Effect of Excess Iodine on Oxidative Stress Markers, Steroidogenic—Enzyme Activities, Testicular Morphology, and Functions in Adult Male Rats

Abstract

Improper iodine intake is a major concern in public health. Chronic intake of low iodine affects gonadal functions of man and animals; however, such effects of excess iodine in male reproduction, specially on testicular morphology, testicular steroidogenic enzyme activities, sperm morphology, sperm viability, and sperm count including male hormonal profiles in reference to iodine status and thyroid hormone profiles are yet to be explored. With this background, adult male rats of 120 ± 10 gm Bw of 90 ± 5 days were divided broadly in two groups depending on the duration of the treatment for 30 and 60 days, respectively. Both the groups consisted of control animals. Excess iodine (100EI), i.e., 100 times more than its recommended level but within its tolerable ranges, was administered through gavage regularly to the first group of experimental animals for 30 and 60 days, respectively, and excessive iodine (500EI), i.e., 500 times more than its recommended level and above tolerable range in the same way and for the same durations, was administered to the other group of experimental animals. Overall results revealed that regular consumption of iodine in excess impairs reproductive functions in adult male rats depending on the dose and duration of its exposure through different mechanisms. Excess iodine accumulates in the testis which results in generation of reactive oxygen species (ROS) as evidenced by higher lipid peroxidation level as well as an imbalance in the pro-/antioxidant status inhibiting the activity of ∆(5) 3β- hydroxysteroid dehydrogenase (HSD) and 17β-HSD resulting to reduced synthesis of testosterone that causes structural and functional changes of the testis. Secondly, persistent generation of ROS in testis as a result of prolonged excess iodine exposure affects hypothalamo-pituitary-adrenal axis that stimulates synthesis and secretion of corticosterone which inhibits LH release that downregulates testosterone synthesis causing further testicular disruption. Thirdly, excess iodine when administered above its tolerable ranges for prolonged duration acts on thyroid itself developing a state of biochemical hypothyroidism (as evident by low T3) which further potentiate the disrupting effect of excess iodine on male gonads by reducing circulating testosterone level.

New insights into morphological, stereological and functional studies of the adrenal gland under exposure to the potent goitrogen thiourea

“…In this investigation the adrenal gland weight was increased following thiourea administration. It was reported previously that such a condition can arise as a result of the stress response, yet it may also occur due to deficient glucocorticoid feedback regulation of ACTH due to toxicity to the adrenal cortex (Chakraborty et al ., 2016). Thus excess thiourea as used in this study might be responsible for producing oxidative stress in the adrenal resulting in the cellular and subcellular alterations.…”

“…It is a gradual process in which free radicals steal electrons from the lipid in the cell membrane. Malonaldehyde (MDA) levels thus formed indicate the intoxication and generation of oxidative stress in this organ, considered an endpoint of oxidative stress formation (Chakraborty et al ., 2016). This clearly suggests that thiourea exposure caused elevation of LPO level or in other words generation of oxidative stress resulting in adrenal gland weight and subsequent changes in the activity of the gland by feedback mechanism to ACTH.…”

“…Examples include oxygen ions and peroxides. Cumulative effects of ROS may result in significant damage to cell structures and have been implicated as an underlying agent in various pathological conditions (Chakraborty et al ., 2016). …”

Genome‐Wide Transcriptional Analysis Reveals the Protection against Hypoxia‐Induced Oxidative Injury in the Intestine of Tibetans via the Inhibition of GRB2/EGFR/PTPN11 Pathways

“…In the GO, the upregulated DE genes were involved in the reactive oxygen species activity, oxygen ions and peroxides, lipid peroxidation and so on; the downregulated DE genes were involved in the decrease of immunological ability. All the changes can be caused by oxidative stress, such as cancer suppressor [23], cell normal functions [24], special responses for pathogens [25], maximal actions, and antigen presentation [26] (Figure 6). Pathway analysis revealed that, in intestinal mucosa tissues of participants from high altitude, many pathway genes had aberrant expression and may be also related with oxidative stress, especially in inflammatory bowel diseases [27, 28], myeloperoxidase [29], ROS production [10], apoptotic cell death [30], tissue damage [31], interleukin-1 [32], oxidative modification [33], cystic fibrosis [34], natural killer cells activity [35], lymphocytes [36], fibrinolysis [37] and so on (Figure 7).…”

Influence of iodine in excess on seminiferous tubular structure and epididymal sperm character in male rats

“…Studies on different assortments of sperm analysis are now a recognized methodology in the appraisal of animal semen destined to breeding. Excess iodine induced alterations on male and female reproductive functions have been reported by our group recently; however, its effect on sperm physiology are yet to be explored in details. Further, sperm chromatin structure that interrupt sperm fertility, apoptosis in mature spermatozoa etc under various incremental doses of relatively high iodine and for different durations have not been evaluated earlier.…”