ArticlePDF Available


Content may be subject to copyright.
Journal of Diabetes, Metabolic Disorders & Control
Impact of zinc on thyroid metabolism
Submit Manuscript |
is essential for normal functioning of metabolic homeostasis, immune
system, cell stimulation, enzyme activity, protection against oxidative
stress, and neural transmission.4,5 It works as co-enzyme factor for
many enzymes which are involved in various metabolic processes
and it is essential for sensitizing the tissues to thyroid hormone.6 Zinc
is also involved in cell differentiation, proliferation, cell repairing
and renewal. The importance of zinc in endocrine system is that it
effect on growth, endocrine homeostasis, and thyroid function and on
glucose metabolism.7 Deciency of zinc in the body may result in
decreased levels of secretion of thyroid hormones which affects the
normal metabolism of the body and resting metabolic rate. Some of
the studies shown that deciency of zinc is associated with enhanced
the expression of hepatic thyroxine-5’-monodeiodinase enzyme
activity which catalyses the thyroid hormone inactivation.8,9
Hypothyroidism and zinc
Zinc is essential trace element for normal levels of thyroid
hormones such as triiodothyronine (T3), tetraiodothyronine (T4), and
thyroid stimulating hormone (TSH) (Table 1). Some of the studies
showed that zinc deciency leads decrease in T3 level. The well known
effect of zinc on some endocrine glands such as pituitary- a master
gland and on hypothalamus is that it appears a role in the synthesis
of releasing hormone such as thyrotrophic releasing hormone (TRH).
Some of the studies showed that in hypothyroidism alteration in zinc
level. Patients with thyroid cancer have signicantly low level s of
zinc.10–12 In Hypothyroidism metabolic rate gets reduce which results
in adverse effect on organ system (Table 2).13 Hypothyroidism can
lead to number of complications in humans such as:
a) Mental health issues such as depression and also cause the slow
functioning of brain.
b) Heart problems because of increase in the level of Low density
lipoprotein (LDL) cholesterol. Sometimes it causes heart failure
and enlarges heart.
c) In hypothyroidism the low levels of thyroid hormone can alter the
process of ovulation which leads to infertility in women.
Hyperthyroidism and zinc
Consumption of high amount of zinc can contribute to
hyperthyroidism or Graves’ disease because zinc acts as a stimulator
to the thyroid gland. Patients suffering from hyperthyroidism have
higher amount of urinary excretion of zinc.14 Over activity of thyroid
gland or some other causes leads to hyperthyroidism (Table 3). When
tissues are exposed to higher concentrations of thyroid hormones then
some physiological, clinical and biochemical alterations occur in the
body (Table 4). Many studies shown that hyperthyroidism affects
many organ systems.15 Some of the researchers reported that zinc
is a fundamental component of enzymatic antioxidant system with
several antioxidant properties. Zinc is required in the body for optimal
activity of many hormones like thyroid hormone.16,17
Table 1 Causes of Hypothyroidism
Autoimmune disease Radiation Therapy
Thyroid surgery Treatment for hyperthyroidism
Medications Pregnancy
Iodine deciency Pituitary disorder
Congenital disorder
Table 2 Symptoms of Hypothyroidism
Elevated blood cholesterol
Muscle weakness, Muscle aches
and stiffness
Slowed heart rate Depression
Excessive sleepiness Constipation
Irregular menstrual periods Weight gain
Thinning of hair Dry skin and puffy face
Table 3 Causes of Hyperthyroidism
Excessive intake of iodine Hyperfunctioining of thyroid
Thyroid cancer Alteration in the secretion of TSH
Inammation in the thyroid
gland Grave’s disease
Postpartum thyroiditis Toxic thyroid adenoma
J Diabetes Metab Disord Control. 2018;5(1): 00134
Volume 5 Issue 1 - 2018
Sabina Khanam
Department of Biological Sciences, Yobe State University, Nigeria
Correspondence: Sabina Khanam, Department of Biological
Sciences, Yobe State University, Damaturu, Nigeria, Email
Received: October 22, 2017 | Published: February 26, 2018
Mini Review
Thyroid gland is the most important endocrine gland in human
body which performs various functions. Thyroid hormones such
as thyroxin and triiodothyronine are essential various metabolic
functions and also required for normal functions of body tissues.
