Corresponding author: Seong-Su Moon http://orcid.org/0000-0001-8881-3927 Department of Internal Medicine, Dongguk University College of Medicine, 123 Dongdae-ro, Gyeongju 38066, Korea E-mail: drmoonss@hanmail.net Recently, there has been increasing concern with regard to health problems due to exposure to environmental pollutants, such as substances found in our food and consumer or industrial products that interfere with our body’s hormone synthesis, secretion, activity, and metabolism [1,2]. Heavy metals are considered as an endocrine-disrupting chemical that can interfere with the normal endocrine system and metabolism of humans. Mercury, the most dangerous of all heavy metals [3], is widely dispersed in the environment including air, soil, dust, water, and the human food chain [4]. Mercury exists in three basic forms: elemental, inorganic, and organic [5-7]. Inorganic mercury is the toxic species found in human tissue after conversion from other forms. Organic forms of mercury from fish and elemental mercury from dental amalgams are the major environmental sources of exposure to mercury [8]. In addition, mercury was also found in cosmetic powders, plastic toys, sea mammals, and thimerosal vaccines. The Environmental Protection Agency in United States reported the safe daily mercury intake to be less than 0.1 μg/kg/day [9]. One dental amalgam filling is estimated to release about 3 to 17 μg of mercury vapor daily [9]. Several kinds of vaccine contain thimerosol as a preservative, which is suspected to be another major source of mercury [6,7,9]. The long-lived large predatory fish such as swordfish, king mackerel, and tuna, which are favorite fish dishes of Koreans, contain about 0.5 to 1 μg of methyl mercury per gram [6,7,9]. Therefore, members of the general population, not only humans in contaminated area, are exposed daily to potential environmental hazards of mercury. Mercury has no known physiologic role in human metabolism, but mercury induces mitochondrial dysfunction and oxidative stress [10,11]. It has been suggested to cause insulin resistance which is one of the underlying pathogenetic mechanism of metabolic syndrome, a constellation of cardiovascular risk factors, including central obesity, dysglycemia, dyslipidemia, and hypertension. Mercury reduces antioxidant defense by binding to sulfhydryl groups of proteins, resulting in inactivation of numerous enzymatic reactions and amino acids and depletion of N-acetyl cysteine, α lipoic acid, and glutathione, which provide about 10% to 50% of the plasma protein antioxidant capacity [12]. Since mercury has a long half-life and the human body has no mechanisms to actively excrete mercury [12], mercury accumulates in human body during lifetime. So far, several in vivo, in vitro, and epidemiologic studies have investigated the metabolic effects of mercury on the risk of obesity, diabetes, and cardiovascular disease. Prevalence of hypertension and cardiovascular diseases, such as myocardial infarction and coronary heart disease, were increased as a consequence of mercury toxicity [13]. Blood mercury concentration showed an association with waist-hip ratio in Korean men [12]. Body mass index (BMI) and waist circumference (WC), indirect measures of adiposity, has been used to estimate the association between blood mercury concentration and obesity, but the findings have been inconsistent. Park et al. [14] showed that the blood mercury concentration was significantly associated with visceral adipose tissue (VAT) as measured by dualenergy X-ray absorptiometry (DXA). Because DXA VAT is considered to be an accurate, direct measure of adiposity, the finding could be more evident than previous studies. Besides Editorial Obesity and Metabolic Syndrome
[1]
K. He,et al.
Association between Blood Mercury Level and Visceral Adiposity in Adults
,
2016,
Diabetes & metabolism journal.
[2]
S. Moon.
Association of lead, mercury and cadmium with diabetes in the Korean population: The Korea National Health and Nutrition Examination Survey (KNHANES) 2009–2010
,
2013,
Diabetic medicine : a journal of the British Diabetic Association.
[3]
Moon Ss.
Association of Lead, Mercury and Cadmium With Diabetes in the Korean Population: The Korea National Health and Nutrition Examination Survey (KNHANES) 2009-2010
,
2013
.
[4]
Bruce Blumberg,et al.
Endocrine disrupting chemicals and disease susceptibility
,
2011,
The Journal of Steroid Biochemistry and Molecular Biology.
[5]
Mark C Houston,et al.
Role of Mercury Toxicity in Hypertension, Cardiovascular Disease, and Stroke
,
2011,
Journal of clinical hypertension.
[6]
Seung-Do Yu,et al.
Relationship Between Blood Mercury Concentration and Waist-to-Hip Ratio in Elderly Korean Individuals Living in Coastal Areas
,
2010,
Journal of preventive medicine and public health = Yebang Uihakhoe chi.
[7]
L. Giudice,et al.
Endocrine-disrupting chemicals: an Endocrine Society scientific statement.
,
2009,
Endocrine reviews.
[8]
A. Yassi,et al.
Lead and mercury exposures: interpretation and action
,
2006,
Canadian Medical Association Journal.
[9]
K. Tsai,et al.
Methylmercury Induces Pancreatic β-Cell Apoptosis and Dysfunction
,
2006
.
[10]
D. Jacobs,et al.
A Strong Dose-Response Relation Between Serum Concentrations of Persistent Organic Pollutants and Diabetes
,
2006,
Diabetes Care.
[11]
K. Tsai,et al.
The Role of Phosphoinositide 3-Kinase/Akt Signaling in Low-Dose Mercury–Induced Mouse Pancreatic β-Cell Dysfunction In Vitro and In Vivo
,
2006,
Diabetes.
[12]
Michael C Henson,et al.
Endocrine Disruption by Cadmium, a Common Environmental Toxicant with Paradoxical Effects on Reproduction
,
2004,
Experimental biology and medicine.
[13]
Laszlo Magos,et al.
The toxicology of mercury--current exposures and clinical manifestations.
,
2003,
The New England journal of medicine.
[14]
I. Shapiro,et al.
Low-level methylmercury exposure causes human T-cells to undergo apoptosis: evidence of mitochondrial dysfunction.
,
1998,
Environmental research.
[15]
R. Schoeny,et al.
Mercury study report to Congress. Volume 1. Executive summary. Sab review draft
,
1996
.
[16]
J. Salonen,et al.
Intake of mercury from fish, lipid peroxidation, and the risk of myocardial infarction and coronary, cardiovascular, and any death in eastern Finnish men.
,
1995,
Circulation.
[17]
J. S. Woods,et al.
Studies on Hg(II)-induced H2O2 formation and oxidative stress in vivo and in vitro in rat kidney mitochondria.
,
1993,
Biochemical pharmacology.
[18]
K. Tsai,et al.
Methylmercury induces pancreatic beta-cell apoptosis and dysfunction.
,
2006,
Chemical research in toxicology.
[19]
L. Magos.
Physiology and toxicology of mercury.
,
1997,
Metal ions in biological systems.