivided into subgroup 3a [hypothyroid adult animals] and subgroup 3b [thyroid hormone-supplemented adult animals]. At the end of the experiment, the animals were killed. Retinal specimens from all groups were processed for light and electron microscopic studies. Biochemical analysis was carried out to measure the serum levels of triiodothyronine, T4, growth hormone, and insulin growth factor-1. In addition, estimations of lipid peroxidation, catalase activity, and antioxidant enzymes were made. Statistical analysis was carried out to measure the retinal thickness. Light and electron microscopic studies showed that thyroid hormone deprivation altered the organization of the retina in juvenile and adult rats. These changes were apparent in the form of significant reduction in the retinal layer thickness. In addition, degenerative changes in some layers were observed. The group with thyroid hormone supplementation showed recovery of both structural changes and retinal thickness, this recovery was apparent in the juvenile group. Adult animals showed minimal recovery. Biochemical analysis of the serum of hypothyroid animals showed a significant increase in lipid peroxidation products and decease in the serum levels of antioxidants, growth hormone, and insulin growth factor-1, comparable with the controls. Administration of thyroid hormone significantly restored their levels especially in the juvenile group. Gestational and lactational hypothyroidism induced marked changes in the developing retina in juvenile and adult rats. These changes were mostly normalized by thyroid hormone administration especially in the juvenile group