Experimentally induced hyperthyroidism influences oxidant and antioxidant status and impairs male gonadal functions in adult rats

Abstract

The objective of the present experiment was to study the effect of hyperthyroidism on male gonadal functions and oxidant/antioxidant biomarkers in testis of adult rats. Induction of hyperthyroidism by L-thyroxine (L-T4, 300 μg kg(-1) body weight) treatment once daily for 3 or 8 weeks caused a decrease in body weight gain as well as in absolute genital sex organs weight. The epididymal sperm counts and their motility were significantly decreased in a time-dependent manner following L-T4 treatment. Significant decline in serum levels of luteinising hormone, follicle stimulating hormone and testosterone along with significant increase in serum estradiol level was observed in hyperthyroid rats compared with euthyroid ones. Significant increase in malondialdehyde and nitric oxide concentration associated with significant decrease in superoxide dismutase and catalase activity was also noticed following hyperthyroidism induction. Both reduced glutathione content and glutathione peroxidase activity were increased in hyperthyroid rats compared with control rats. Marked histopathological alterations were observed in testicular section of hyperthyroid rats. These results provide evidence that hypermetabolic state induced by excess level of thyroid hormones may be a causative factor for the impairment of testicular physiology as a consequence of oxidative stress.

The role of fish oil in attenuating cardiac oxidative stress, inflammation and fibrosis in rat model of thyrotoxicosis

“…Patients with hyperthyroidism usually notice a loss in their body weights, which is not consistent with observations in animal models of hyperthyroidism. Previous studies have observed a reduction [18], an increase [19, 20] or no change in body weight in hyperthyroid animals [21].…”

Therapeutic Potential of Date Palm Pollen for Testicular Dysfunction Induced by Thyroid Disorders in Male Rats

“…The elevated MDA level may be partly attributed to the high content of polyunsaturated fatty acids in the male germ cells membranes [ 13 ], thus rendering them particularly prone to lipid peroxidation. NO may cause spermatozoal dysfunction and infertility by inhibiting testicular T secretion, suppressing antioxidant enzyme activities [ 60 ] and generating peroxynitrite that is a more powerful oxidant [ 6 ]. GSH plays a pivotal role in the proliferation and differentiation of spermatogenic cells [ 50 ].…”

“…Group III: (hyperthyroid group), animals received L-T4 (300μg kg −1 , i.p.) dissolved in alkaline saline [ 6 ]. Group IV: (L-T4+DPP group), animals received DPP extract (150 mg kg −1 , p.o.)…”

“…The mechanism underlying testicular dysfunction that results from thyroid disorders is still vague. However, observations from previous reports suggest oxidative stress, lipid peroxidation [ 6 , 8 ] and cellular apoptosis [ 9 , 10 ] as major culprits. THs modulate oxidative stress as they profoundly promote mitochondrial oxygen consumption [ 11 ].…”

Evaluation of Arginine-Nitric Oxide Pathway in Patients with Hyperthyroidism

“…Our main objective in this study was to investigate the arginine-NO pathway by measuring plasma total nitrite, arginase and Mn in hyperthyroidism. Although there are some studies dealing with NO levels, NOS activity and plasma concentration of asymmetric dimethylarginine, an endogenous inhibitor of NOS in the hyperthyroidism [1,[15][16][17][18][19], to our knowledge, this is the first report which has investigated arginase activity and Mn levels together with NO levels in hyperthyroidism.…”