T3 fails to restore mitochondrial thiol redox status altered by experimental hypothyroidism in rat testis.

Oxidative stress impaired sperm function might lead to infertility. The objective of this study was to evaluate the effects of altered thyroid hormone levels on regulation of mitochondrial glutathione redox status and its dependent antioxidant defense system in adult rat testis and their correlation with testicular function. Adult male Wistar rats were rendered hypothyroid by administration of 6-n-propyl-2-thiouracil in drinking water for six weeks.

Thiol redox status critically influences mitochondrial response to thyroid hormone-induced hepatic oxidative injury: A temporal analysis.

Liver is a major target organ for thyroid hormone. The objective of the present study was to investigate temporal regulation of mitochondrial glutathione and protein-bound thiol redox status in hyperthyroid liver. Mitochondria were isolated from control and hyperthyroid rat liver tissues at different time intervals, i.

Effect of T3 treatment on glutathione redox pool and its metabolizing enzymes in mitochondrial and post-mitochondrial fractions of adult rat testes.

T3 (3,3', 5-triiodo-L-thyronine; 20 microg/100 g body weight/day in 0.01 N NaOH, i.p for 1, 3 and 5 days) treatment modulated reduced (GSH) and oxidized (GSSG) glutathione contents along with the activities of its metabolizing enzymes (such as glutathione peroxidase, glutathione reductase and glutathione S-transferase) in the testis of Wistar rats.