These thyroid hormones affect metabolic rate and consumption on
oxygen.1 The most important constituent of thyroid hormones is
iodine. The geographical areas where the amount of iodine is less
thyroid dysfunction and diseases are very common. Thyroid disease
is the commonest endocrine disorder in the whole world. Thyroid
diseases are caused due to over secretion and under secretion of
thyroid hormones. These diseases are more common in females.2,3
Zinc is essential trace element for human body in limited amount. It
Citation: Khanam S. Impact of zinc on thyroid metabolism. J Diabetes Metab Disord Control. 2018;5(1): 00134. DOI: 10.15406/jdmdc.2018.05.00134
Impact of zinc on thyroid metabolism 28
©2018 Khanam
Table 4 Symptoms of Hyperthyroidism
Fast and Irregular heartbeat Vomiting , Nausea
Difculty in sleeping Weight loss
Increased appetite Dizziness and shortness of breath
Brittle hair and hair loss Development of breast in men
Congestive heart failure Protruding eyes
Fertility problems Paralysis
Increased sweating Light menstrual periods
Conict of interest
1. Kologlu S, Erdogan G. Thyroid: general remark and information. In:
Erdogan G, editor. Kologlu Endocrinology. Basis and Clinic. 2nd ed. Ankara:
Nobel Bookstore; 2005:155-72.
2. Fabrizio M. Classication of thyroid diseases: suggestions for a revision. J
Clin Endocrinol Metab. 2003;88(4):1428-1432.
3. Garber JR, Cobin RH, Gharib H, et al. Clinical practice guidelines for
hypothyroidism in adults: cosponsored by the American Association of
Clinical Endocrinologists and the American Thyroid Association. Endocr
Pract. 2012;18(6):988-1028.
4. Rundles-Cunningham S. Zinc modulation of immune function: Specicity
and mechanism of action. J Lab Clin Med. 1996;128(1):9-11.
5. King JC, Cousins RJ. Zinc. In: Shils ME, Shike M, Ross AC, Caballero B,
Cousins RJ, editors. Modern nutrition in health and disease. Philadelphia:
Lippincott Williams and Wilkins, 2006; 271-285.
6. Kaya S, Kececi T, Halilo S. Effect of zinc and vitamin supplements on
plasma level of thyroid hormone, cholesterol, glucose and egg yolk
cholesterol of laying hens. Res Vet Sci. 2001;71(2):135-139.
7. Maret W. Zinc in Human Disease. Met Ions Life Sci. 2013;13:389-414.
8. El-sisy GA, Abdel-Razek AM, Younis AA, et al. Effects of dietary zinc or
selenium supplementation on some reproductive hormone levels in
male Baladi Goats. Global Veternaria. 2008;2:46-50.
9. Oliver JW, Sachan DS, Su P, et al. Effects of zinc deciency on thyroid
function. Drug-Nutrient Interactions. 1987;5(2):113-124.
10. Brandao Neto J, Saturnino A, Leite LD De, et al. Lack of acute zinc
effect on thyrotropin releasing hormone-stimulated thyroid-stimulating
hormone secretion during oral zinc tolerance test in healthy men. Nutr
Res; 2006;26(10):493-496.
11. Majewask U, Braziewicz J, Banas D, et al. Zinc concentration in thyroid
tissue and whole blood of women with different diseases of thyroid. Biol
Trace Elem Res. 2001;80:193-199.
12. Kucharzewski M, Braziewich J, Majewska U, et al. Copper, zinc, and
selenium in whole blood and thyroid tissue of people with various
thyroid diseases. Biol Trace Elem Res. 2003;93(1-3):9-18.
13. Golden SH, Robinson KA, Saldanha I, et al. Clinical review: prevalence
and incidence of endocrine and metabolic disorders in the United States:
a comprehensive review. J Clin Endocrinol Metab. 2009;94(6):1853-1878.
14. Aihara K, Nishi Y, Hatano S, et al. Zinc, copper, manganese, and selenium
metabolism in thyroid disease. American Journal of Clinical Nutrition.
15. Ludgate M, Crips M, Lance C, et al. The thyrotropin receptor in thyroid
eye disease. Thyroid. 1998;8(5):411-423.
16. Formigari A, Irato P, Santon A. Zinc, antioxidant systems and
metallothionein in metal mediated-apoptosis: biochemical and
cytochemical aspects. Comp Biochem Physiol C Toxicol Pharmacol.
