An Overview of Boron, Lithium, and Strontium in Human Health and Profiles of These Elements in Urine of Japanese

The biological, medical and environmental roles of trace elements have attracted considerable attention over the years. In spite of their relevance in nutritional, occupational and toxicological aspects, there is still a lack of consistent and reliable measurement techniques and reliable information on reference values. In this review our understandings of the urinary profilings of boron, lithium and strontium are summarized and fundamental results obtained in our laboratory are discussed. Over the past decade we have successfully used inductively coupled plasma emission spectrometry for the determination of reference values for urinary concentrations of boron, lithium and strontium. Taking into account the short biological half-life of these elements and the fact that their major excretion route is via the kidney, urine was considered to be a suitable material for monitoring of exposure to these elements. We confirmed that urinary concentrations of boron, lithium and strontium follow a lognormal distribution. The geometric mean reference values and 95% confidence intervals were 798 μg/l (398–1599 μg/l) for boron, 23.5 μg/l (11.0–50.5 μg/l) for lithium and 143.9 μg/l (40.9–505.8 μg/l) for strontium. There were no discrepancies between our values and those previously reported. Our reference values and confidential intervals can be used as guidelines for the health screening of Japanese individuals to evaluate environmental or occupational exposure to these elements.

An overview of boron, lithium, and strontium in human health and profiles of these elements in urine of Japanese

The biological, medical and environmental roles of trace elements have attracted considerable attention over the years. In spite of their relevance in nutritional, occupational and toxicological aspects, there is still a lack of consistent and reliable measurement techniques and reliable information on reference values. In this review our understandings of the urinary profilings of boron, lithium and strontium are summarized and fundamental results obtained in our laboratory are discussed.Over the past decade we have successfully used inductively coupled plasma emission spectrometry for the determination of reference values for urinary concentrations of boron, lithium and strontium. Taking into account the short biological half-life of these elements and the fact that their major excretion route is via the kidney, urine was considered to be a suitable material for monitoring of exposure to these elements. We confirmed that urinary concentrations of boron, lithium and strontium follow a lognormal distribution. The geometric mean reference values and 95% confidence intervals were 798 μg/l (398-1599 μg/l) for boron, 23.5 μg/l (11.0-50.5 μg/l) for lithium and 143.9 μg/l (40.9-505.8 μg/l) for strontium. There were no discrepancies between our values and those previously reported. Our reference values and confidential intervals can be used as guidelines for the health screening of Japanese individuals to evaluate environmental or occupational exposure to these elements.

Determination of Reference Concentrations of Strontium in Urine by Inductively Coupled Plasma Atomic Emission Spectrometry

Objective: The aim of this study was to establish reference concentrations of urinary strontium by inductively coupled plasma atomic emission spectrometry (ICP-AES). Methods: For the determination of strontium, urine samples were collected from healthy Japanese (n=146; 115 males, 31 females; mean age, 33±9 years; age range, 18 to 58 years). The urine samples stored at or below −20°C were thawed with incubation at 40°C for 30 min and sediments were dissolved by vigorous shakings. Then, the samples were centrifuged at 3000 g for 5 min, and the supernatant was directly aspired into a P-5200-3600/1200 ICP-AES system from Hitachi Ltd., Tokyo, Japan. Results: A steeper increase in the S/N ratio and a good effective linearity of the calibration line was obtained at 407.771 nm in the range of 0–300 μg/L strontium standard solution. Urine samples having the same background signal as that of 18 MΩ cm ultrapure blank water, a good correspondence of the single peak pattern of the spectra, accuracy and precision of spike recovery were also confirmed. Urinary strontium concentrations showed a log-normal distribution and a geometric mean concentration of 143.9 μg/L, with 5–95% confidential interval of 40.9–505.8 μg/L. Conclusion: The results of this study will be useful as guidelines for the biological monitoring of strontium in normal subjects and in individuals therapeutically or environmentally exposed to strontium.

