Iodine excess induces hepatic, renal and pancreatic injury in female mice as determined by attenuated total reflection Fourier‐transform infrared spectrometry

Abstract

Limited knowledge of the long‐term effects of excessive iodine (EI) intake on biomolecular signatures in the liver/pancreas/kidney prompted this study. Herein, following 6 months of exposure in mice to 300, 600, 1200 or 2400 μg/L iodine, the biochemical signature of alterations to the liver/pancreas/kidney was profiled using attenuated total reflection Fourier‐transform infrared (ATR‐FTIR) spectroscopy coupled with principal component analysis‐linear discriminant analysis (PCA‐LDA). Our research showed that serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN), serum creatinine (Scr), insulin, blood glucose levels and homeostasis model assessment for insulin resistance (HOMA‐IR) index in the 1200 and 2400 μg/L iodine‐treated groups were significantly increased compared with those in the control group. Moreover, histological analysis showed that the liver/kidney/pancreas tissues of mice exposed to EI treatment displayed substantial morphological abnormalities, such as a loss of hepatic architecture, glomerular cell vacuolation and pancreatic neutrophilic infiltration. Notably, EI treatment caused distinct biochemical signature segregation between EI‐exposed versus the control liver/pancreas/kidney. The main biochemical alterations between EI‐exposed and control groups were observed for protein phosphorylation, protein secondary structures and lipids. The ratios of amide I‐to‐amide II (1674 cm−1/1570 cm−1), α‐helix‐to‐β‐sheet (1657 cm−1/1635 cm−1), glycogen‐to‐phosphate (1030 cm−1/1086 cm−1) and the peptide aggregation (1 630 cm−1/1650 cm−1) level of EI‐treated groups significantly differed from the control group. Our study demonstrated that EI induced hepatic, renal and pancreatic injury by disturbing the structure, metabolism and function of the cell membrane. This finding provides the new method and implication for human health assessment regarding long‐term EI intake.

Excess Iodine Consumption Induces Oxidative Stress and Pancreatic Damage Independently of Chemical Form in Male Wistar Rats: Participation of PPAR-γ and C/EBP-β

“…Furthermore, the deficiency or excessive consumption of iodine has been associated with the risk of presenting insulin resistance [9]. Similarly, in our study, excess iodate caused high insulin levels and a decrease in IR, which correlates with other studies that show that low levels insulin levels and low levels of IR are associated with pancreatic fibrosis, insulin resistance, and alterations in insulin gene regulation [3,4,[7][8][9][10].…”

“…In murine models, the consumption of 3.5 mg of potassium iodide (KI)/100 g body weight, which is 500 times the physiological daily dosage of iodide, for 60 days causes a hyperglycemic and hypercholesteremic status and severe destruction of the pancreatic structure [9]. In mice, the excessive consumption of 1200 or 2400 µg/L of iodide alters insulin, blood glucose levels, and the homeostasis model assessment for insulin resistance (HOMA-IR) index after 6 months [10]. In contrast, low iodine and 25(OH)D concentrations have been associated with complications in diabetic patients [8], and excessive consumption of iodine is associated with pancreatic damage in epidemiological studies [3][4][5][6][7]11].…”

“…Both are public health strategies for the prevention of pathologies associated with iodine deficiency. However, the lack of monitoring programs or regulation of its consumption has led to reported cases of excess iodine consumption in the population, and this could be a risk factor for the development of diabetes, hypothyroidism, and hypertriglyceridemia [3][4][5][6][7][8][9][10][11]. Studies done in models in vitro and in vivo have shown that I2 has antioxidant properties (in low doses) and acts as a free radical scavenger (in high doses); it also acts as an oxidant and can have cytotoxic effects by inducing apoptosis at high concentrations [15][16][17].…”

Investigating the impact of elevated urinary trace elements on non-alcoholic fatty liver disease using vibration-controlled transient elastography

“…Excessive iodine intake is associated with thyroid disease; however, research on the association between urinary iodine and NAFLD is lacking. However, some studies have suggested that excessive iodine consumption may disrupt the structure, metabolism, and function of cell membranes, potentially leading to liver, kidney, and pancreatic damage ( 32 ). This disruption could explain the non-linear dose-dependent relationship observed here between I levels and NAFLD.…”

Associations between urinary iodine concentration and the prevalence of metabolic disorders: a cross-sectional study

“…Second, chronic inflammatory states and oxidative stress appear to be central to the pathophysiology of MetS. Excess iodine puts cells in a state of high oxidative stress, which predisposes them to organ damage and is detrimental to disease recovery ( 59 ). Moreover, iodine functions as both a pro-oxidant and an antioxidant ( 60 , 61 ), and it can balance oxidative homeostasis at the physiological and molecular levels of the cell ( 62 ).…”