Folic acid alleviates oxidative stress and hyperhomocysteinemia involved in testicular dysfunction of hypothyroid rats.

Although there is general agreement that thyroid hormone is an important hormonal regulator of testis physiology during development period, its role in the post-pubertal and adult testes is still controversial. Furthermore, most experimental studies to date have focused on thyroid hormone effects on the developing testes and only limited data are available on its role in spermatogenesis. This study evaluated some biochemical alterations in post-pubertal hypothyroidism and its impact on testicular function. Additionally, the ameliorating role of folic acid supplementation was investigated. Fifty male albino rats were randomly divided into five groups (group I, control; group II, folic acid; group III, 0.05% propylthiouracil-induced hypothyroid rats; group IV, co-treatment; group V, post-treatment). Plasma total homocysteine, total NO metabolites, malondialdehyde and GSSG/GSH ratio quantified by HPLC significantly (P<0.05) increased in hypothyroid rats as compared to controls. These biochemical alterations at least in part disrupted spermatogenesis in these experimental models. Folic acid supplemented after restoration of the euthyroid state (group V) presented better amelioration to spermatogenesis over its concurrent supplementation (group IV). This postulates an indirect negative impact of post-pubertal hypothyroidism on testicular function through development of these alterations. This is plus the observed role of folic acid supplementation in enhancing spermatogenesis, boosting sperm concentration and building up the antioxidant status against the oxidants in the present study. If confirmed in human beings, our results could propose that folic acid can be used as an adjuvant therapy in hypothyroidism disorders with thyroxin replacement therapy.