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. However, the magnitude and nature of changes in the above biochemical parameters in response to T3 treatment were noticed to be different between mitochondrial and post-mitochondrial fractions. This was accompanied with elevated levels of lipid hydroperoxide and ascorbic acid in the crude homogenate of testis. The level of hydrogen peroxide in the post-mitochondrial fractions of testes did not change on first day, decreased on 3rd day and increased on 5th day of the hormone treatment when compared to respective controls. Nevertheless, its content in mitochondria was significantly elevated in response to all the three durations of the hormone treatment having the highest induction on 3rd day. The changes observed in the levels of GSH and GSSG and its metabolizing enzymes in response to T3 treatment reflect an alteration in the redox state of testis, which may be a causative factor for the impairment of testicular physiology as a consequence of oxidative stress.

Experimental hyperthyroidism-induced oxidative stress and impairment of antioxidant defence system in rat testis.

Short-term hyperthyroidism, induced by daily administration of T3 (20 microg/100g body weight) for one, three, and five days consecutively, modulates oxidative stress and antioxidant defence parameters in mitochondrial and postmitochondrial fractions of testis in adult rats. Alteration in antioxidant defences along with oxidative stress parameters in testis by thyroid hormone was found to be associated with a decline in the number of sperms and disturbances in histoarchitecture of seminiferous tubules in the testes; the results indicated that induced hyperthyroid state altered testicular physiology by influencing antioxidant defence system of testes.