Increased germ cell apoptosis during testicular development and maturation by experimentally induced transient and persistent hypothyroidism

Oxidative stress is known to be one of the major factors to induce germ cell apoptosis. In our earlier research, it was reported that neonatal persistent and transient hypothyroidism cause prevalence of oxidative stress marked by elevated lipid peroxide levels, protein carbonyl contents with decreased antioxidant enzyme levels. Alteration in germ cell population was also marked in persistent and transient hypothyroid rat testis. In the present investigation, germ cell apoptosis were assessed by TUNEL in testicular sections and was found that significant apoptosis occurred in germ cells in the experimentally induced persistent and transient hypothyroid rats by 6-n-propyl-2-thiouracil (PTU). The number of TUNEL-positive cells (bright green spots) increases dramatically in case of the PTU-treated rat testis both for transient and persistent hypothyroidism in comparison to the controls. Nuclei were stained with DAPI and emitted blue fluorescence when excited with 405nm blue-diode laser. This also establishes the fact that hypothyroidism caused by PTU is linked with high testicular germ cell death rates. Such type of altered testicular physiology by hypothyroidism is reflected in adulthood with hampered fertility as evidenced by reduced total viable germ cells and sperm counts.