We see claims of every sort in relation to iodine intake. When people take high doses, they often claim to feel well on it and hope they are protecting themselves from some cancers. I hope that they both do feel well and are protecting themselves. This paper, however, suggests that the impact might be rather more complex, profound and with a level of feedback which enhances the impact - and not in a good way.
Biol Trace Elem Res. 2015 Dec 23. [Epub ahead of print]
Effect of Excess Iodine on Oxidative Stress Markers, Steroidogenic-Enzyme Activities, Testicular Morphology, and Functions in Adult Male Rats.
Chakraborty A1, Mandal J1, Mondal C1, Sinha S1, Chandra AK2.
Author information
1Endocrinology & Reproductive Physiology Laboratory, Department of Physiology, University of Calcutta, University College of Science and Technology, 92, Acharya Prafulla Chandra Road, Kolkata, 700 009, West Bengal, India.
2Endocrinology & Reproductive Physiology Laboratory, Department of Physiology, University of Calcutta, University College of Science and Technology, 92, Acharya Prafulla Chandra Road, Kolkata, 700 009, West Bengal, India. physiology.ac@gmail.com.
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.
KEYWORDS:
Corticosterone; Excessive iodine; Pro-/antioxidant status; Reactive oxygen species; Steroidogenic enzymes; Testosterone
PMID: 26701334 [PubMed - as supplied by publisher]