Determination of reference concentrations of strontium in urine by inductively coupled plasma atomic emission spectrometry

<p><b>OBJECTIVE</b>The aim of this study was to establish reference concentrations of urinary strontium by inductively coupled plasma atomic emission spectrometry (ICP-AES).</p><p><b>METHODS</b>For the determination of strontium, urine samples were collected from healthy Japanese (n=146; 115 males, 31 females; mean age, 33±9 years; age range, 18 to 58 years). The urine samples stored at or below -20°C were thawed with incubation at 40°C for 30 min and sediments were dissolved by vigorous shakings. Then, the samples were centrifuged at 3000 g for 5 min, and the supernatant was directly aspired into a P-5200-3600/1200 ICP-AES system from Hitachi Ltd., Tokyo, Japan.</p><p><b>RESULTS</b>A steeper increase in the S/N ratio and a good effective linearity of the calibration line was obtained at 407.771 nm in the range of 0-300 μg/L strontium standard solution. Urine samples having the same background signal as that of 18 MΩ cm ultrapure blank water, a good correspondence of the single peak pattern of the spectra, accuracy and precision of spike recovery were also confirmed. Urinary strontium concentrations showed a log-normal distribution and a geometric mean concentration of 143.9 μg/L, with 5-95% confidential interval of 40.9-505.8 μg/L.</p><p><b>CONCLUSION</b>The results of this study will be useful as guidelines for the biological monitoring of strontium in normal subjects and in individuals therapeutically or environmentally exposed to strontium.</p>

Hepatic injury and gluconeogenesis after subcutaneous injection of monochloroacetic acid in rats

<p><b>OBJECTIVE</b>Monochloroacetic acid (MCA) is corrosive to skin, and causes not only chemical injury but also fatal systemic poisoning. Little is known about the cause of death. We studied the acute toxicity of MCA before clinical symptoms appeared in fasting rats.</p><p><b>METHODS</b>Blood samples were analyzed 2 h after subcutaneous MCA injection (Ld(90): 162 mg/ml kg body weight). Control rats were injected with saline.</p><p><b>RESULTS</b>Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were about 1.5-fold higher than in the controls, and mitochondrial AST (mAST) was 2-fold higher. Blood urea nitrogen and creatinine were significantly increased, while serum glucose was significantly decreased in the treated group. Lactate was 6-fold higher and pyruvate was 13-fold higher than in the controls.</p><p><b>CONCLUSIONS</b>MCA caused injury to the liver and kidneys but these injuries were slight. However, the larger increase in mAST indicated that hepatocellular mitochondria were selectively targeted. Hepatocellular mitochondrial injury decreased gluconeogenesis and caused hypoglycemia and extremely high levels of lactate and pyruvate. Hypoglycemia and lactic acidosis were insidious before the critical symptoms appeared and this combination accelerated to death, affecting other organs such as the heart and brain. Nosotropic therapy of these abnormalities up to the appearance of symptoms may help to establish an early therapy for skin exposure to MCA.</p>

Hepatic Injury and Gluconeogenesis After Subcutaneous Injection of Monochloroacetic Acid in Rats

Objective: Monochloroacetic acid (MCA) is corrosive to skin, and causes not only chemical injury but also fatal systemic poisoning. Little is known about the cause of death. We studied the acute toxicity of MCA before clinical symptoms appeared in fasting rats. Methods: Blood samples were analyzed 2 h after subcutaneous MCA injection (LD90: 162 mg/ml kg body weight). Control rats were injected with saline. Results: Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were about 1.5-fold higher than in the controls, and mitochondrial AST (mAST) was 2-fold higher. Blood urea nitrogen and creatinine were significantly increased, while serum glucose was significantly decreased in the treated group. Lactate was 6-fold higher and pyruvate was 13-fold higher than in the controls. Conclusions: MCA caused injury to the liver and kidneys but these injuries were slight. However, the larger increase in mAST indicated that hepatocellular mitochondria were selectively targeted. Hepatocellular mitochondrial injury decreased gluconeogenesis and caused hypoglycemia and extremely high levels of lactate and pyruvate. Hypoglycemia and lactic acidosis were insidious before the critical symptoms appeared and this combination accelerated to death, affecting other organs such as the heart and brain. Nosotropic therapy of these abnormalities up to the appearance of symptoms may help to establish an early therapy for skin exposure to MCA.