17. Catania AS, Barros CR, Ferreira SR. Vitamins and minerals with
antioxidant properties and cardio metabolic risk; controversies and
perspectives. Endocrinol Metabol. 2009;53(5):550-559.
... Its role is very complex in thyroid function and normal thyroid homeostasis (11). Zinc is a fundamental component needed by the body for the optimal activity of many organs, such as thyroid hormone secretion (12). Zinc is an important micronutrient for human health because it has many structural and biochemical functions. ...
... Zinc affects growth factors, endocrine homeostasis, thyroid function, and glucose metabolism. Zinc deficiency in the body can cause a decrease in the level of thyroid hormone secretion, which affects the body's normal metabolism and metabolic rate at rest (12). The results of this study are not in line with those found by Nishi et al., who reported abnormal zinc metabolism in patients with thyroid dysfunction (17). ...
... A study by Sinha et al. also reported a correlation between zinc deficiency and hyperthyroidism (16). Khanam reported that zinc deficiency can cause hypothyroidism (12). ...
Full-text available
Introduction: Melasma is an acquired hyperpigmentation disorder, clinically identified by symmetrical blackish-brown macules, especially on the facial area. Several factors are thought to play a role, including thyroid dysfunction and zinc deficiency. The aim of this study was to determine serum zinc levels in melasma and non-melasma patients with and without thyroid dysfunction. Methods: A cross-sectional study was conducted in Jakarta in September 2019. There were 60 melasma patients and 60 non-melasma patients. The two groups were matched for age and sex. Atomic absorption spectrophotometry was used to measure serum zinc levels. Blood laboratory tests were used to check thyroid function by measuring thyroid stimulating hormone and free T4. Statistical analysis was performed using SPSS software. Results: The mean serum zinc level in the melasma group was 10.25 ± 1.89 μmol/l and in the non-melasma group 10.29 ± 1.46 μmol/l (< 0.901). The mean serum zinc level in melasma patients with thyroid dysfunction was 8.77 ± 0.69 μmol/l, in melasma patients without thyroid dysfunction 10.33 ± 1.89 μmol/l, in non-melasma patients with thyroid dysfunction 10.48 ± 2.4 μmol/l, and in non-melasma patients without thyroid dysfunction 10.27 ± 1.4 μmol/l (< 0.184). Conclusions: There was no significant difference between serum zinc levels in the melasma and non-melasma groups with and without thyroid dysfunction.
... Вміст цинку та кобальту в раціоні обстежених також був зниженим. Дослідження показали важливу роль цинку в обміні гормонів ЩЗ, зокрема в регуляції активності дейодиназ та синтезі ТТГ, а також впливі на фактори транскрипції, що беруть участь у синтезі тиреоїдних гормонів [41][42]. Стосовно кобальту, дані щодо його впливу на функціонування ЩЗ суперечливі. ...
... However, DIT, T 3 , and T 4 levels were found to be reduced significantly which can be correlated with the reduced levels of T 3 and T 4 in the serum as observed in the present study. The T 3 and T 4 levels were found to be elevated significantly when combined lithium and zinc-treated animals were compared with lithium-treated rats alone (Table 6), thus indicating that zinc is playing a protective role in the regulation of the levels of T 3 and T 4 [26]. ...
Full-text available
Lithium is an integral drug used in the management of acute mania, unipolar and bipolar depression, and prophylaxis of bipolar disorders. Thyroid abnormalities have been associated with treatment with lithium. Zinc is an essential trace element that plays a role in several biological activities. Therefore, the present study was aimed at investigating the potential role of zinc in the thyroid gland following lithium administration to explore the role of zinc under such conditions. To achieve this goal, male Wistar rats (150–195 g) were divided into four groups: Group 1 animals were fed standard pellet feed and tap water ad lib; Group 2 rats were fed lithium in the form of lithium carbonate through diet at a concentration of 1.1 g/kg body weight; Group 3 animals received zinc treatment in the form of zinc sulfate (ZnSO4·7H2O) at a dose level of 227 mg/L mixed with drinking water of the animals; and Group 4 animals were given lithium and zinc in a similar manner as was given to the animals belonging to groups 2 and 4 respectively. The role of zinc on thyroid functions in lithium-treated rats was studied after 2, 4, and 8 weeks of different treatments. Zinc has been observed to have the capability to nearly normalize the altered 2-h uptake of 131I, biological and effective half-lives of 131I, and circulating T4 levels that were altered after lithium treatment. The present study concludes that zinc may be an effective agent in normalizing the adverse effects caused by lithium on thyroid functions.
