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

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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.

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Acknowledgments

The authors are thankful to Prof. T. G. Srivastava, National Institute for Health and Family Welfare (NIHFW)—Govt. of India, New Delhi, India for his generous help in providing corticosterone kits. The authors are grateful to Prof. Arun K. Ray, Fellow, Alexander von Humboldt Foundation, Germany and Ex-Senior Professor and Emeritus Scientist (CSIR), Division of Molecular Medicine, Bose Institute, Calcutta for the review and language improvement of the manuscript.

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Correspondence to Amar K. Chandra.

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The entire work was financially supported by Major Research Project under University Grants Commission (UGC), New Delhi, Govt. of India [Sanction No.41-84/2012(SR) dated 11th July 2012].

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The authors declared no potential conflicts of interest with respect to the authorship, research, or publication of this article.

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Chakraborty, A., Mandal, J., Mondal, C. et al. Effect of Excess Iodine on Oxidative Stress Markers, Steroidogenic—Enzyme Activities, Testicular Morphology, and Functions in Adult Male Rats. Biol Trace Elem Res 172, 380–394 (2016). https://doi.org/10.1007/s12011-015-0581-3

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