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Toxicol Mech Methods. 2019 Feb;29(2):110-118. doi: 10.1080/15376516.2018.1528647. Epub 2018 Nov 28.

Excess iodine-induced lymphocytic impairment in adult rats.

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a Endocrinology and Reproductive Physiology Laboratory, Department of Physiology , University College of Science and Technology, University of Calcutta , Kolkata , India.
b Department of Physiology , Serampore College , Hooghly , India.


Altered lymphocytic activity and its subset ratio found responsible for initiating abnormal autoimmune responses in men and animals after excess iodine exposure. Study objective is to reveal excess iodine-induced impairment of peripheral blood lymphocytes (PBL), its functional status, antioxidant balance, DNA damage, proliferation assay, and serum cytokine levels (IL6 and TNF α)in adult male rats to understand the onset of autoimmune alterations if any indirectly that is unexplored. Experimental animals were grouped depending on doses of iodine(KI) treatment with moderately excess-7 mg/kg bw (100EI) and excessively excess-35 mg/kg bw (500EI)for 30 days to analyze IL6 and TNF α, hematological indices, oxidative stress, lymphocytic DNA damage, and proliferation status. Significant impairment in superoxide dismutase, catalase, GPx activities including elevated NO, LPO in lymphocytes of treated group, with increased IL6 and TNF α level, lymphocyte proliferation and DNA damage depending on doses of iodine. Therefore, excess iodine consumption leads to lymphocytic impairment that may be the potential cause of autoimmune thyroid diseases in long run. Highlights Excess iodine triggers the oxidative stress in lymphocytes. Excess iodine promotes the activity of pro-inflammatory cytokines. Excess iodine causes impairment of functional status of lymphocytes leading to immune-cytotoxicity. Excess iodine exacerbates the autoimmunity.


DNA damage; Excess iodine; cytokine; oxidative stress; peripheral blood lymphocytes

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