... In hypothyroidism, the low levels of thyroid hormone can alter the process of ovulation which leads to infertility in women [8]. ...
Full-text available
The thyroid produces and secretes adequate amounts of hormones that regulate various physiological processes, including growth, development, metabolism, and reproductive function. The production and metabolism of thyroid hormones are dependent on micronutrients such as iodine, selenium, zinc and iron. Iodine is essential for the proper synthesis of thyroid hormones. The risk of iodine deficiency is high in places where the food consumed comes from iodine-deficient sources. To avoid complications, various government strategies have been developed to enrich food with this element. Selenium is incorporated in the deiodinases, which are enzymes that also play an essential role in the metabolism of thyroid hormones, in addition to contributing to the antioxidant defense in the thyroid. Zinc participates in the process of deiodination, in addition to being necessary for the T3 receptor to adopt its biologically active confirmation. Iron is found in hemeproteins, including thyroid peroxidase (TPO), which participates in the first two stages of thyroid hormone biosynthesis. Deficiencies of these elements can impair thyroid function. In general, the influence of micronutrients on thyroid function reveals the need for more research to increase scientific knowledge so that preventive and therapeutic measures can be taken regarding thyroid dysfunctions, to maintain a healthy thyroid.
Full-text available
Oxygen reactive species (ROS) are generated during cellular processes. In excess, they may cause damages to the cell. Oxidative stress is an imbalance in the redox state that favors oxidation. Endogenous enzymes and some vitamins and minerals participate in the plasma antioxidant defense. Vitamin E is found in the plasma and in the LDL particle, avoiding lipid peroxidation. Observational studies reported an inverse association between vitamin E consumption and cardiometabolic (CM) risk. However, clinical trials were not able to prove the efficacy of its supplementation on CM endpoints. Vitamin C participates in the vitamin E regeneration system, keeping the plasma's antioxidant potential. Data about beneficial effects of its supplementation in CM risk reduction are inconclusive. The antioxidant activity of carotenoids is partially responsible for its protective role against cardiovascular diseases and cancer. Supplementation of this nutrient did not provide consistent findings in terms of CM risk reduction. Recently, zinc and selenium's participation in the antioxidant defense has been studied, yet its supplementation in individuals with normal levels and adequate ingestion of these nutrients does not seem necessary. In summary, the role of these micronutrients for CM risk is still very controversial. Epidemiological studies suggest that diets rich in antioxidants, or simply in fruit and vegetables intake, can reduce CM risk. Further studies are needed before recommending antioxidant supplements for this purpose.
The vast knowledge of the physiologic functions of zinc in at least 3000 proteins and the recent recognition of fundamental regulatory functions of zinc(II) ions released from cells or within cells links this nutritionally essential metal ion to numerous diseases. However, this knowledge so far has had remarkably limited impact on diagnosing, preventing, and treating human diseases. One major roadblock is a lack of suitable biomarkers that would detect changes in cellular zinc metabolism and relate them to specific disease outcomes. It is not only the right amount of zinc in the diet that maintains health. At least as important is the proper functioning of the dozens of proteins that control cellular zinc homeostasis, regulate intracellular traffic of zinc between the cytosol and vesicles/organelles, and determine the fluctuations of signaling zinc(II) ions. Cellular zinc deficiencies or overloads, a term referring to zinc concentrations exceeding the cellular zinc buffering capacity, compromise the redox balance. Zinc supplementation may not readily remedy zinc deficiency if other factors limit the capability of a cell to control zinc. The role of zinc in human diseases requires a general understanding of the wide spectrum of functions of zinc, how zinc is controlled, how it interacts with the metabolism of other metal ions, in particular copper and iron, and how perturbation of specific zinc-dependent molecular processes causes disease and influences the progression of disease.
