Compromised Rat Testicular Antioxidant Defence System by Hypothyroidism before Puberty

Abstract

Altered thyroid function during early stages of development is known to affect adversely testicular growth, physiology, and antioxidant defence status at adulthood. The objective of the present study is to investigate the modulation of antioxidant defence status in neonatal persistent hypothyroid rats before their sexual maturation and also to identify the specific testicular cell populations vulnerable to degeneration during neonatal hypothyroidism in immature rats. Hypothyroidism was induced in neonates by feeding the lactating mother with 0.05% 6-n-propyl-2-thiouracil (PTU) through the drinking water. From the day of parturition till weaning (25 day postpartum), the pups received PTU through mother's milk (or) drinking water and then directly from drinking water containing PTU for the remaining period of experimentation. On the 31st day postpartum, the animals were sacrificed for the study. An altered antioxidant defence system marked by elevated SOD, CAT, and GR activities, with decreased GPx and GST activities were observed along with increased protein carbonylation, disturbed redox status in hypothyroid immature rat testis. This compromised testicular antioxidant status might have contributed to poor growth and development by affecting the spermatogenesis and steroidogenesis in rats before puberty as indicated by reduced germ cell number, complete absence of round spermatids, decreased seminiferous tubule diameter, and decreased testosterone level.

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

“…The current study revealed that hyperthyroid induced rats were characterised by a significant increase in testicular MDA and NO concentrations along with a decrease in SOD and CAT activities. Altered thyroid status has been shown to influence several oxidative stress and enzymatic antioxidant defence parameters in rat testis (Choudhury et al ., ; Zamoner et al ., ; Sahoo et al ., ; Sakai et al ., ; Sahoo & Roy, ). These results indicate that thyroid hormone treatment caused a high oxidative insult to the testis.…”

Effects of concomitant diabetes mellitus and hyperthyroidism on testicular and epididymal histoarchitecture and steroidogenesis in male animals

“…In books, it ranges from 10-80 ng/ml (Foster et al, 1983) to (4700±300) ng/ml (Delahunty and Beamer, 2007). However, the published data of research articles after 2010 show the total T4 level in control subjects as ranging from (13.0±3.92) ng/ml (Sahoo and Roy, 2012) to (39 280.0±11 970) ng/ml (Kim et al, 2012). Such enormous differences in data might be due to the use of different blood samples such as serum or plasma and diverse analytical kits such as RIA and enzyme-linked immunosorbent assay (ELISA).…”

Assessment of sperm morphology, chromatin integrity, and catSper genes expression in hypothyroid mice

“…ROS as by-products of tissue metabolism is normally scavenged by physiological antioxidants defense systems. In reproductive system, intrinsic antioxidants maintain the functional integrity of the cell membrane, spermatogenesis, sperm morphology, and motility [7,11,31,32]. There are increasing bodies of evidence that show hypothyroidism is associated with the high production of ROS in testis.…”

“…There are increasing bodies of evidence that show hypothyroidism is associated with the high production of ROS in testis. It is well known that high amounts of ROS negatively affect the quality of sperm DNA as well as sperm morphology and motility [11,22,31,32,38]. This study was conducted to determine the effect of hypothyroidism on the alteration of sperm chromatin, sperm morphology, and CatSper 1 and CatSper 2 genes expression.…”