| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2801184 | General and Comparative Endocrinology | 2010 | 9 Pages |
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. At the end of the treatment period, a subset of the hypothyroid rats was treated with T3 (20 μg/100 g body weight/day for 3 days). Mitochondria were isolated from euthyroid, hypothyroid and hypothyroid + T3-treated rat testes, and sub-fractionated into sub-mitochondrial particles and matrix fractions. Mitochondrial respiration, oxidative stress indices and antioxidant defenses were assayed. The results were correlated with daily testicular sperm production and epididymal sperm viability. Increased pro-oxidant level and reduced antioxidant capacity rendered the hypothyroid mitochondria susceptible to oxidative injury. The extent of damage was more evident in the membrane fraction. This was reflected in higher degree of oxidative damages inflicted upon membrane lipids and proteins. While membrane proteins were more susceptible to carbonylation, thiol residue damage was evident in matrix fraction. Reduced levels of glutathione and ascorbate further weakened the antioxidant defenses and impaired testicular function. Hypothyroid condition disturbed intra-mitochondrial thiol redox status leading to testicular dysfunction. Hypothyroidism-induced oxidative stress condition could not be reversed with T3 treatment.
Research highlights► Mitochondrial thiol redox status in testis of hypothyroid rat is fundamental during spermatogenetic process such as apoptosis, sperm function and sperm quality. ► A compromised antioxidant defense system during hypothyroidism might be the key factor in contributing towards oxidative stress in testicular mitochondria, reflected in higher levels of oxidatively damaged membrane lipids and proteins ultimately leading to tissue injury and dysfunction which cannot be alleviated by extraneous thyroid hormone treatment.