Objective Hypothyroidism has multiple etiologies and manifestations. Appropriate treatment requires an accurate diagnosis and is influenced by coexisting medical conditions. This paper describes evidence-based clinical guidelines for the clinical management of hypothyroidism in ambulatory patients. Methods The development of these guidelines was commissioned by the American Association of Clinical Endocrinologists (AACE) in association with American Thyroid Association (ATA). AACE and the ATA assem bled a task force of expert clinicians who authored this article. The authors examined relevant literature and took an evidence-based medicine approach that incor porated their knowledge and experience to develop a series of specific recommendations and the rationale for these recommendations. The strength of the recommen dations and the quality of evidence supporting each was rated according to the approach outlined in the American Association of Clinical Endocrinologists Protocol for Standardized Production of Clinical Guidelines—2010 update. Results Topics addressed include the etiology, epide miology, clinical and laboratory evaluation, management, and consequences of hypothyroidism. Screening, treatment of subclinical hypothyroidism, pregnancy, and areas for future research are also covered. Conclusions Fifty-two evidence-based recommenda tions and subrecommendations were developed to aid in the care of patients with hypothyroidism and to share what the authors believe is current, rational, and optimal medi cal practice for the diagnosis and care of hypothyroidism. A serum thyrotropin is the single best screening test for primary thyroid dysfunction for the vast majority of outpa tient clinical situations. The standard treatment is replace ment with L-thyroxine. The decision to treat subclinical hypothyroidism when the serum thyrotropin is less than 10 mIU/L should be tailored to the individual patient.
It is known that zinc interacts with thyroid hormones, altering plasma thyroid-stimulating hormones (TSH), triiodothyronine (T3), and tetraiodothyronine (T4) in rats and humans. To investigate whether zinc affects thyrotropin-releasing hormone (TRH)–stimulated TSH, 5 healthy men were tested at 8:00 am after an overnight fast. Elemental zinc (37.5 mg, as heptahydrated zinc sulfate) was administered orally, and TRH (200 μg) was administered intravenously for 1 minute. Blood samples were collected from an antecubital vein at −30, 0, 30, 60, 90, 150, 210, 240, 270, and 300 minutes. Serum zinc remained constant throughout the control period. However, serum zinc was significantly elevated after oral zinc administration in the experimental group (P < .05). Plasma TSH levels increased after TRH injection in the control and in the experimental group, although not significantly when comparing both groups. Moreover, no significant areas under the curves and no correlation between serum zinc and plasma TSH levels were detected in both groups studied. This is the first study that showed the relationship between TRH-stimulated TSH secretion during oral zinc tolerance test in healthy men. These results suggest that a single oral dose of zinc did not change TSH secretion after TRH injection. Furthermore, acute increases in blood TRH and TSH did not alter serum zinc levels.
There has not been a comprehensive compilation of data regarding the epidemiology of all endocrine and metabolic disorders in the United States. We included 54 disorders with clinical and public health significance. We identified population-based studies that provided U.S. prevalence and/or incidence data by searching PubMed in December 2007 for English-language reports, hand-searching reference lists of six textbooks of endocrinology, obtaining additional resources from identified experts in each subspecialty, and searching epidemiological databases and web sites of relevant organizations. When available, we selected articles with data from 1998 or later. Otherwise, we selected the article with the most recent data, broadest geographical coverage, and most stratifications by sex, ethnicity, and/or age. Ultimately, we abstracted data from 70 articles and 40 cohorts. Endocrine disorders with U.S. prevalence estimates of at least 5% in adults included diabetes mellitus, impaired fasting glucose, impaired glucose tolerance, obesity, metabolic syndrome, osteoporosis, osteopenia, mild-moderate hypovitaminosis D, erectile dysfunction, dyslipidemia, and thyroiditis. Erectile dysfunction and osteopenia/osteoporosis had the highest incidence in males and females, respectively. The least prevalent conditions, affecting less than 1% of the U.S. population, were diabetes mellitus in children and pituitary adenoma. Conditions with the lowest incidence were adrenocortical carcinoma, pheochromocytoma, and pituitary adenomas. Certain disorders, such as hyperparathyroidism and thyroid disorders, were more common in females. As expected, the prevalence of diabetes mellitus was highest among ethnic minorities. Sparse data were available on pituitary, adrenal, and gonadal disorders. The current review shows high prevalence and incidence of common endocrine and metabolic disorders. Defining the epidemiology of these conditions will provide clues to risk factors and identify areas to allocate public health and research resources.
Interactive combinations of altered zinc and thyroid states were studied in rats to assess pathophysiologic effects. Clinical signs of zinc deficiency or thyroid alteration were limited to effects on growth rate. Changes in organ and glandular weights and serum thyrotropin levels reflected changes in serum thyroid hormone concentrations. Significantly (probability less than .001), zinc-deficient rats had enhanced hepatic thyroxine-5'-monodeiodinase activity. In addition, the zinc-deficient state was found to be protective against thiouracil-induced suppression of the microsomal-monooxygenase and thyroxine-5'-monodeiodinase enzyme complex. This protective effect was evident by greater thyroxine-5'-monodeiodinase and reduced nicotinamide-adenine dinucleotide phosphate cytochrome c reductase activities, as well as cytochrome P-450 content, in zinc-deficient/thiouracil-treated animals. Thus, the enzyme complex had increased triiodothyronine-generating capacity in conditions of zinc deficiency, which may be important because of the greater biological reactivity of triiodothyronine. Primary zinc deficiency conditions of the magnitude seen in this study and in this-age rat did not appear to alter serum thyroid hormone levels or organ/glandular function. However, concurrent zinc deficiency and altered thyroid status did change thyroid hormone response and disposition, which may be important to populations at risk because of thyroid dysfunctional states.
This study was designed to evaluate trace metal metabolism in adults with thyroid diseases. Erythrocyte zinc values were significantly lower than normal in hyperthyroidism and higher in hypothyroidism. A significantly higher than normal urinary excretion of zinc was observed in hyperthyroidism. The mean concentrations of plasma and erythrocyte copper were significantly above normal in hyperthyroidism. Plasma selenium levels were significantly lower than normal in hyperthyroidism. No statistically significant difference was found in plasma zinc, erythrocyte manganese, or urine copper values between patients with thyroid diseases and healthy controls. The erythrocyte manganese content correlated well with thyroxine and triiodothyronine levels. Plasma prealbumin and retinol-binding protein correlated well with the erythrocyte zinc content but not with plasma zinc levels. There was no correlation between erythrocyte superoxide dismutase activity and erythrocyte copper or zinc concentrations. The results of this study suggest that the metabolism of zinc, copper, manganese, and selenium is abnormal in thyroid diseases.
Thyroid eye disease (TED) has an autoimmune etiology, but the nature of the autoantigen that is the target of the initiating event remains unknown. A number of candidates have been proposed based on Western blotting, library screening, and deduction from sequence similarity. A strong favorite is the thyrotropin receptor (TSHR), which is the target of the thyroid stimulating antibodies (TSAB) of Graves' disease (GD). We have recently demonstrated TSHR transcripts in orbital adipose tissue from a patient with TED by Northern blot, transcripts in normal adipose tissue being at the limit of detection. We have shown that the transcripts are translated into protein by immunohistochemical analysis using two monoclonal antibodies to the TSHR generated by genetic immunization. TSHR immunoreactivity is associated with elongated cells with the appearance of a fibroblast, often adjacent to clusters of adipocytes, in orbital biopsies from patients with TED but not in strabismus or pseudotumor biopsies. In animal studies, we have transferred thyroiditis to naive BALBc and NOD mice, using T cells primed to the human TSHR, either using the receptor expressed as a bacterial fusion protein or by genetic immunization. The BALBc develop a Th2-type response to the receptor, but the NOD a Th1-type with thyrocyte destruction. Orbital pathology, edema, infiltration by mast cells and lymphocytes, and adipose accumulation was also induced in 68% of the BALBc but none of the NOD mice. Together these data indicate that the preadipocyte expresses the TSHR and that a Th2 autoimmune response to the receptor may be an initiating event in TED.
The Zn concentration in thyroid tissue and whole blood of patients with Graves' disease, thyroid cancer, and nodular goiter disease was determined using the total-reflection X-ray fluorescence method. The dependence of obtained concentrations on the clinical stage of the examined disease, histopathological grading, and kind of analyzed material (thyroid tissue and blood) was studied. The determined concentration of Zn was the lowest in the thyroid tissue of patients with thyroid cancer (23.1 microg/g) and it was the highest in the case of Graves' disease (41.7 microg/g), whereas in the blood samples, the reverse results were found (7.1 microg/g and 4.8 microg/g, respectively). The physical basis of the method used, the experimental setup, and the procedure of sample preparation are described.